Use of asarone in the preparation of a medicament for treating and / or preventing eye diseases and a composition and use thereof

Abstract

This invention provides the application of asarone in the preparation of drugs for treating and / or preventing eye diseases, and a composition thereof, belonging to the field of biomedical technology. The asarone composition of this invention comprises the following components: asarone, soybean oil, egg yolk lecithin, glycerol, sodium hydroxide, and water, wherein the asarone includes at least one of α-asarone, β-asarone, and γ-asarone. The asarone or asarone composition of this invention, administered via eye drops, oral administration, or injection, can effectively reduce intraocular pressure, protect retinal ganglion cells, improve retinal function, reduce vascular leakage caused by neovascular age-related macular degeneration, and reduce MDA content in the retinal tissue of optic neuritis and cataracts, reduce retinal cell apoptosis in diabetic retinopathy, and increase tear secretion in rats with dry eye. This invention provides an effective basis for the treatment and / or prevention of the aforementioned eye diseases using asarone.

Description

Technical Field

[0001] This invention relates to the field of biomedical technology, and more particularly to the use of α-asarone in the preparation of medicaments for the treatment and / or prevention of eye diseases, and a composition thereof. Background Technology

[0002] The optic nerve is composed of axons from retinal ganglion cells (RGCs), which converge at the optic disc, pass through the cribriform lamina of the sclera, run posteriorly within the eye socket, and then penetrate the optic canal into the cranial fossa, connecting to the diencephalon via the optic chiasm and optic tract. As the optic nerve is part of the visual organ formed by the outward projection of the brain during embryonic development, it belongs to the central nervous system. Its three layers of sheath, covered by the dura mater, arachnoid mater, and pia mater, are also continuations of the three layers of meninges. The optic nerve is a crucial component of the visual pathway, transmitting visual information acquired by the retina to the brain. Due to its anatomical characteristics, the optic nerve is easily damaged, including primary injuries from direct mechanical trauma, axonal interruption, and shear stress, as well as secondary injuries caused by inflammation, neurotoxic factors, and vascular dysfunction. Statistics show that 0.5%–5% of closed head injuries are accompanied by optic nerve injury, primarily affecting young adults. Optic nerve injury can cause secondary death of retinal ganglion cells and axonal degeneration, leading to severe visual impairment such as decreased vision, visual field defects, and color vision loss, ultimately resulting in irreversible vision loss. The low regenerative capacity of residual surviving retinal ganglion cells after optic nerve injury, the lack of neurotrophic factors, the formation of glial scars, and the inhibitory environment of myelin further limit the recovery of visual function. Optic nerve injury is a serious disease that causes great inconvenience to patients' lives and is difficult for clinicians to treat, placing a heavy burden on patients' families and society. Many ophthalmological diseases are closely related to optic nerve damage, such as glaucoma, optic neuritis, traumatic optic nerve injury, and diabetic retinopathy.

[0003] Glaucoma is a disease characterized by intermittent or persistent elevation of intraocular pressure, with optic nerve atrophy and visual field defects as common features. Pathological elevation of intraocular pressure is its main risk factor. Sustained high intraocular pressure can damage various tissues of the eyeball and visual function, causing decreased vision and narrowed visual field. It is a blinding eye disease characterized by progressive visual field defects, leading to irreversible and non-selective death of retinal ganglion cells. Clinically, glaucoma is classified into primary glaucoma, angle-closure glaucoma, open-angle glaucoma, secondary glaucoma, and congenital glaucoma. Treatment strategies include promoting optic nerve repair, ferroptosis, pyroptosis, glutamate excitotoxicity, and oxidative stress. However, due to the complexity of the pathogenesis of glaucoma, the understanding of these factors and their interactions is still incomplete, and there remains a significant unmet clinical need for glaucoma treatment.

[0004] Optic neuritis (ON) refers to all inflammatory lesions related to the optic nerve, with decreased or lost vision as the main clinical manifestation, with or without pain on eye movement, and usually affecting only one eye. Internationally, ON is often divided into typical ON and atypical ON. Typical ON is an idiopathic inflammatory demyelinating disease, usually associated with multiple sclerosis (MS), and is mostly unilateral and subacute, with patients experiencing decreased vision within hours or days of onset. Atypical ON is often associated with autoimmune diseases and infectious diseases, and is divided into ON associated with neuromyelitis optica spectrum disorder (NMOSD), chronic relapsing inflammatory optic neuropathy, and ON associated with systemic diseases. Currently, the main treatments for ON include hormone therapy, immunosuppression, MS correction therapy, plasma exchange, immunoadsorption, as well as traditional Chinese medicine compound therapy and acupuncture. The above therapies have problems such as significant adverse reactions and poor treatment compliance, therefore, the development of new drugs for the treatment of ON is of great significance.

[0005] Diabetic retinopathy (DR) is one of the most common eye complications in diabetic patients. With the increasing global prevalence of diabetes, the global prevalence of DR is also increasing. The International Diabetes Federation estimates that by 2045, there will be 700 million people with type 1 and type 2 diabetes worldwide, with approximately 6% of them experiencing vision-threatening DR. If DR is not treated promptly, it can lead to retinal edema, hemorrhage, and neovascularization, potentially causing retinal detachment and, in severe cases, threatening vision. The causes of DR are currently unclear. Based on the severity and characteristics of the lesions, DR is generally classified into non-proliferative and proliferative types. Non-proliferative diabetic retinopathy (NPDR) manifests as microaneurysms and microaneurysmal lesions; while proliferative diabetic retinopathy (PDR) mainly involves neovascularization, which can lead to severe retinal detachment. Current treatment methods include retinal laser photocoagulation, anti-VEGF drugs, corticosteroids, and combination therapies.

[0006] Neovascular age-related macular degeneration (nAMD) is characterized by choroidal neovascularization (CNV) in the macular region or retinal neovascularization, and may also be accompanied by retinal edema, retinal exudates, hemorrhages, and scarring. Its pathogenesis is currently unclear, but it is likely related to multiple factors including age, environment, genetics, oxidative stress, lipid metabolism, and immune response. Vascular endothelial growth factor (VEGF) has been shown to play a crucial role in neovascularization in nAMD. Currently, anti-VEGF therapy has become the most important targeted treatment for nAMD patients. However, anti-VEGF therapy also presents many challenges and difficulties, such as the need for multiple intravitreal injections, progression of macular atrophy during treatment, formation of retinal fibrosis, and patients' vision returning to baseline levels after 5 years of treatment. Furthermore, some patients have poor or no response to anti-VEGF therapy. Therefore, exploring new treatment strategies to achieve better therapeutic effects is of great significance.

[0007] Cataracts are caused by damage to the lens capsule due to various factors, leading to increased permeability and loss of its barrier function, or causing metabolic disorders in the lens, resulting in lens protein denaturation and clouding. The pathogenesis of cataracts is related to oxidative stress, apoptosis, autophagy, and epithelial-mesenchymal transition. Currently, there is no effective drug treatment for cataracts. Early-stage cataracts are often treated with eye drops, while mid-to-late-stage patients are primarily treated surgically. Therefore, developing drugs that can treat or slow the progression of cataracts is of great significance.

[0008] Dry eye syndrome (Xerophthalmia), also known as keratoconjunctivitis sicca, is one of the most common ophthalmic diseases caused by insufficient lacrimal secretion due to various ocular and / or systemic factors, leading to abnormal tear film and dry ocular surface epithelium. It is an ocular surface disease caused by various impairments in the natural function and protective mechanisms of the external eye, resulting in tear film instability during blinking. Clinically, it is often classified according to the cause of insufficient tear production into aqueous tear deficiency (ATD) and lipid tear deficiency (LTD), primarily due to immune inflammation and apoptosis, and hormonal changes. Current treatments include artificial tears, immunomodulators, and surgery, but the effects are often unsatisfactory.

[0009] In summary, there are currently no effective drugs available in clinical practice for the prevention and treatment of the aforementioned eye diseases. Summary of the Invention

[0010] To address the aforementioned problems, the present invention provides the use of asarone in the preparation of medicaments for treating and / or preventing eye diseases, and a composition thereof.

[0011] To achieve the above-mentioned objectives, the present invention provides the following technical solution:

[0012] This invention provides the use of asarone in the preparation of medicaments for the treatment and / or prevention of eye diseases, including retinal ganglion cell damage diseases as well as macular degeneration, cataracts, or dry eye syndrome.

[0013] Preferably, the retinal ganglion cell damage disease includes glaucoma, optic neuritis, or diabetic retinopathy.

[0014] The present invention also provides a composition comprising at least one of α-asarone, β-asarone, and γ-asarone at an effective concentration, preferably α-asarone, wherein the final concentration of α-asarone is 0.5–30 g / L. The structural formulas of α-asarone, β-asarone, or γ-asarone are shown below:

[0015]

[0016] Preferably, the composition further includes an oil solvent, an emulsifier, an osmotic pressure regulator, a pH regulator, and water.

[0017] Preferably, the oil solvent includes soybean oil, the emulsifier includes egg yolk lecithin, the osmotic pressure regulator includes glycerol, and the pH regulator includes sodium hydroxide.

[0018] Preferably, the dosage form of the composition is an eye drop, an oral preparation, or an injection.

[0019] Preferably, the eye drops use water as a solvent and contain the following components at the following concentrations: asarum 0.5-5 g / L, soybean oil 4-50 g / L, egg yolk lecithin 1-15 g / L, glycerin 2-25 g / L, and sodium hydroxide 0.001-0.005 g / L.

[0020] Preferably, the oral or injectable preparation uses water as a solvent and contains the following components at the following concentrations: α-asarone 4-30 g / L, soybean oil 80-300 g / L, egg yolk lecithin 10-20 g / L, glycerol 20-30 g / L, and sodium hydroxide 0.02-0.1 g / L.

[0021] The present invention also provides the use of the described composition in the preparation of medicaments for the treatment and / or prevention of eye diseases, including glaucoma, optic neuritis, diabetic retinopathy, macular degeneration, cataracts, or dry eye syndrome.

[0022] By adopting the above technical solution, the present invention has the following beneficial effects: The asarone composition of the present invention comprises at least one of α-asarone, β-asarone, and γ-asarone, preferably α-asarone, soybean oil, egg yolk lecithin, glycerol, sodium hydroxide, and water. When the asarone or asarone composition of the present invention is administered via eye drops, oral administration, or injection, it can effectively reduce intraocular pressure, protect retinal ganglion cells, improve retinal function, reduce vascular leakage caused by neovascular age-related macular degeneration, and reduce MDA content in the retinal tissue of optic neuritis and cataracts, reduce retinal cell apoptosis in diabetic retinopathy, and increase tear secretion in rats with dry eye. The present invention provides an effective basis for the treatment and / or prevention of the above-mentioned eye diseases using α-asarone. Attached Figure Description

[0023] Figure 1 The intraocular pressure (IOP) statistics for Example 3 are as follows: one week of pre-administration and model establishment followed by one to four weeks of further administration (n=10).

[0024] Figure 2 The following is a statistical chart of the dark adaptation 3.0 ERG a-wave amplitude of each group (n=10) after one week of pre-administration and modeling followed by 1 to 4 weeks of further administration in Example 3.

[0025] Figure 3 The following is a statistical chart of the dark adaptation 3.0 ERG b-wave amplitude of each group (n=10) after one week of pre-administration and modeling followed by 1 to 4 weeks of further administration in Example 3.

[0026] Figure 4 The chart shows the statistical changes in the amplitude of visual evoked potentials (F-VEP) in each group after one week of pre-administration and two weeks of modeling in Example 4 (n=8).

[0027] Figure 5 The images show the retinal thickness of each group (n=10) after one week of pre-administration and two weeks of post-modeling in Example 4. Compared with the model control group, ***P<0.001.

[0028] Figure 6 The following is a statistical chart of the dark-adapted ERG a-wave amplitude of each group (n=10) after one week of pre-administration and two weeks of modeling in Example 5.

[0029] Figure 7 The following is a statistical chart of the dark-adapted ERG b-wave amplitude of each group (n=10) after one week of pre-administration and two weeks of modeling in Example 5.

[0030] Figure 8 The chart shows the statistical changes in the amplitude of visual evoked potentials (F-VEP) in each group after one week of pre-administration and two weeks of modeling in Example 5 (n=8).

[0031] Figure 9 Example 6 shows the leakage level scores of fundus angiography images of each group after 3 days of pre-administration and 7 days of modeling. Compared with the model control group, *P<0.05.

[0032] Figure 10 Example 6 shows the statistical chart of the maximum central thickness of the choroidal vascular bundle (CNV) in each group (n=8) after pre-administration for 3 days and modeling followed by 7 days of further administration.

[0033] Figure 11 The bar chart shows the effect of α-asarone on glutamate-induced apoptosis in R28 cells in Example 7 (n=6).

[0034] Figure 12 The chart shows the statistical content of MDA in the retina of rats in each group in Example 8 (n=10).

[0035] Figure 13 This is a statistical graph showing the number of apoptotic retinal cells in each group of Example 9 (n=10).

[0036] Figure 14 This is a statistical chart showing the MDA content in the retina of rats in each group in Example 10.

[0037] Figure 15 This is a statistical chart of tear secretion in each group of rats in Example 11. Detailed Implementation

[0038] This invention provides the use of asarone in the preparation of medicaments for the treatment and / or prevention of eye diseases, including retinal ganglion cell damage diseases as well as macular degeneration, cataracts, or dry eye syndrome. The retinal ganglion cell damage diseases include glaucoma, optic neuritis, or diabetic retinopathy.

[0039] The present invention also provides a composition comprising at least one of α-asarone, β-asarone, and γ-asarone at an effective concentration, preferably α-asarone, wherein the final concentration of α-asarone is 0.5–30 g / L, more preferably 10–20 g / L, and even more preferably 15 g / L. The composition further comprises an oil solvent, an emulsifier, an osmotic pressure regulator, a pH adjuster, and water. In the present invention, the oil solvent comprises soybean oil, the emulsifier comprises egg yolk lecithin, the osmotic pressure regulator comprises glycerol, and the pH adjuster comprises sodium hydroxide.

[0040] The dosage form of the composition described in this invention is an eye drop, an oral preparation, or an injection.

[0041] In this invention, the eye drops use water as a solvent and contain the following components at the following concentrations: α-asarone 0.5-5 g / L, soybean oil 4-100 g / L, egg yolk lecithin 1-15 g / L, glycerin 2-25 g / L, and sodium hydroxide 0.001-0.005 g / L.

[0042] The concentration of α-asarone in the eye drops is 0.5–5 g / L, more preferably 1–4 g / L, and even more preferably 2 g / L;

[0043] The concentration of soybean oil is 4–100 g / L, more preferably 20–80 g / L, and even more preferably 50 g / L;

[0044] The concentration of egg yolk lecithin is 1-15 g / L, more preferably 5-10 g / L, and even more preferably 8 g / L;

[0045] The concentration of glycerol is 2-25 g / L, more preferably 10-20 g / L, and even more preferably 15 g / L;

[0046] The concentration of sodium hydroxide is 0.001 to 0.005 g / L, more preferably 0.002 to 0.004 g / L, and even more preferably 0.003 g / L.

[0047] In this invention, the oral or injectable preparation uses water as a solvent and contains the following components at the following concentrations: α-asarone 4-30 g / L, soybean oil 80-300 g / L, egg yolk lecithin 10-20 g / L, glycerol 20-30 g / L, and sodium hydroxide 0.02-0.1 g / L.

[0048] The concentration of α-asarone in oral or injectable form is 4–30 g / L, more preferably 10–20 g / L, and even more preferably 15 g / L;

[0049] The concentration of soybean oil is 80-300 g / L, more preferably 100-200 g / L, and even more preferably 150 g / L;

[0050] The concentration of egg yolk lecithin is 10-20 g / L, more preferably 12-18 g / L, and even more preferably 15 g / L;

[0051] The concentration of glycerol is 20-30 g / L, more preferably 22-28 g / L, and even more preferably 25 g / L;

[0052] The concentration of sodium hydroxide is 0.02–0.1 g / L, more preferably 0.04–0.08 g / L, and even more preferably 0.06 g / L.

[0053] The soybean oil, egg yolk lecithin, and glycerin mentioned in this invention are preferably injectable soybean oil, injectable egg yolk lecithin, and injectable glycerin.

[0054] When necessary, the compositions of the present invention may also contain pharmaceutically acceptable antibacterial agents, such as acids, alcohols, quaternary ammonium salts, para-hydroxybenzoates, benzoic acid, sorbic acid, etc.

[0055] The present invention also provides the use of the described composition in the preparation of medicaments for the treatment and / or prevention of eye diseases, including glaucoma, optic neuritis, diabetic retinopathy, macular degeneration, cataracts, or dry eye syndrome.

[0056] The technical solutions provided by the present invention will be described in detail below with reference to the embodiments, but they should not be construed as limiting the scope of protection of the present invention.

[0057] The high-pressure homogenizer used in this embodiment of the invention is a Duoning Bio-Experimental High-Pressure Nano Homogenizer, model: AH-NANO-TKE061; SD rats and C57BL / 6 mice were purchased from Chengdu Dashuo Experimental Animal Co., Ltd.

[0058] Example 1: Preparation of α-Asarum Oral Emulsion / α-Asarum Emulsion Injection

[0059] 1. Preparation process

[0060] Table 1 Raw Materials and Usage

[0061] materials effect Prescription quantity α-Asarum Main drug 0.5kg Soybean oil for injection Solvent, carrier 5.0kg Egg yolk lecithin for injection emulsifier 0.6kg Glycerin for injection isotonic agent 1.125kg Sodium hydroxide pH adjuster 1.25g Water for Injection solvent 50L

[0062] 1) Pour the soybean oil for injection into the oil tank, start the stirrer and start heating. Then add α-asarone and egg yolk lecithin for injection at 70℃. Keep the oil temperature at 70℃ and stir at 3000rpm / min to make the lecithin evenly dispersed in the oil phase. Stir for 20 minutes to make the lecithin completely dissolved.

[0063] 2) Add 45L of water for injection to the preparation tank. Then add the weighed glycerol for injection and sodium hydroxide, start the stirrer and mix thoroughly. Filter the mixture through a 0.22μm, 5-inch PP filter (Hangzhou Kebaite Instrument Co., Ltd.) into the aqueous phase tank. Control the aqueous phase temperature at 70℃. Purge with nitrogen for protection and adjust the aqueous phase to the required volume.

[0064] 3) Under the condition of stirring speed of 3000 rpm / min, the oil phase is slowly injected into the water phase with nitrogen gas, the flow rate is controlled, and the transfer is completed in about 5 minutes to obtain the primary emulsion.

[0065] 4) The colostrum is homogenized twice using a high-pressure homogenizer, each time for 30 minutes, with the solution temperature controlled at 60℃. The homogenization conditions for each step are as follows:

[0066] Table 2 Pressure and Temperature of High Pressure Homogenizer

[0067] Homogenization times Homogeneous pressure (bar) Temperature control after homogenization Homogenization time 1 700bar±50 60℃ 30min 2 700bar±50 60℃ 30min

[0068] After homogenization begins, adjust the homogenization pressure until the specified pressure is reached before transferring the liquid to the next storage tank.

[0069] 2. Filling, sterilization, and storage

[0070] 1) After homogenization, cool the solution to 30°C, transfer it to a settling tank for storage, and await filling. The solution is then pressure filtered with nitrogen and sent to the filling station.

[0071] 2) Filling and sealing

[0072] The prepared emulsion is filled into the washed ampoules through a 5μm PP filter cartridge (20 inches, Hangzhou Kebote Filter Material Co., Ltd.) by a filling machine, and immediately protected with nitrogen and then sealed.

[0073] 3) Sterilization

[0074] The product is sterilized in a rotary sterilizer (121℃×10min, F0 value≥12).

[0075] 4) Packaging and storage

[0076] After sterilization, the product is inspected by light and then packed into a cardboard box to obtain α-asarone emulsion injection with a concentration of 10 mg / mL.

[0077] Example 2: Preparation of α-Asarum Emulsion Eye Drops

[0078] 1. Preparation process

[0079] Table 3 Raw Materials and Usage

[0080] materials effect Prescription quantity α-Asarum Main drug 2.0g Soybean oil for injection Solvent, carrier 50g Egg yolk lecithin for injection emulsifier 12g Glycerin for injection isotonic agent 22.5g Sodium hydroxide pH adjuster 0.025g Water for Injection solvent 1.0L

[0081] The raw materials and dosages of the α-asarone emulsion eye drops in this embodiment are shown in Table 3, and the preparation method is the same as in Example 1.

[0082] 2. Sterilization, filling, and storage

[0083] 1) Sterilization

[0084] A non-terminal sterilization process is used, employing a vaporized hydrogen peroxide sterilization chamber to sterilize the polyester (PET) packaging materials. Meanwhile, the filling and sealing process for the preparation of α-asarone emulsion eye drops must be carried out under appropriate clean environment conditions.

[0085] 2) Filling

[0086] After homogenization, the drug solution is cooled to 30°C and transferred to a settling tank for storage, awaiting filling. The drug solution is then pressure filtered with nitrogen and sent to the filling station. The prepared emulsion is passed through a 5μm PP filter cartridge (20-inch, Hangzhou Kebote Filter Material Co., Ltd.) and filled by a filling machine into pre-washed, dried, and sterilized packaging containers made of polyester (PET).

[0087] 3) Packaging and storage

[0088] After being inspected by light, the product is packed into a cardboard box to obtain α-asarone emulsion eye drops with a concentration of 2.0 mg / mL.

[0089] Comparative Example 1

[0090] Unlike Example 2, Comparative Example 1 prepared an emulsion eye drop without α-asarone. Except for the absence of α-asarone, the other reagents and preparation methods were the same as in Example 2. The following experiment is referred to as "blank emulsion eye drops".

[0091] Example 1: Protective effect of α-Asarum syringe emulsion eye drops on a rat model of chronic ocular hypertension glaucoma induced by magnetic microspheres.

[0092] 1. Reagents and Materials

[0093] Thirty male SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g; magnetic polystyrene microspheres (PS); α-asarone emulsion eye drops (prepared according to the method in Example 2, concentration 2.0 mg / mL).

[0094] 2. Animal grouping and administration method

[0095] The experimental rats were randomly divided into three groups: normal control group (Control group, n=10), model control group (PS group, n=10), and α-asarone emulsion eye drops group (α-asarone group, n=10).

[0096] One week prior to the start of the treatment, rats in the α-asarone emulsion eye drop group were administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 AM to 6:00 PM daily. On day 8, in both the model control group and the α-asarone group, 10 μL of 5 μm diameter, 50 mg / mL magnetic polystyrene microspheres were injected into the right anterior chamber of the rats under a surgical microscope to induce unilateral intraocular pressure elevation. The normal control group received an equal volume of sterile saline injected into the same area of ​​the eye. After model establishment, rats in the α-asarone group were administered 20 μL of α-asarone emulsion eye drops every 3.5 hours from 8:30 AM to 6:00 PM daily for 4 weeks. The PS group was simultaneously administered an equal volume of blank emulsion eye drops without α-asarone.

[0097] 3. Evaluation Methods and Results

[0098] Intraocular pressure was measured in rats before modeling and at 1, 2, 3, and 4 weeks after modeling. The results are as follows: Figure 1 As shown in Table 4, the ERG waveform changes were detected using the dark adaptation 3.0 method in weeks 1, 2, 3, and 4, and the results are as follows. Figures 2-3 The results are shown in Tables 5 and 6. Data are presented as mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (for homogeneity of variance) or the Dunnett-t test (for heterogeneity of variance). A p-value < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPad Prism 9.3.0. Specific results are as follows:

[0099] Table 4 Comparison of intraocular pressure in rats of different groups before modeling and after drug administration. (mmHg)(n=10)

[0100] Control group PS Group α-Asarum brain group Before molding 12.97±1.89 13.80±0.36 13.24±1.25 Week 1 13.63±4.37**** 27.31±3.12 24.28±1.63* Week 2 11.82±2.41**** 25.62±1.70 20.50±2.76**** Week 3 12.26±1.97**** 26.80±2.23 17.26±1.04**** Week 4 13.54±2.20**** 28.10±3.14 16.74±2.05****

[0101] Table 5. Dark adaptation 3.0 ERG a-wave amplitude variation (μV)(n=10)

[0102] Control group PS Group α-Asarum brain group Week 1 83.21±22.40** 56.25±14.62 60.25±18.53 Week 2 88.74±18.09*** 48.39±14.04 73.68±25.56** Week 3 96.85±29.58*** 55.75±23.52 89.33±12.03** Week 4 84.37±22.30** 53.45±19.53 78.18±15.95**

[0103] Table 6. Amplitude variation of dark-adapted 3.0 ERGb wave (μV)(n=10)

[0104] Control group PS Group α-Asarum brain group Week 1 207.58±24.41**** 92.01±23.79 168.17±32.34**** Week 2 226.90±29.32**** 123.00±46.78 197.54±37.26*** Week 3 239.28±47.07**** 102.33±21.72 180.09±49.01*** Week 4 201.74±32.08**** 122.09±36.72 193.08±22.67****

[0105] Note: Compared with the PS group, *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001.

[0106] The a wave is generated by the outer retinal cells (mainly rod and cone cells) and reflects the function of the photoreceptors; the b wave is generated by the inner retinal cells (mainly bipolar and Muller cells) and reflects the function of the middle retinal layer.

[0107] From Tables 4-6 and Figures 1-3 It was observed that after 4 weeks of continuous administration, the intraocular pressure of rats decreased slowly. Under dark-adapted flash stimulation, the amplitude at each time point was ranked as follows: Control group > α-asarone group > PS group. The α-asarone group and the PS group showed significant or highly significant differences (P<0.001 or P<0.0001), indicating that prophylactic administration of α-asarone can effectively reduce intraocular pressure, increase the amplitude of flash stimulation, and improve retinal function in mice with chronic high intraocular pressure.

[0108] Through experimental research, the inventors discovered that the pharmacodynamic performance of α-asarone emulsion eye drops was essentially consistent with that of the α-asarone emulsion injection group administered via intraperitoneal injection (ip) at a dose of 30 mg / kg and via oral gavage (ig) at a dose of 60 mg / kg. Furthermore, α-asarone exhibited similar or identical efficacy to β-asarone or γ-asarone in the treatment and / or prevention of ocular diseases. For simplicity, the following experiments only present the pharmacodynamic results of α-asarone emulsion eye drops.

[0109] Example 2: Protective effect of α-Asarum-based emulsion eye drops on N-methyl-D-aspartate (NMDA)-induced retinal ganglion cell damage.

[0110] 1. Reagents and Materials

[0111] Twenty-eight male SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g; NMDA; α-asarone emulsion eye drops (prepared according to the method in Example 2, concentration 2.0 mg / mL).

[0112] 2. Animal grouping and administration method

[0113] The experimental rats were randomly divided into three groups: normal control group (Control group, n=10), model control group (NMDA group, n=10), and α-asarone emulsion eye drops group (α-asarone group, n=10).

[0114] One week prior to the start of the treatment, rats in the α-asarone emulsion eye drop group were administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 AM to 6:00 PM daily. On day 8, 3 μL of NMDA (50 mM) solution was slowly injected into the vitreous cavity of the right eye of rats in both the model control and α-asarone groups under an optical microscope using a 33G needle to induce neuroexcitotoxicity. The normal control group received an equal volume of sterile saline in their eyes. After model establishment, rats in the α-asarone group were administered 20 μL of α-asarone emulsion eye drops every 3.5 hours from 8:30 AM to 6:00 PM daily for two weeks. The NMDA group was simultaneously administered an equal volume of blank emulsion eye drops without α-asarone.

[0115] 3. Evaluation Methods and Results

[0116] The amplitude changes of flash visual evoked potentials (F-VEP) in rats of each group were detected in the second week after modeling. The results are as follows: Figure 4 As shown in Table 7; in the second week, paraffin sections of the eyes of rats in each group were prepared, stained with hematoxylin and eosin (HE), and the retinal thickness of rats in each group was recorded. The results are as follows. Figure 5 Table 8 shows the data results. The data are presented as mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (for homogeneity of variance) or the Dunnett-t test (for heterogeneity of variance). A p-value < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPad Prism 9.3.0. Specific results are as follows:

[0117] Table 7 Variations in the amplitude of visual evoked potentials (F-VEP) (n=10)

[0118] Control group NMDA Group α-Asarum brain group N1-P1 amplitude (μV) 45.29±4.31**** 17.14±9.11 29.74±5.72***

[0119] Table 8. Changes in retinal thickness in rats of different groups. (n=10)

[0120] Control group NMDA Group α-Asarum brain group Retinal thickness (μm) 208.71±10.85**** 160.11±24.83 194.82±17.49***

[0121] Note: Compared with the NMDA group, ***P<0.001; ****P<0.0001.

[0122] From Tables 7-8 and Figures 4-5It was observed that after two weeks of continuous administration, the thickness of the rat retina increased and some electrophysiological functions were restored. The treatment group showed significant or highly significant differences compared with the model group (P<0.001 or P<0.0001), indicating that α-asarone prophylaxis has a protective effect against intravitreal injection of 50mM NMDA-induced rat RGC death, retinal morphology and optic nerve function damage.

[0123] Experimental Example 3: The therapeutic effect of α-Asarum cerebroside emulsion eye drops on traumatic optic neuropathy in rats.

[0124] 1. Reagents and Materials

[0125] Thirty male SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g; α-Asarum lactone emulsion eye drops (prepared according to the method in Example 2, concentration 2.0 mg / mL).

[0126] 2. Animal grouping and administration method

[0127] The experimental rats were randomly divided into three groups: normal control group (Control group, n=10), optic nerve crush model control group (ONC group, n=10), and α-asarone emulsion eye drops group (α-asarone group, n=10).

[0128] One week prior to the treatment, rats in the α-asarone emulsion eye drop group were administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 AM to 6:00 PM daily. On day 8, optic nerve clipping surgery was performed on the model control group and the α-asarone emulsion eye drop group, while the normal control group received no treatment. After model establishment, rats in the α-asarone emulsion group were administered 20 μL of α-asarone emulsion eye drops every 3.5 hours from 8:30 AM to 6:00 PM daily for 2 weeks. The ONC group was simultaneously administered an equal volume of blank emulsion eye drops without α-asarone.

[0129] 3. Evaluation Methods and Results

[0130] ERG waveform changes were observed during the second week after modeling, and the results are as follows: Figures 6-7 The results are shown in Tables 9 and 10. Simultaneously, the amplitude changes of flash visual evoked potentials (F-VEPs) in each group of rats were measured during week 2, and the results are as follows: Figure 8Table 11 shows the data results. The data are presented as mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (for homogeneity of variance) or the Dunnett-t test (for heterogeneity of variance). A p-value < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPadPrism 9.3.0. Specific results are as follows:

[0131] Table 9. Variation of ERG a-wave amplitude in dark adaptation (μV)(n=10)

[0132]

[0133] Table 10. Variation of dark-adapted ERG b-wave amplitude (μV)(n=10)

[0134]

[0135] Table 11 Variations in the amplitude of visual evoked potentials (F-VEP) (n=10)

[0136] Control group ONC Group α-Asarum brain group N1-P1 amplitude (μV) 36.19±4.87**** 12.56±2.40 25.56±6.61****

[0137] Note: Compared with the ONC group, *P<0.05; **P<0.01; ****P<0.0001.

[0138] From Tables 9-11 and Figure 13 It can be seen that after being stimulated with different light intensities in sequence, the amplitudes measured one week after pre-treatment and two weeks after modeling were ranked as follows: Control group > α-asarone group > ONC group. This indicates that α-asarone preventive eye drops can effectively increase the amplitude of each flash stimulus and alleviate optic nerve damage in rats caused by external pressure.

[0139] Example 4: Protective effect of α-Asarum cerebroside emulsion eye drops on laser-induced mouse choroidal neovascularization model

[0140] 1. Reagents and Materials

[0141] Thirty male C57BL / 6 mice, aged 7-8 weeks, SPF grade, weighing 19-21g, were used; α-asarone oral emulsion / α-asarone emulsion eye drops (prepared according to the method in Example 1, concentration 10mg / mL).

[0142] 2. Animal grouping and administration method

[0143] The experimental mice were randomly divided into two groups: a normal control group (Control group, n=6), a choroidal neovascularization model control group (CNV group, n=12), and an α-asarone emulsion eye drop group (α-asarone group, n=12).

[0144] Three days prior to the event, rats in the α-asarone emulsion eye drop group were administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours between 8:30 AM and 6:00 PM daily. On day 4, 532 nm laser photocoagulation was used to establish the CNV group and the α-asarone group, while the normal control group received no treatment. After model establishment, rats in the α-asarone emulsion group were administered 20 μL of α-asarone emulsion eye drops every 3.5 hours between 8:30 AM and 6:00 PM daily for two weeks. The CNV group was simultaneously administered an equal volume of blank emulsion eye drops without α-asarone.

[0145] 3. Evaluation Methods and Results

[0146] Seven days after laser photocoagulation, mice in each group underwent fluorescein fundus angiography (FFA), and the results were as follows: Figure 9 The results are shown in Table 12. Simultaneously, paraffin sections were prepared from the eyeballs of each group of mice, stained with hematoxylin and eosin (HE), and the maximum central thickness of the CNV in each group was calculated. Figure 10 Table 13 shows the results. The data are presented as mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (homogeneous variance) or the Dunnett-t test (unequal variance). P < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPadPrism 9.3.0.

[0147] Table 12 Leakage scores of fundus angiography in mice of each group (n=12)

[0148] CNV Group α-Asarum brain group Number of Level 3 (percentage) 21 / 43(49％) 9 / 40(23％) Average leakage level 2.11±1.00 1.65±0.92*

[0149] Table 13 Changes in maximum central thickness of CNV in each group of mice (μm)(n=12)

[0150]

[0151]

[0152] Note: Compared with the CNV group, *P<0.05; **P<0.01; ****P<0.0001.

[0153] From Tables 12-13 and Figures 9-10 It is evident that pre-administration for 3 days followed by continuous administration for 7 days can reduce fluorescein leakage from laser-induced spots in laser-induced mice and decrease CNV formation. The results of ex vivo eyeball HE staining and fundus fluorescein angiography are basically consistent, and there are significant differences between the administration group and the model group (P<0.05). This indicates that α-asarone prophylactic administration can effectively inhibit the formation of CNV in laser-induced mice and has a certain therapeutic effect on CNV in laser-induced mice.

[0154] Experimental Example 5: Protective effect of α-asarone on glutamate-damaged R28 cells

[0155] 1. Reagents and Materials

[0156] Rat retinal progenitor cell line (R28) was obtained from Wuhan Pronosei Biotechnology Co., Ltd.; L-glutamate (Maclean, L810369); CCK-8 (Biosharp, BS350C); DMEM / F12 medium (containing antibiotics) (KGI Biotechnology, KGM12500-500); fetal bovine serum (ZETA, 120214018-4S); PBS (KGI Biotechnology, KGB5001); DMSO (Solepro, D8371).

[0157] 2. Experimental Procedure

[0158] 1) Screening of glutamate concentration for modeling: R28 cells were cultured with different concentrations of glutamate for 24 hours. It was found that the cell viability was about 60% in the presence of 10mM glutamate. Therefore, a concentration of 10mM glutamate was selected for modeling.

[0159] 2) Screening of α-Asarum pharmacodynamics: R28 cells in the logarithmic growth phase cultured in complete culture medium were subjected to a 1×10⁻⁶ HCl treatment. 4Cells were seeded at a density of 100 μL / well in 96-well plates, with edge wells filled with sterile PBS. Cells were incubated at 37°C and 5% CO2 for 24 h until complete adhesion. The supernatant was discarded, and 50 μL of α-asarone solution (final concentrations of 0.5 μM, 1 μM, and 2 μM) was added to each well. Cells were incubated at 37°C and 5% CO2 for 2 h. Then, 50 μL of glutamate solution diluted with serum-free medium to a final concentration of 10 mM was added to each well of the above-mentioned drug-treated groups, and the cells were incubated at 37°C and 5% CO2 for another 24 h. The control group received only the same volume of serum-free medium. The model group received 50 μL of serum-free medium followed by 50 μL of glutamate solution diluted with serum-free medium to a final concentration of 10 mM. All other procedures for the control and model groups were the same as those for the drug-treated groups. Then, 110 μL of 10% CCK-8 solution was added to each well, and the cells were cultured at 37°C and 5% CO2 for 2 h. The OD value at 450 nm was detected using a microplate reader, and the viability of R28 cells was calculated according to the following formula.

[0160] Cell viability = (average absorbance of experimental group - average absorbance of zeroing well) / (average absorbance of normal control group - average absorbance of zeroing well).

[0161] Figure 11 The cellular efficacy results were measured after pretreatment with α-asarone at final concentrations of 0.5, 1, and 2 μM for 2 hours, followed by administration of glutamate at a final concentration of 10 mM for 24 hours. As shown in the figure, compared with the Glu group, the absorbance of the different prophylactic administration groups was significantly increased, with the highest cell viability observed at 2 μM. This indicates that prophylactic administration of α-asarone has a protective effect on R28 cells.

[0162] Example 6: Protective effect of α-Asarum cerebroside emulsion eye drops on an inflammation-induced rat model of optic neuritis.

[0163] 1. Reagents and Materials

[0164] Thirty-four female SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g; guinea pig spinal cord homogenate; Complete Freund Adjuvant (CFA); pertussis vaccine; α-asarone emulsion eye drops (prepared according to Example 2, concentration 2 mg / mL).

[0165] 2. Animal grouping and administration method

[0166] After one week of acclimatization, 10 SD rats were randomly selected as the normal control group (Control group, n=10). The remaining 24 SD rats were injected subcutaneously into the paw pads with guinea pig spinal cord homogenate mixed with complete Freund's adjuvant (CFA) as the antigen, and pertussis vaccine was injected subcutaneously into the hind limbs to establish a rat model of experimental autoimmune encephalomyelitis (EAE). The Control group was injected with the same amount of physiological saline in the same manner. Twelve rats that successfully developed the α-asarone group were randomly selected and administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 to 18:00 daily for three consecutive weeks. The remaining twelve rats were administered an equal volume of blank emulsion without α-asarone every 3.5 hours from 8:30 to 18:00 daily for three consecutive weeks.

[0167] 3. Evaluation Methods and Results

[0168] Three weeks after drug administration, rat retinas were harvested to detect MDA content. Results are shown in Table 14. Figure 12 As shown. Data results are presented in the form of mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (homogeneous variance) or the Dunnett-t test (unequal variance). P < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPadPrism 9.3.0.

[0169] Table 14 MDA content in the retina of rats in each group (n=10)

[0170]

[0171] Note: Compared to the EAE group. **** P<0.0001.

[0172] The results are shown in Table 14. Figure 12 As shown, the MDA content detection results showed that the MDA content in the EAE group was significantly higher than that in the Control group and the α-asarone group, and the difference was statistically significant; while there was no significant difference between the Control group and the α-asarone group. This indicates that the EAE group suffered severe oxidative damage, while the α-asarone group did not suffer significant damage. Therefore, α-asarone can alleviate the damage to the retina caused by inflammation.

[0173] Example 7: Protective effect of α-Asarum syringe eye drops on a streptozotocin-induced diabetic retinopathy rat model.

[0174] 1. Reagents and Materials

[0175] Thirty-four male SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g, were used; streptozotocin (STZ) and α-asarone emulsion eye drops (prepared in Example 2, concentration 2 mg / mL) were used.

[0176] 2. Animal grouping and administration method

[0177] After 1 week of acclimatization, 10 SD rats were randomly selected as the normal control group (Control group, n=10). The remaining 24 SD rats were given STZ solution (60mg / kg) via intraperitoneal injection (ip). The model was considered successful when the blood glucose level was ≥16.7mmol / L three times randomly measured 72h after STZ injection. The Control group was injected with the same amount of physiological saline in the same way.

[0178] Twelve rats that successfully developed the α-asarone group were randomly selected and administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 to 18:00 daily for 12 consecutive weeks. The remaining 12 rats were assigned to the STZ group and administered an equal volume of blank emulsion eye drops without α-asarone every 3.5 hours from 8:30 to 18:00 daily for 12 consecutive weeks.

[0179] 3. Evaluation Methods and Results

[0180] Twelve weeks after drug administration, rat eyeballs were removed for TUNEL staining to observe retinal cell apoptosis. The results are shown in Table 15. Figure 13 As shown. Data results are presented in the form of mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (homogeneous variance) or the Dunnett-t test (unequal variance). P < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPad Prism 9.3.0.

[0181] Table 15 Number of Apoptotic Cells in the Retinal Region (n=10)

[0182] Control group STZ group α-Asarum brain group Number of apoptotic cells / cell 3±1*** 114±38 7±1***

[0183] Note: Compared with the STZ group, ***P<0.001.

[0184] The results are shown in Table 15. Figure 13 As shown, TUNEL staining results indicated that the number of apoptotic cells in the STZ group was significantly higher than that in the α-asarone group and the Control group, with a statistically significant difference; while there was no significant difference between the Control group and the α-asarone group. This suggests that the STZ group suffered severe damage due to hyperglycemia, while the α-asarone group did not suffer significant damage. Therefore, α-asarone can alleviate the damage to retinal cells caused by STZ-induced hyperglycemia.

[0185] Example 8: Protective effect of α-Asarum-based emulsion eye drops on a rat model of D-galactose-induced cataracts.

[0186] 1. Reagents and Materials

[0187] Thirty-four male SD rats aged 6–8 weeks, SPF grade, weighing 180–220 g; D-galactose; α-asarone emulsion eye drops (prepared in Example 2, concentration 2 mg / mL).

[0188] 2. Animal grouping and administration method

[0189] After 1 week of acclimatization, 10 SD rats were randomly selected as the normal control group (Control group, n=10). The remaining 24 SD rats were given D-galactose (200mg / kg) subcutaneously once a day for 4 consecutive weeks. The degree of lens opacity of the rats was observed under slit lamp irradiation. If lens opacity appeared, the model was considered to have been successfully established. The Control group was injected with the same amount of physiological saline in the same way.

[0190] Twelve rats that successfully developed the α-asarone group were randomly selected and administered 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 to 18:00 daily for four consecutive weeks. The remaining twelve rats were administered an equal volume of blank emulsion eye drops without α-asarone every 3.5 hours from 8:30 to 18:00 daily for 12 consecutive weeks.

[0191] 3. Evaluation Methods and Results

[0192] Three weeks after drug administration, rat retinas were harvested to detect MDA content. The results are shown in Table 16. Figure 14As shown. Data results are presented in the form of mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (homogeneous variance) or the Dunnett-t test (unequal variance). P < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPadPrism 9.3.0.

[0193] Table 16 shows the MDA content in the retina of rats in each group. (n=10)

[0194]

[0195] Note: Compared with the Veh group, ****P<0.0001.

[0196] The results are shown in Table 16. Figure 14 As shown, the MDA results indicated that the MDA content in the Veh group was significantly higher than that in the Control group and the α-asarone group, with a statistically significant difference; while there was no significant difference between the Control group and the α-asarone group. This suggests that the Veh group suffered severe oxidative damage due to hyperglycemia, while the α-asarone group showed no significant damage, indicating that α-asarone can alleviate oxidative damage to the retina induced by D-galactose.

[0197] Example 9: Protective effect of α-Asarum Brain Emulsion Eye Drops on a scopolamine hydrobromide-induced dry eye rat model.

[0198] 1. Reagents and Materials

[0199] Thirty-four 6- to 8-week-old SD rats, SPF grade, female, weighing 180-220g; scopolamine hydrobromide (SCOP); α-asarone emulsion eye drops (prepared according to the method in Example 2, concentration 2.0mg / mL).

[0200] 2. Animal grouping and administration method

[0201] After acclimatizing for one week, 10 SD rats were randomly selected as the normal control group (Control group, n=10), and the remaining 24 SD rats were given SCOP (12.5mg / kg) subcutaneously every 3 hours (9:00, 12:00, 15:00, 18:00).

[0202] Twelve rats were randomly selected as the α-asarone group after modeling. The rats in the α-asarone group were given 20 μL of α-asarone emulsion eye drops (2.0 mg / mL) every 3.5 hours from 8:30 to 18:00 every day for one week. The remaining 12 rats were given an equal volume of blank emulsion eye drops without α-asarone every 3.5 hours from 8:30 to 18:00 every day for one week.

[0203] 3. Evaluation Methods and Results

[0204] The tear secretion of rats in each group was measured on day 7 after modeling. The results are shown in Table 17. Figure 15 As shown. Data results are presented in the form of mean ± standard deviation. After testing the normality and homogeneity of variance of the experimental data, one-way ANOVA was used for statistical analysis. Post-hoc comparisons were performed using the LSD test (homogeneous variance) or the Dunnett-t test (unequal variance). P < 0.05 was considered statistically significant. All data were processed and analyzed using IBM SPSS Statistics 27, and all statistical graphs were created using GraphPadPrism 9.3.0.

[0205] Table 17 Tear secretion in rats of each group (n=10)

[0206] Detection Control group SCOP Group α-Asarum brain group Tear secretion / mm 11.45±1.71**** 5.98±0.97 7.50±1.70*

[0207] Note: Compared with the SCOP group, *P<0.05; ****P<0.0001.

[0208] The results are shown in Table 17. Figure 15 As shown, the tear secretion of rats in each group was significantly less than that in the Control group and the α-asarone group, and the difference was statistically significant. This indicates that the SCOP group caused a significant reduction in tear secretion, which led to dry eye syndrome. In contrast, the α-asarone group was able to alleviate the reduction in tear secretion induced by SCOP and play a protective role on the ocular surface.

[0209] As can be seen from the above embodiments, the α-asarone and its composition of the present invention can effectively treat and / or prevent diseases related to retinal ganglion cell damage (such as glaucoma, optic neuritis, diabetic retinopathy), neovascular age-related macular degeneration, cataracts, and dry eye.

[0210] The above description is only a preferred embodiment of the present invention. It should be noted that for those skilled in the art, several improvements and modifications can be made without departing from the principle of the present invention, and these improvements and modifications should also be considered within the scope of protection of the present invention.

Claims

1. The use of asarone as the sole active ingredient in the preparation of drugs for the treatment and / or prevention of eye diseases, wherein the eye diseases are retinal ganglion cell damage diseases, cataracts or dry eye syndrome; wherein the asarone is α-asarone; The retinal ganglion cell damage diseases mentioned are glaucoma or diabetic retinopathy.

2. Use according to claim 1, characterized in that, The application methods of the asarone include eye drops, oral preparations or injections; The eye drops use water as a solvent and contain the following components at the following concentrations: α-asarone 0.5~5g / L, soybean oil 4~50g / L, egg yolk lecithin 1~15g / L, glycerin 2~25g / L, and sodium hydroxide 0.001~0.005g / L.

3. Use according to claim 1, characterized in that, The application methods of the asarone include eye drops, oral preparations or injections; The oral or injectable preparation uses water as a solvent and contains the following components at the following concentrations: α-asarone 4~30 g / L, soybean oil 80~300 g / L, egg yolk lecithin 10~20 g / L, glycerol 20~30 g / L, and sodium hydroxide 0.02~0.1 g / L.

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