Application of eriodictyol in preparation of medicine for treating nano-plastic induced ovarian injury
By using sago phenol to regulate multiple antioxidant and apoptotic signaling pathways, the problem of difficulty in reversing nanoplastics in the prior art is solved, and the effect of significantly improving ovarian and reproductive endocrine functions is achieved.
Patent Information
- Application Number
- CN202510713311.0
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-05-30
- Publication Date
- 2025-06-27
AI Technical Summary
Existing intervention methods are difficult to effectively reverse nanoplastic-induced ovarian damage. Traditional antioxidants cannot target key damage sites and have dose-dependent toxicity problems, so they cannot cope with the composite toxic effect of nanoplastics and other pollutants.
The use of saccharophorol as a drug for treating nanoplastics-induced ovarian injury, and reverses ovarian injury through the multi-target synergy mechanism of the "antioxidation-anti-inflammatory-anti-apoptotic network" that regulates the Nrf2/KEAP1 antioxidant pathway and inhibits the Bax/Caspase-3 apoptotic signaling pathway.
Saccharomycephalus significantly improves ovarian morphology and follicle development levels, improves estradiol and anti-Muller hormone levels, reduces follicle stimulating hormone levels, reverses reproductive endocrine disorders caused by nanoplastics, and efficiently repairs ovarian damage through a multi-path coordinated mechanism.
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Abstract
Description
Technical Field
[0001] The present invention belongs to the technical field of biomedicine, and particularly relates to the application of eriodyctiol in the preparation of a drug for treating ovarian injury induced by nanoplastics. Background Art
[0002] Plastic pollution has become a global environmental problem. After entering the environment, plastic pollutants are extremely difficult to completely degrade and often decompose into micro-nanoplastics with a particle size of 1 nm to 5 mm. Micro-nanoplastics are ubiquitous in the environment and can enter organisms through diet, drinking water, etc., posing significant risks to the ecosystem and human health. The reproductive system has always been considered one of the main targets of plastic pollution. Research shows that nanoplastics can cause apoptosis of granulosa cells, hormone secretion disorders, and decreased fertility, and can also trigger ovarian injury by inducing oxidative stress, mitochondrial dysfunction, and inflammatory responses.
[0003] Regarding ovarian injury induced by nanoplastics, existing intervention methods mainly rely on antioxidants, but the effects are significantly insufficient. Traditional antioxidants mainly act by scavenging reactive oxygen species, but they cannot target key injury sites such as ovarian granulosa cells or mitochondria, resulting in low protection efficiency; there is also a problem of dose-dependent toxicity. High-dose antioxidants may cause cytotoxicity and even interfere with normal physiological functions. For example, excessive vitamin C leads to iron overload. And nanoplastics often combine with heavy metals, antibiotics, persistent organic pollutants, etc. in the environment to form combined toxic effects, which are difficult to cope with by existing intervention methods. For example, research shows that nanoplastics such as nylon and polystyrene can adsorb antibiotics, reduce their biological activity, and promote the generation of drug-resistant bacteria, resulting in the failure of traditional antibiotic treatment. Some studies have tried physical means, such as magnetic nanoiron to adsorb or remove nanoplastics in the body, but physical removal can only reduce the accumulation of nanoplastics in the body and cannot reverse pathological changes such as the decrease in mitochondrial membrane potential and apoptosis that have already occurred. Therefore, there is an urgent need to find a drug that can efficiently reverse ovarian injury induced by nanoplastics.
[0004] Eriodyctiol is a natural dihydroflavonoid compound widely present in vegetables, fruits, and traditional Chinese medicines, and has the effects of antioxidation, anti-inflammation, analgesia, and improvement of diabetes and diabetic complications. However, whether it can be used as a drug that can effectively reverse ovarian injury induced by nanoplastics remains to be explored. Summary of the Invention
[0005] To solve the above problems, the present invention provides the application of eriocitrin in the preparation of a drug for treating nano-plastic-induced ovarian injury. Eriocitrin can significantly improve ovarian morphology and follicular development levels, increase estradiol levels and anti-Müllerian hormone levels, decrease follicle-stimulating hormone levels, and reverse the reproductive endocrine disorders caused by nano-plastics. It can also efficiently repair nano-plastic-induced ovarian injury in mice through the "antioxidant-inflammatory-apoptosis resistance network" multi-target synergistic mechanism of regulating the Nrf2 / KEAP1 antioxidant pathway and inhibiting the Bax / Caspase-3 apoptosis signaling pathway. Moreover, it has the advantages of natural low toxicity and flexible dosage forms, and has potential application value in the preparation of drugs for repairing reproductive toxicity caused by nano-plastics.
[0006] The present invention provides the application of eriocitrin in the preparation of a drug for treating nano-plastic-induced ovarian injury, and the structural formula of the eriocitrin is shown in formula (I): 。
[0007] Further, the nano-plastic is polystyrene nano-plastic.
[0008] Further, the eriocitrin is used for preparing a drug for reversing the reproductive endocrine disorders caused by polystyrene nano-plastics.
[0009] Further, the eriocitrin is used for preparing a drug for improving ovarian morphology or regulating follicular development levels or regulating sex hormone levels.
[0010] Further, the drug for regulating sex hormone levels is a drug for increasing estradiol levels or anti-Müllerian hormone levels or decreasing follicle-stimulating hormone levels.
[0011] Further, the eriocitrin is used for preparing a drug for inhibiting cell apoptosis caused by nano-plastics.
[0012] Further, the eriocitrin is used for preparing a drug for decreasing the Bax / Bcl-2 ratio or inhibiting the activation of Caspase-3.
[0013] Further, the drug for decreasing the Bax / Bcl-2 ratio is a drug for decreasing the expression level of apoptosis-promoting protein Bax or increasing the level of apoptosis-inhibiting protein Bcl-2.
[0014] Further, the eriocitrin is used for preparing a drug for reversing the oxidative stress-inflammation vicious cycle induced by nano-plastics.
[0015] Further, the eriocitrin is used for preparing a drug for up-regulating the expression level of SOD1 or down-regulating the expression level of HO-1 or stabilizing the Nrf2 / KEAP1 system.
[0016] Furthermore, the drug uses eriodyctiol as the sole active ingredient.
[0017] Furthermore, the drug is composed of eriodyctiol and pharmaceutically acceptable excipients.
[0018] Furthermore, the drug is an oral preparation or an injection.
[0019] Furthermore, the oral preparation is any one of oral liquid, tablets, capsules, pills, powders and granules.
[0020] Furthermore, the injection is an injection solution or a sterile powder for injection.
[0021] Compared with the prior art, the beneficial effects of the present invention are as follows: The present invention for the first time reveals that the natural flavonoid compound eriodyctiol can be used to prepare a drug for treating ovarian damage induced by nanoplastics. Experiments show that: (1) Eriodyctiol can significantly improve the ovarian morphology of mice and reduce the number of atretic follicles, providing a good basis for the normal development of follicles and the stable secretion of hormones. (2) Eriodyctiol can significantly increase the levels of estradiol and anti-Müllerian hormone in the serum of mice and significantly reduce the level of follicle-stimulating hormone, while estradiol, anti-Müllerian hormone and follicle-stimulating hormone are important indicators for evaluating ovarian function. (3) Eriodyctiol can efficiently repair ovarian damage in mice induced by nanoplastics through a multi-target synergistic mechanism of an "antioxidant-inflammatory-antiapoptotic network" that regulates the Nrf2 / KEAP1 antioxidant pathway and inhibits the Bax / Caspase-3 apoptotic signaling pathway.
[0022] Eriodyctiol is a natural flavonoid compound with a wide source. It can be extracted from plants such as lemons, peanuts, and ginkgo, or synthesized by microorganisms. It has low cost and is easy to produce on a large scale. Eriodyctiol does not interfere with the normal endocrine function of the ovaries and has the ability to regulate multiple pathways synergistically. It has the advantages of natural low toxicity and flexible dosage forms, and has potential application value in repairing reproductive toxicity caused by nanoplastics. Compared with traditional intervention methods, the systematic repair mechanism of eriodyctiol can more efficiently reverse ovarian damage and provide new ideas for the prevention and treatment of nano-pollution-related diseases.
[0023] In summary, eriodyctiol has the advantages of "natural low toxicity - multi-effect synergy", providing a safe and efficient new strategy for the protection of reproductive toxicity caused by nano-pollution, and has broad application prospects in the fields of clinical treatment of premature ovarian failure and polycystic ovary syndrome, occupational protection and reproductive protection of occupationally exposed populations. Description of the Drawings
[0024] To more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the following will briefly introduce the drawings required for the description of the embodiments or the prior art. Obviously, the drawings in the following description are only some embodiments of the present invention. For those of ordinary skill in the art, without creative efforts, other drawings can also be obtained based on these drawings.
[0025] Figure 1 It is the hematoxylin-eosin staining result of mouse ovaries; Figure 1 Figure A of [reference] is the blank group, Figure 1 Figure B of [reference] is the injury group, Figure 1 Figure C of [reference] is the eriocitrin treatment group.
[0026] Figure 2 It is the statistical chart of the number of follicles at all levels in mice of the blank group, injury group, and eriocitrin group. * indicates p <0.05, ** indicates p <0.01, *** indicates p <0.001.
[0027] Figure 3 It is the statistical chart of the content of sex hormones in the serum of mice in the blank group, injury group, and eriocitrin group; Figure 3 Figure A of [reference] is the statistical chart of the level of anti-Müllerian hormone in the serum of mice in each group, Figure 3 Figure B of [reference] is the statistical chart of the level of estradiol hormone in the serum of mice in each group, Figure 3 Figure C of [reference] is the statistical chart of the level of follicle-stimulating hormone in the serum of mice in each group. ** indicates p <0.01, *** indicates p <0.001.
[0028] Figure 4 It is the expression of apoptosis signal-related proteins in mice of the blank group, injury group, and eriocitrin group. Among them, Figure 4 Figure A of [reference] is the expression of Caspase-3 protein, Bax protein, Bcl-2 protein, and actin internal reference protein; Figure 4 Figure B of [reference] is the ratio of Bax / Bcl-2 in each group of mice; Figure 4 Figure C of [reference] is the relative expression of Caspase-3 in each group of mice. * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.
[0029] Figure 5 It is the expression of Nrf2 / HO-1 pathway-related proteins in mice of the blank group, injury group, and eriocitrin group. Among them, Figure 5 Figure A of [reference] is the expression of HO-1 protein, Nrf2 protein, KEAP1 protein, SOD1 protein, and actin internal reference protein; Figure 5Figure B shows the relative expression levels of Nrf2 in mice of the blank group, injury group, and eriocitrin group; Figure 5 Figure C shows the relative expression levels of KEAP1 in mice of the blank group, injury group, and eriocitrin group; Figure 5 Figure D shows the relative expression levels of SOD1 in mice of the blank group, injury group, and eriocitrin group; Figure 5 Figure E shows the relative expression levels of HO-1 in mice of the blank group, injury group, and eriocitrin group; * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001. Detailed implementation manners
[0030] The following describes the detailed implementation manners of the present invention in detail, but it should be understood that the protection scope of the present invention is not limited by the detailed implementation manners. Based on the embodiments of the present invention, all other embodiments obtained by those of ordinary skill in the art without creative efforts belong to the protection scope of the present invention. The experimental methods described in the embodiments of the present invention are all conventional methods unless otherwise specified. The materials, reagents, etc. used in the following embodiments can be obtained from commercial channels unless otherwise specified.
[0031] In the present invention, eriodyctiol was purchased from Shanghai Yuanye Bio-Technology Co., Ltd., with a purity of ≥98% and the product number B21160; the mouse anti-Müllerian hormone ELISA kit was purchased from Jianglai Biotech Co., Ltd., with the product number JL20476; the mouse estradiol ELISA kit was purchased from Jianglai Biotech Co., Ltd., with the product number JL50852; the mouse follicle-stimulating hormone ELISA kit was purchased from Jianglai Biotech Co., Ltd., with the product number JL10239; in the present invention, the primary antibody solutions and secondary antibody solutions of Bax, Bcl-2, Caspase3, SOD1, Nrf2, KEAP1, and HO-1 were all purchased from Wuhan Sanying Biotechnology Co., Ltd. The detailed information is as follows: the product number of BAX Monoclonal antibody is 60267-1-Ig; the product number of Bcl2 Polyclonal antibody is 26593-1-AP; the product number of Cleaved Caspase 3 Polyclonal antibody is 25128-1-AP; the product number of SOD1 Polyclonal antibody is 10269-1-AP; the product number of NRF2, NFE2L2 Polyclonal antibody is 16396-1-AP; the product number of HO-1 / HMOX1 Monoclonal antibody is 66743-1-IG; the product number of KEAP1 Polyclonal antibody is 10503-2-AP; the product number of HRP-conjugated Goat Anti-Rabbit IgG is SA00001-2; the product number of HRP-conjugated Goat Anti-Mouse IgG is SA00001-1; in the present invention, nanoplastics are labeled as NPs.
[0032] The reproductive system is one of the main targets of plastic pollution. Research has shown that nanoplastics can cause apoptosis of granulosa cells, hormone secretion disorders, and decreased fertility, and can also induce ovarian damage by inducing oxidative stress, mitochondrial dysfunction, and inflammatory responses. Existing intervention methods mainly rely on antioxidants, but traditional antioxidants have problems such as being unable to target key damage sites, having low protection efficiency, and dose-dependent toxicity. In addition, nanoplastics often combine with other pollutants in the environment to form combined toxic effects, making it difficult for existing intervention methods to cope. Physical methods such as magnetic nanoiron can reduce the accumulation of nanoplastics in the body, but cannot reverse the pathological changes that have occurred. Therefore, there is an urgent need to find a drug that can efficiently reverse nanoplastics-induced ovarian damage. Eriodyctiol is a natural dihydroflavonoid compound with antioxidant, anti-inflammatory, analgesic, and effects in improving diabetes and diabetic complications, but whether it can be used as a drug to effectively reverse nanoplastics-induced ovarian damage remains to be explored.
[0033] The present invention provides an application of eriocitrin in the preparation of a drug for treating nanoplastics-induced ovarian injury. The present invention has verified through systematic experiments that eriocitrin has a reparative effect on nanoplastics-induced ovarian injury in mice. Specifically, after treatment with eriocitrin, the ovarian morphology of mice was significantly improved. Hematoxylin-eosin staining showed a reduction in atretic follicles and inhibition of abnormal luteal hyperplasia, and follicular development recovered to normal levels. Serum hormone detection experiments confirmed that eriocitrin effectively increased the levels of estradiol and anti-Müllerian hormone and decreased the level of follicle-stimulating hormone, reversing the reproductive endocrine disorders caused by nanoplastics. Electrophoresis experiments further revealed that eriocitrin blocked apoptosis by reducing the Bax / Bcl-2 ratio and inhibiting the activation of Caspase-3. By stabilizing the Nrf2 / KEAP1 system, upregulating the expression of SOD1 and downregulating the overactivation of HO-1, the redox balance was reconstructed, and the ovarian injury induced by nanoplastics could be reversed synergistically through multiple pathways.
[0034] Example 1: Reparative effect of eriocitrin on the ovarian morphology of mice exposed to NPs 1. Establishment of a mouse ovarian injury model Thirty 6-week to 8-week-old ICR female mice were selected. After one week of adaptive feeding, they were randomly divided into an injury group, an eriocitrin group, and a blank group, with 10 mice in each group.
[0035] Injury group: Intragastric administration of 25-nm-sized polystyrene nanoplastics for 42 consecutive days, and the intragastric administration dose of polystyrene nanoplastics was 1 mg / kg / day.
[0036] Eriocitrin group: Intragastric administration of 25-nm-sized polystyrene nanoplastics for 42 consecutive days, and at the same time, eriocitrin was intragastrically administered. The intragastric administration dose of polystyrene nanoplastics was 1 mg / kg / day, and the intragastric administration dose of eriocitrin was 100 mg / kg.
[0037] Blank group: Intragastric administration of normal saline with the same volume as eriocitrin.
[0038] After 42 consecutive days of treatment in the injury group, the eriocitrin group, and the blank group, the mice in each group were fasted for 24 h before sampling without water deprivation, and weighed before sampling. Blood was collected by the method of eye enucleation, and then the mice were sacrificed by cervical dislocation. The ovaries of the mice were taken for subsequent experiments.
[0039] 2. Evaluation of pathological manifestations of mouse ovaries Paraffin sections of mouse ovarian tissues were prepared and stained with hematoxylin-eosin according to the following steps.
[0040] S1. Fixation and sectioning: The mouse ovarian tissues obtained after establishing the mouse ovarian injury model were fixed, dehydrated, and paraffin-embedded to obtain mouse ovarian tissue wax blocks. Then, the mouse ovarian tissue wax blocks were made into 5-μm sections and baked in an oven at 60 °C for 2 h.
[0041] S2. Dewaxing and rehydration: Dewax the sections obtained in step S1 with xylene for 20 min, then sequentially place the sections in 100 wt% ethanol, 95 wt% ethanol, 90 wt% ethanol, 80 wt% ethanol, 70 wt% ethanol, and 50 wt% ethanol for static treatment for 3 min each, and then place them in PBS for static treatment for 5 min. Repeat this step once.
[0042] S3. Staining: Immerse the sections obtained in S2 in hematoxylin staining solution for static staining for 5 min, then rinse with tap water to wash off the unattached dye. Then sequentially immerse the sections in hydrochloric acid-ethanol solution for differentiation for 2 s, immerse in ammonia water for infiltration and blueing for 3 s, and immerse in eosin staining solution for soaking for 3 min. Wash off the unattached dye with tap water. Then sequentially place the sections in 75 wt% ethanol, 80 wt% ethanol, 90 wt% ethanol, 96 wt% ethanol, and 100 wt% ethanol for 5 min each, soak in xylene for 10 min, then drop neutral resin onto the cleared sections, and cover with a coverslip for sealing.
[0043] S4. Microscopic examination: Observe the stained tissue sections under a microscope.
[0044] From Figure 1 It can be seen from the staining results shown that the development of ovarian follicles at all levels in the blank group and the eupatilin group of mice is normal; compared with the blank group and the eupatilin group of mice, the ovarian follicles in the injury group of mice develop poorly, follicular atresia occurs, large follicles coexist with corpora lutea, and the number of corpora lutea increases.
[0045] As Figure 2 shown, after statistically analyzing the numbers of ovarian follicles at all levels in the blank group, the eupatilin group, and the injury group of mice respectively, it was found that compared with the blank group, the numbers of primordial follicles and growing follicles in the injury group of mice decreased, and the number of atretic follicles increased; compared with the injury group, the number of atretic follicles in the eupatilin group decreased.
[0046] Example 2: Recovery of the reproductive endocrine function of eupatilin in NPs-exposed mice According to the instruction steps of the mouse anti-Müllerian hormone ELISA kit, the mouse estradiol ELISA kit, and the mouse follicle-stimulating hormone ELISA kit respectively, determine the contents of anti-Müllerian hormone, estradiol, and follicle-stimulating hormone in the mouse serum.
[0047] S1. Collect the blood samples of each group of mice obtained by establishing the mouse ovarian injury model in Example 1. After the blood samples coagulate at room temperature for 30 min, centrifuge at 3000 g for 15 min, and aspirate the upper serum samples.
[0048] S2. Take out the required strips from the aluminum foil bag that has been equilibrated at room temperature for 10 min, and seal the remaining strips with a self-sealing bag and return them to 4°C.
[0049] S3, Sample addition: Add the samples or standard products with different concentrations into the wells at 50 μL / well respectively. Add 50 μL of the universal diluent into the blank well. Immediately add 50 μL of the Biotin-antibody working solution to each well. After covering with the sealing film, incubate at 37 °C for 1 h.
[0050] S4, Plate washing: Discard the liquid. Add 300 μL of 1× washing solution to each well, let stand for 1 min, discard the washing solution, and pat dry on the absorbent paper. Repeat this step 3 times.
[0051] S5, Add enzyme conjugate working solution: Add 100 μL of the enzyme conjugate working solution to each well. After covering with the sealing film, incubate at 37 °C for 30 min.
[0052] S6, Plate washing: Discard the liquid and wash the plate 5 times.
[0053] S7, Add substrate: Add 90 μL of the substrate TMB to each well, cover with the sealing film, and incubate at 37 °C in the dark for 15 min.
[0054] S8, Add stop solution: Add 50 μL of the stop solution to each well, and immediately measure the OD value of each well at a wavelength of 450 nm.
[0055] The results are as Figure 3 shown. The contents of anti-Müllerian hormone and estradiol in the serum of the injury group were significantly lower than those of the blank group, and the content of follicle-stimulating hormone in the serum of the injury group was significantly higher than that of the blank group. However, after treatment with eriodictyol, the levels of anti-Müllerian hormone, estradiol, and follicle-stimulating hormone in the serum of the eriodictyol group were effectively alleviated compared with those of the injury group.
[0056] Example 3: Improvement of eriodictyol on ovarian apoptosis in NPs-exposed mice Extract the ovarian tissue proteins of each group of mice obtained by establishing the mouse ovarian injury model in Example 1, and perform SDS-PAGE electrophoresis separation. After transfer membrane and blocking, add the primary antibody solutions of apoptosis-related factors Bax, Bcl-2, and Caspase3 and incubate overnight at 4 °C. Then wash the membrane 3 times with TBST buffer, incubate in the secondary antibody solution at room temperature for 1 h, and detect the protein expression level using an imaging system.
[0057] The results are as Figure 4 shown. Compared with the blank group, the injury group led to an increase in the Bax / Bcl-2 ratio, which is usually related to the activation of cell apoptosis. However, in the ovarian proteins of mice with nanoplastic injury treated with eriodictyol, the increase in the Bax / Bcl-2 ratio was inhibited, and the activation of Caspase-3 was also significantly reduced, indicating that eriodictyol can effectively inhibit the apoptotic signal transduction induced by nanoplastics.
[0058] Example 4: Verification of eriodictyol regulating the Nrf2 / HO-1 pathway Extract the ovarian tissue proteins of the mice in each group obtained from the mouse ovarian injury model in Example 1, and perform SDS-PAGE electrophoresis separation. After transfer and blocking, add the primary antibody solutions of SOD1, Nrf2, KEAP1, and HO-1 and incubate overnight at 4°C. Then wash the membrane 3 times with TBST buffer, incubate in the secondary antibody solution at room temperature for 1 h, and detect the protein expression level using an imaging system.
[0059] The results are as Figure 5 shown. Compared with the blank group, the protein expression levels of Nrf2, KEAP1, and SOD1 in the injury group decreased, while the protein expression level of HO-1 increased. However, after treatment with eriodictyol, the protein expression levels of Nrf2, KEAP1, and SOD1 increased, and the expression level of HO-1 decreased, indicating that eriodictyol can stabilize the Nrf2 / KEAP1 system and precisely regulate the expression of antioxidant enzymes, effectively reversing the vicious cycle of oxidative stress-inflammation induced by NPs.
[0060] It should be noted that when the present invention involves a numerical range, it should be understood that any value between the two endpoints of each numerical range and the two endpoints can be selected. Since the steps and methods adopted are the same as those in the examples, in order to prevent repetition, the present invention describes the preferred embodiments. Although the preferred embodiments of the present invention have been described, those skilled in the art can make additional changes and modifications to these embodiments once they know the basic creative concept. Therefore, the appended claims are intended to be interpreted as including the preferred embodiments and all changes and modifications falling within the scope of the present invention.
[0061] Obviously, those skilled in the art can make various changes and modifications to the present invention without departing from the spirit and scope of the present invention. Thus, if these modifications and variations of the present invention fall within the scope of the claims of the present invention and their equivalent technologies, the present invention is also intended to include these modifications and variations.
Claims
1. Application of eriocitrin in the preparation of a drug for treating ovarian injury induced by nanoplastics.
2. Use of eriocitrin according to claim 1 in the preparation of a medicament for treating nanoplastics-induced ovarian injury, characterized in that, The nanoplastics are polystyrene nanoplastics.
3. Use of eriocitrin according to claim 1 in the preparation of a medicament for treating nano-plastic-induced ovarian injury, characterized in that, The eriocitrin is used for preparing a drug for reversing reproductive endocrine disorders caused by nanoplastics.
4. Use of eriocitrin according to claim 3 in the preparation of a drug for treating nano-plastic-induced ovarian injury, characterized in that, The eriocitrin is used for preparing a drug for improving ovarian morphology or regulating follicular development level or regulating sex hormone level.
5. Use of eriocitrin according to claim 4 in the preparation of a medicament for treating nano-plastic-induced ovarian injury, characterized in that, The drug for regulating sex hormone level is a drug for increasing estradiol level or anti-Müllerian hormone level or decreasing follicle-stimulating hormone level.
6. Use of eriocitrin according to claim 1 in the preparation of a medicament for treating nano-plastic-induced ovarian injury, characterized in that, The drug takes eriocitrin as the sole active ingredient.
7. Use of eriocitrin according to claim 1 in the preparation of a medicament for treating nano-plastic-induced ovarian injury, characterized in that, The drug is composed of eriocitrin and pharmaceutically acceptable excipients.
8. Use of eriocitrin according to claim 1 in the preparation of a drug for treating nanoplastics-induced ovarian injury, characterized in that, The drug is an oral preparation or an injection.
Citation Information
Patent Citations
Application of chrysoeriol in preparation of products for promoting embryonic development
CN115896007A