Lycium barbarum polypeptide selenium nanoparticles, preparation method and pharmaceutical application

Abstract

This invention relates to the field of biopharmaceutical manufacturing technology, and discloses Lycium barbarum glycopeptide selenium nanoparticles, their preparation method, and their pharmaceutical applications. By preparing Lycium barbarum glycopeptide selenium nanoparticles, drugs prepared from them can inhibit oxidative stress-mediated mitochondrial damage and promote abnormal mitochondrial degradation, thereby maintaining mitochondrial homeostasis and inhibiting cGAS-STING pathway activation. Drugs prepared from Lycium barbarum glycopeptide selenium nanoparticles address the issues of insufficient local drug concentration and unclear mechanisms of targeted mitochondrial homeostasis in the treatment of chronic prostatitis.

Description

TECHNICAL FIELD

[0001] The present application relates to the technical field of biopharmaceutical manufacturing, in particular to a wolfberry glycopeptide selenium nanoparticle, a preparation method and a pharmaceutical application. BACKGROUND

[0002] The prostate is an important part of the male urethra (prostatic urethra), connecting the urinary system and the reproductive system. Due to the unique anatomical position of the prostate in the urogenital system, it is easily affected by various pathogenic factors, eventually evolving into chronic prostatitis (CP).

[0003] Oxidative stress and abnormal immune response (autoimmune-related inflammatory response) are recognized as important theories of the pathogenesis of chronic nonbacterial prostatitis (CNP). Oxidative stress is an important mechanism of CNP, and improving the antioxidant capacity of the prostate and rapidly removing oxidative stress metabolites is one of the important strategies for treating CNP; inhibiting the excessive activation of the immune system mediated by the initial pathogenic factor is another important strategy for treating CNP; however, whether oxidative stress and abnormal immune response have a causal relationship; the specific mechanism of how oxidative stress induces or promotes abnormal local immune response in the prostate is not clear, which greatly limits the use of its efficacy in the treatment of CNP.

[0004] Selenium (Se) and wolfberry glycopeptide (LBP) have various biological activities, especially special effects in antioxidant. Both have significant reducing, superoxide radical scavenging and inhibiting hydrogen peroxide abilities. The potential mechanisms include: selenium is the key active center of many antioxidant enzymes; wolfberry glycopeptide can reduce the loss of key active group sulfhydryl in antioxidant enzymes, thereby inhibiting the inactivation of antioxidant enzymes and maintaining intracellular antioxidant levels, such as SOD, CAT and glutathione peroxidase (GPX4), which can synergistically improve intracellular antioxidant levels. Studies have found that the level of mitochondrial damage-related molecules in prostate cells increases in chronic prostatitis, which may be potentially related to the increase in oxidative stress. After inhibiting mitochondrial damage, prostatitis tends to be relieved and symptoms are reduced, which indicates that oxidative stress-mediated mitochondrial damage may play an important role in the development of prostatitis. Among them, further improving the level of intracellular autophagy, promoting damaged mitochondria to enter autophagic lysosomes for degradation (mitophagy), maintaining normal mitochondrial levels in cells, and achieving a dynamic balance (homeostasis) of mitochondrial damage-degradation, which may be one of the potential mechanisms for inhibiting mitochondrial damage and relieving prostatitis.

[0005] It is difficult for prostate drugs to penetrate, resulting in low local drug concentration and poor treatment effect. The main reason is related to the unique anatomical structure and physiological barrier of the prostate. The outer envelope of the prostate is dense, the internal gland structure is complex, and the presence of the blood-prostate barrier limits the entry of drug molecules into the gland tissue. Although selenium and glycosylated peptides have unique biological effects in terms of antioxidant capacity, the special anatomical structure of the prostate makes the proportion and time of selenium and glycosylated peptides supplemented by intravenous injection to stay in the prostate tissue unsatisfactory. Studies have shown that nanomedicines have the effect of passive targeting to inflammatory sites, known as the ELVIS effect (increased vascular permeability and inflammatory cell uptake at inflammatory sites). In the inflammatory microenvironment, the blood vessels around the inflammation proliferate and expand. When nanomedicines pass through the blood vessels at the inflammation site, they will leak from the enlarged vascular gap and accumulate at the inflammation site through the mediation of inflammatory cells.

[0006] Therefore, it is necessary to combine selenium and glycosylated peptides to develop a high biocompatibility medical nanomedicine for treating chronic prostatitis. It can relieve chronic prostatitis by inhibiting oxidative stress-mediated mitochondrial damage and promoting abnormal mitochondrial degradation. SUMMARY

[0007] The purpose of the present application is to overcome the shortcomings of the prior art and provide a glycosylated peptide selenium nanoparticle, a preparation method and a pharmaceutical application. The drug prepared therefrom has the effect of inhibiting oxidative stress-mediated mitochondrial damage and promoting abnormal mitochondrial degradation, thereby maintaining mitochondrial homeostasis and inhibiting the activation of the cGAS-STING pathway. The drug prepared from the glycosylated peptide selenium nanoparticle solves the problems of insufficient local drug concentration and unclear targeted mitochondrial homeostasis precise treatment mechanism in the treatment of chronic prostatitis.

[0008] To solve the above technical problems, the present application discloses the use of a glycosylated peptide selenium nanoparticle in the preparation of a drug for treating chronic prostatitis.

[0009] Preferably, the drug for treating chronic prostatitis has the following effects: regulating mitochondrial homeostasis by inhibiting mitochondrial damage and promoting damaged mitochondrial degradation, and inhibiting the cGAS-STING pathway.

[0010] Preferably, the drug for treating chronic prostatitis comprises a preparation made of a glycosylated peptide selenium nanoparticle and a pharmaceutically acceptable carrier or additive.

[0011] Preferably, the drug for treating chronic prostatitis comprises an intravenous dosage form.

[0012] Further, the drug for treating chronic prostatitis comprises an intravenous drip agent made of a glycosylated peptide selenium nanoparticle and physiological saline.

[0013] This invention also discloses a method for preparing selenium-enriched wolfberry glycopeptide nanoparticles, comprising the following steps: Sodium selenite was added to an aqueous solution of wolfberry glycopeptide and stirred. Then vitamin C was added and stirred again. The resulting product was dialyzed and filtered, and then freeze-dried to obtain wolfberry glycopeptide selenium nanoparticles.

[0014] Preferably, when preparing the selenium nanoparticles of goji berry glycopeptide, the concentration of goji berry glycopeptide in the aqueous solution of goji berry glycopeptide is 2 mg / mL.

[0015] Preferably, in the preparation of wolfberry glycopeptide selenium nanoparticles: the concentration of sodium selenite added is 10 mM; the concentration of vitamin C added is 40 mM.

[0016] Preferably, the stirring conditions for preparing the goji berry glycopeptide selenium nanoparticles are: stirring at 25°C for 6 hours.

[0017] Preferably, when preparing the wolfberry glycopeptide selenium nanoparticles, the vitamin C is added at a rate of 1 drop / second.

[0018] Preferably, the stirring time is 1-3 minutes during the preparation of wolfberry glycopeptide selenium nanoparticles.

[0019] Preferably, the goji berry glycopeptide selenium nanoparticles are prepared using the method described above.

[0020] This invention also discloses the application of the above-mentioned wolfberry glycopeptide selenium nanoparticles in constructing a CNP mouse model.

[0021] Preferably, it includes the following steps: Step 1: Select mice as experimental subjects and place them in a sleep deprivation device to establish a CNP mouse model; Step 2: Apply selenium-enriched wolfberry glycopeptide nanoparticles to mice with CNP and test the effect of selenium-enriched wolfberry glycopeptide nanoparticles on treating prostatitis in CNP mice.

[0022] The present invention also discloses a CNP mouse model based on the above-mentioned wolfberry glycopeptide selenium nanoparticles.

[0023] Compared with the prior art, the beneficial effects of the present invention are as follows: 1. This invention utilizes nanotechnology to integrate the biological activities of selenium and Lycium barbarum glycopeptides, designing them into selenium Lycium barbarum glycopeptide nanoparticles (Se@LBP nanoparticles). The synthesis method of Se@LBP nanoparticles is simple, yields high quantities, and exhibits stable properties. Furthermore, through the ELVIS effect, they can efficiently aggregate in prostatitis tissue, achieving high local drug concentrations. In the synthesis process of Se@LBP nanoparticles, this invention explores the optimal preparation ratio by adjusting the feed ratio of Se and LBP, thereby achieving the goal of both Se and LBP being non-toxic and maximizing their biological activity. In addition, Se@LBP nanoparticles can continuously release Se and LBP, allowing drugs prepared from Se@LBP nanoparticles to achieve long-term therapeutic effects, solving the dilemma of poor drug penetration and low drug concentration leading to unsatisfactory therapeutic effects in prostate diseases.

[0024] 2. The oxidative stress-related cGAS-STING pathway plays a crucial role in the development and progression of CNP. Specifically, increased prostatic oxidative stress promotes mitochondrial damage and releases mitochondrial DNA (mtDNA), thereby activating the cGAS-STING pathway and secreting the effector cytokine IFN-β. Subsequently, inflammatory cells are recruited to infiltrate the prostate, forming a local inflammatory microenvironment and promoting the development and progression of prostatitis. This invention links the abnormal etiologies of oxidative stress and immune response to explore the therapeutic mechanism of CNP and demonstrates that the drug prepared from Se@LBP nanoparticles can regulate mitochondrial homeostasis through a dual pathway, inhibiting the cGAS-STING pathway, thereby treating CNP.

[0025] Specifically, Se@LBP nanoparticles, upon entering cells, can enhance intracellular antioxidant capacity and reduce the level of oxidative stress products, thereby decreasing the continuous increase of damaged mitochondria (first pathway: reducing the source). Secondly, the goji berry glycopeptides in Se@LBP nanoparticles can enhance intracellular autophagic flux and increase autophagy levels, promoting the degradation of damaged mitochondria within autolysosomes, further reducing the accumulation of damaged mitochondria (second pathway: promoting degradation). Based on these two pathways, Se@LBP nanoparticles have a synergistic inhibitory effect on the cGAS-STING pathway, and drugs prepared from Se@LBP nanoparticles can achieve the therapeutic goal of CNP by inhibiting the cGAS-STING pathway. Attached Figure Description

[0026] Figure 1 These are TEM images of the selenium glycopeptide nanoparticles (Se@LBP nanoparticles) and Se nanoparticles prepared in Example 1 of this invention; Figure 1In the image, (a1) is a TEM image of Se nanoparticles under a 200 nm scale, (a2) is a TEM image of Se nanoparticles under a 100 nm scale, (b1) is a TEM image of Se@LBP nanoparticles under a 200 nm scale, and (b2) is a TEM image of Se@LBP nanoparticles under a 100 nm scale. Figure 2 This is a graph showing the surface Zeta potential changes of Se@LBP nanoparticles and Se nanoparticles prepared in Example 1 of this invention; Figure 3 These are the UV absorption and infrared spectra of Se@LBP nanoparticles and Se nanoparticles and Lycium barbarum glycopeptide (LBP) prepared in Example 1 of this invention. Figure 3 In the figure, (a) is the UV absorption spectrum of wolfberry glycopeptide, Se nanoparticles and Se@LBP nanoparticles, and (b) is the infrared spectrum of wolfberry glycopeptide, Se nanoparticles and Se@LBP nanoparticles. Figure 4 This is an elemental mapping diagram of the Se@LBP nanoparticles prepared in Example 1 of this invention; Figure 5 The images show the original cell images and intracellular green ROS probe co-localization test images of the control group, Se@LBP nanoparticle group, LPS group, and LPS+Se@LBP nanoparticle group in the in vitro cell experiment of Example 1 of this invention. Figure 5 In the image, (a) is the original cell image, and (b) is the intracellular green ROS probe colocalization test image. Figure 6 The above are flow cytometry results of mitochondrial damage in the control group, Se@LBP nanoparticle group, LPS group, and LPS+Se@LBP nanoparticle group in the in vitro cell experiment of Example 1 of the present invention. Figure 6 In the figure, (a) is a flow cytometry plot of mitochondrial damage detection, and (b) is a statistical graph of the flow cytometry results of mitochondrial damage detection. Figure 7 The images show mitochondrial damage fluorescence in the control group, Se@LBP nanoparticle group, LPS group, and LPS+Se@LBP nanoparticle group during the in vitro cell experiment of Example 1 of this invention. Figure 8 This is a diagram showing the colocalization of mitochondria and mitochondrial DNA (double-stranded DNA) in the in vitro cell experiment of Example 1 of the present invention, in the control group, Se@LBP nanoparticle group, LPS group, and LPS+Se@LBP nanoparticle group. Figure 9 This is a Western blot image of the key proteins (TBK1 and IRF3) of the cGAS-STING pathway and their phosphorylated protein (GAPDH) in the control group, Se@LBP nanoparticle group, LPS group, and LPS+Se@LBP nanoparticle group in the in vitro cell experiment of Example 1 of the present invention. Figure 10 This is a graph showing the change in Se ion content after treatment with physiological saline, Se nanoparticles, and Se@LBP nanoparticles in Example 1 of the present invention; Figure 10 In the figure, (a) shows the change in Se ion content after 1 week of intravenous treatment with saline, Se nanoparticles, and Se@LBP nanoparticles, and (b) shows the change in Se ion content 3 days after the drug was discontinued after 1 week of intravenous treatment with saline, Se nanoparticles, and Se@LBP nanoparticles. Figure 11 HE staining images of the normal control group, CNP modeling group, and CNP modeling + Se@LBP group in Example 2 of this invention; Figure 12 These are immunofluorescence staining images of prostate tissues from the normal control group, CNP model group, and CNP model + Se@LBP group in Example 2 of this invention; the scale bar for each image is 100 μm. Figure 13 These are images showing the inflammatory factor test results of prostate tissues in the normal control group, CNP model group, and CNP model + Se@LBP group in Example 2 of this invention. Figure 14 These are blood inflammatory factor test images from the normal control group, CNP model group, and CNP model + Se@LBP group in Example 2 of this invention. Figure 15 This is a Western blot image of the key proteins (TBK1 and IRF3) of the cGAS-STING pathway and their phosphorylated protein (GAPDH) in the normal control group, CNP modeling group, and CNP modeling + Se@LBP group in Example 2 of the present invention. Detailed Implementation

[0027] The present invention will be further illustrated below through specific embodiments. The following embodiments are specific implementations of the present invention, but the implementation of the present invention is not limited to the following embodiments. Any changes, modifications, substitutions, combinations, or simplifications made without departing from the spirit and principle of the present invention shall be considered equivalent substitutions and are included within the protection scope of the present invention.

[0028] In the description of this invention, it should be noted that Lycium barbarum glycopeptide is referred to as LBP in this invention.

[0029] Example 1 This embodiment discloses a method for preparing selenium-containing glycopeptides from wolfberry, comprising the following steps: 10 mM sodium selenite was added to a 2 mg / mL aqueous solution of Lycium barbarum glycopeptide and stirred at 25 °C for 6 h. Then, 40 mM vitamin C was added at a rate of 1 drop / second. After the addition was complete, stirring was continued for 3 min. The resulting product was dialyzed and filtered with distilled water (MWCO: 3500 Da) for 48 h and then freeze-dried to obtain Lycium barbarum glycopeptide selenium nanoparticles, denoted as Se@LBP. The wolfberry glycopeptide was purchased from Ningxia Tianren Wolfberry Biotechnology Co., Ltd.

[0030] The physicochemical properties of selenium-containing wolfberry glycopeptide nanoparticles (Se@LBP) were analyzed, and the results are as follows: Figure 1 As shown.

[0031] The morphology of Se nanoparticles and Se@LBP nanoparticles was observed using transmission electron microscopy (TEM, Hitachi HT7700), and their fine structure was observed using high-resolution TEM (HR-TEM) on a Talos F200S system (Thermo Fisher Scientific) to evaluate whether the structure and other characteristics of the selenium nanoparticles changed after surface modification. Figure 1 In the figures, (a1) and (a2) are TEM images of Se nanoparticles, and (b1) and (b2) are TEM images of Se@LBP nanoparticles. The test results in the figures show that the shape and core structure of the Se nanoparticles did not change after modification with LBP, indicating that the modified LBP with blurred boundaries can be observed.

[0032] The size distribution and surface charge changes of the material were detected using a Zetasizer Nano ZS90. Figure 2 The figure shows the change in zeta potential on the surface of Se@LBP nanoparticles after modification with Se nanoparticles and Lycium barbarum glycopeptide LBP. The test results in the figure show that after modification with negatively charged LBP, the zeta potential of Se nanoparticles changes from about 2mV to -13mV, which indirectly indicates that the modification was successful.

[0033] Fourier transform infrared spectrophotometer (FTIR) (Nexus 470) and X-ray photoelectron spectroscopy (XPS) (Escalab 250 Xi) were used to evaluate the characteristic absorption peaks, chemical elemental composition and content of Se@LBP, respectively, in order to assess the success and amount of material modification at each step. Figure 3 To obtain the ultraviolet absorption peaks and infrared spectra of the raw materials LBP, Se, and Se@LBP nanoparticles, Figure 4 The image shows the elemental mapping of Se@LBP nanoparticles. The test results in the image show that the position of the main absorption peak did not change, but the peak value changed, indicating that LBP modification of Se nanoparticles was successful.

[0034] In summary, the size and elemental composition of the wolfberry glycopeptide selenium nanoparticles prepared by this invention meet the target requirements.

[0035] The effects and mechanisms of selenium lycine glycopeptide nanoparticles (Se@LBP nanoparticles) on regulating mitochondrial homeostasis and inhibiting the cGAS-STING axis were investigated and analyzed. The results are as follows: Figures 5 to 9 As shown.

[0036] RWPE-1 prostatic epithelial cells were seeded in 96-well culture dishes (approximately 10,000 cells / well). When the cell density reached approximately 60%, an in vitro inflammatory environment was simulated using lipopolysaccharide (LPS) (according to the method described in Redox Biol. 2019, 24:101215). After treating RWPE-1 prostatic epithelial cells with LPS for 4 h, Se@LBP nanoparticles were added and co-incubated for 12 h. The incubation products were then analyzed.

[0037] Cells were collected to detect changes in intracellular ROS levels (fluorescent probe) and mitochondrial membrane potential (JC-1 staining). The effects of Se@LBP treatment on these indicators were observed to evaluate its antioxidant and mitochondrial function protection efficacy.

[0038] Cells were collected to detect mitophagy markers (mitochondrial lysosomal fluorescence colocalization) and to assess the biological function of Se@LBP-induced damage to mitochondrial degradation.

[0039] Cells were collected to detect changes in key proteins of the cGAS-STING pathway (p-TBK1 / TBK1, p-IRF3 / IRF3) and to assess their impact on the cGAS-STING pathway and their efficacy in inhibiting inflammation.

[0040] Figure 5 This is a diagram showing the co-localization of the original cell image and the intracellular green ROS probe, created by... Figure 5 The test results show that Se@LBP inhibits the increase of ROS after liposome LPS stimulation; Figure 6 This is a flow cytometry result of Se@LBP inhibiting mitochondrial damage after liposome LPS stimulation. Figure 7 The image shows the fluorescence of mitochondrial damage after Se@LBP inhibits liposome LPS stimulation (using Hoechst fluorescent dye). Figure 6 and Figure 7 The test results show that LPS stimulation alters the mitochondrial membrane potential, indicating mitochondrial damage caused by oxidative stress. Treatment with Se@LBP nanoparticles after LPS stimulation significantly inhibits this change in mitochondrial membrane potential, demonstrating that Se@LBP nanoparticles can significantly suppress LPS-induced mitochondrial damage and protect mitochondrial function. Figure 8This is a map of mitochondrial and mitochondrial DNA colocalization assays, by... Figure 8 The test results show that mitochondrial DNA release mediated by mitochondrial damage increases after liposome LPS stimulation, while Se@LBP can significantly inhibit mitochondrial DNA levels, which may be related to autophagy promoting the degradation of damaged mitochondria. Figure 9 Western blot images of key proteins (TBK1 and IRF3) and their phosphorylated proteins (GAPDH) in the cGAS-STING pathway, by... Figure 9 The test results show that Se@LBP inhibits the activation of the cGAS-STING pathway mediated by mitochondrial DNA release after liposome LPS stimulation.

[0041] In summary, the anti-inflammatory effects of Se@LBP nanoparticles were verified through in vitro cell experiments. The results showed that, compared with the control group, LPS stimulation significantly increased intracellular oxidative stress (ROS), caused mitochondrial damage, and activated the cGAS-STING inflammatory pathway, inducing sustained inflammation. Se@LBP nanoparticles could significantly inhibit the above-mentioned inflammatory processes.

[0042] Example 2 This embodiment discloses a method for evaluating the regulation of mitochondrial homeostasis and inhibition of the cGAS-STING axis by selenium nanoparticles of Lycium barbarum glycopeptide using a CNP mouse model, including the following steps: ICR mice were selected as experimental subjects and placed in a transparent cylindrical sleep deprivation device with a height of 25 cm and a diameter of 30 cm for 7 days of acclimatization. The sleep deprivation device was turned off for 1 hour after every 5 hours of work, so that the mice could stay awake for 20 hours a day as a CNP model. Control group mice were placed in the same sleep deprivation device and given ample water, food, and normal sleep. Mice successfully modeled using the above method were randomly divided into three groups: a normal control group, a CNP modeling + Se@LBP group (mice were intravenously injected with Se@LBP nanoparticles at a concentration of 5 mg / kg daily after successful modeling), and a CNP modeling group + PBS buffer group (mice were intravenously injected with the same volume of PBS as Se@LBP daily after successful modeling). Inflammation of prostate tissue, inflammatory cytokines (IL-6, PGE2, and TNF-α), and pelvic pain response were detected in each group of mice to evaluate the role of Se@LBP in treating prostatitis in CNP mice.

[0043] The aggregation and anti-prostatitis effects of selenium lycine glycopeptide nanoparticles (Se@LBP nanoparticles) were analyzed, and the results are as follows: Figures 10 to 15 As shown.

[0044] Figure 10 Figure (a) shows the changes in Se ion content after one week of intravenous treatment with Se@LBP nanoparticles and Se nanoparticles at the same Se dose. The results show that the Se@LBP nanoparticles aggregated to achieve the highest Se ion concentration, indicating significant drug aggregation.

[0045] Figure 10 (b) shows the changes in Se ion content 3 days after the cessation of intravenous treatment with Se@LBP nanoparticles and Se nanoparticles at the same Se dose for 1 week. The results show that the drug concentration of Se@LBP nanoparticles decreases slowly, and the drug concentration 3 days after the cessation of treatment is more than twice that of Se nanoparticles, indicating that Se@LBP nanoparticles can release drugs for a long time and achieve a sustained therapeutic effect.

[0046] The effective human dosage range of this invention can be derived by conversion from the animal experimental dosages in the examples, as shown in the following conversion formula: Human dose concentration (mg / kg) = Mouse dose concentration (mg / kg) ÷ 10.

[0047] Figure 11 HE staining images of the normal control group, CNP modeling group, and CNP modeling + Se@LBP group in the experiment. Figure 11 The test results show that, compared with the control group, the CNP modeling group successfully constructed an animal model of chronic prostatitis (CNP), and after treatment with Se@LBP nanoparticles, the prostate matrix infiltrating inflammatory cells disappeared in the CNP modeling + Se@LBP group. Figure 12 This is an immunofluorescence staining image of prostate tissue, by Figure 12 The test results show that, compared with the control group, the CNP modeling group successfully established a chronic prostatitis (CNP) animal model. After treatment with Se@LBP, the infiltrating inflammatory cells in the CNP modeling + Se@LBP group disappeared (where red staining represents inflammatory cells CD45). + ); Figure 13 A map of inflammatory factors in prostate tissue, created by... Figure 13 The test results show that after treatment with Se@LBP nanoparticles, the levels of prostaglandins (PGE2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-β (IFN-β) in the prostate tissue of the CNP model + Se@LBP group all decreased to normal levels. Figure 14 A graph of inflammatory factors in the blood (serum), by Figure 14The test results show that after treatment with Se@LBP nanoparticles, the blood inflammatory factors (PGE2, TNF-α, IL-6 and IFN-β) in the CNP model + Se@LBP group all decreased to normal levels.

[0048] Figure 15 Western blot images of key proteins (TBK1 and IRF3) and their phosphorylated proteins (GAPDH) in the cGAS-STING pathway, by... Figure 15 The test results show that after treatment with Se@LBP nanoparticles, the cGAS-STING pathway activated in mice in the CNP model + Se@LBP group was significantly inhibited, indicating that the cure of prostatitis is related to the inhibition of the cGAS-STING pathway.

[0049] In summary, after one week of treatment with Se@LBP nanoparticles (5 mg / kg) via intravenous injection, prostate inflammation in mice significantly subsided, and inflammatory factors in blood and prostate tissue decreased significantly to normal levels, demonstrating a significant anti-prostatitis effect. IFN-β is a key upstream factor regulating the activation of the cGAS-STING pathway.

[0050] It should be noted that the embodiments described above are only for explaining the present invention and do not constitute any limitation on the present invention. The present invention has been described with reference to typical embodiments, but it should be understood that the words used therein are descriptive and explanatory terms, not limiting terms. Modifications can be made to the present invention within the scope of the claims, and revisions can be made to the present invention without departing from the scope and spirit of the present invention. Although the present invention described herein relates to specific methods, materials, and embodiments, it does not mean that the present invention is limited to the specific examples disclosed herein; on the contrary, the present invention can be extended to all other methods and applications with the same function.

Claims

1. The application of selenium-enriched wolfberry glycopeptide nanoparticles in the preparation of drugs for treating chronic prostatitis, characterized in that, The method for preparing the wolfberry glycopeptide selenium nanoparticles includes the following steps: Sodium selenite was added to an aqueous solution of wolfberry glycopeptide and stirred. Then vitamin C was added and stirred again. The resulting product was dialyzed and filtered, and then freeze-dried to obtain wolfberry glycopeptide selenium nanoparticles. The drug for treating chronic prostatitis has the following effects: it regulates mitochondrial homeostasis by inhibiting mitochondrial damage and promoting the degradation of damaged mitochondria, and inhibits the cGAS-STING pathway.

2. The application of the selenium-enriched wolfberry glycopeptide nanoparticles according to claim 1 in the preparation of a drug for treating chronic prostatitis, characterized in that, The wolfberry glycopeptide selenium nanoparticles were prepared using the method described above.

3. The application of the selenium-enriched wolfberry glycopeptide nanoparticles according to claim 1 in the preparation of a drug for treating chronic prostatitis, characterized in that, The medication for treating chronic prostatitis includes formulations made from selenium-containing lycine glycopeptide nanoparticles and pharmaceutically acceptable carriers or additives.

4. The application of the selenium-enriched wolfberry glycopeptide nanoparticles according to claim 1 in the preparation of a drug for treating chronic prostatitis, characterized in that, The medications used to treat chronic prostatitis include intravenous formulations.

5. The application of the selenium-enriched wolfberry glycopeptide nanoparticles according to claim 1 in the preparation of a drug for treating chronic prostatitis, characterized in that, The medication for treating chronic prostatitis includes an intravenous infusion made from selenium-enriched wolfberry glycopeptide nanoparticles and saline solution.

6. The application of the wolfberry glycopeptide selenium nanoparticles as described in claim 2 in the construction of a CNP mouse model.

7. The application according to claim 6, characterized in that, Includes the following steps: Step 1: Select mice as experimental subjects and place them in a sleep deprivation device to establish a CNP mouse model; Step 2: Apply selenium-enriched wolfberry glycopeptide nanoparticles to mice with CNP and test the effect of selenium-enriched wolfberry glycopeptide nanoparticles on treating prostatitis in CNP mice.

8. A CNP mouse model based on the wolfberry glycopeptide selenium nanoparticles of claim 2.

9. The model according to claim 8, characterized in that, The following steps are included in the construction process: Step 1: Select mice as experimental subjects and place them in a sleep deprivation device to establish a CNP mouse model; Step 2: Apply selenium-enriched wolfberry glycopeptide nanoparticles to mice with CNP and test the effect of selenium-enriched wolfberry glycopeptide nanoparticles on treating prostatitis in CNP mice.

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