Application of alpha-solanine in preparation of medicine for treating Alzheimer's disease

Abstract

The invention relates to application of alpha-solanine in preparation of a medicine for treating Alzheimer's disease, and belongs to the technical field of biological medicine. The invention discloses the new application of alpha-solanine in preparation of the medicine for treating the Alzheimer's disease by regulating microglial cell autophagy for the first time. Firstly, based on a 5xFAD model mouse, it is found that alpha-solanine can improve the cognitive function of the Alzheimer's disease model mouse and relieve related pathological phenotypes. Secondly, in-vitro primary microglial cells are utilized to clarify that alpha-solanine inhibits apoptosis of the microglial cells by promoting autophagy of the microglial cells so as to play a role in treating the Alzheimer's disease. The results show that the alpha-solanine can obviously reduce or improve related pathological indexes of the Alzheimer's disease, can be used for preparing the medicine for treating the Alzheimer's disease, and has important significance in research and development of the medicine for treating the Alzheimer's disease.

Description

Technical Field

[0001] The invention relates to application of alpha-solanine in preparing a drug for treating Alzheimer's disease, and belongs to the technical field of biomedicine. Background Art

[0002] Alzheimer's disease (AD) is the most common neurodegenerative disease. The pathological changes and pathogenesis of AD are complex. First-line clinical drugs, including cholinesterase inhibitors and glutamate receptor antagonists, still have their own treatment limitations, and an effective cure has not yet been found. Therefore, exploring the pathogenesis of AD and developing new drugs to treat AD are current research hotspots.

[0003] Autophagy refers to the process in which eukaryotic cells use lysosomes to degrade their own cytoplasmic proteins and damaged organelles under the regulation of autophagy related genes (Atg). It is characterized by participating in the renewal and quality control of organelles, removing damaged or dysfunctional organelles, maintaining the stability of the intracellular environment, thereby inhibiting apoptosis, and helping cells adapt and survive. Genomic and proteomic evidence shows that microglia are similar to macrophages in other tissues and mainly play an immune function. As the main immune cells of the central nervous system, microglia play a key role in the development of Alzheimer's disease in the elderly. Their autophagy will inhibit microglial apoptosis, leading to enhanced neuroprotective function, thereby delaying the occurrence and development of AD.

[0004] α-solanine is a natural compound extracted from Solanaceae plants that can induce autophagy through multiple mechanisms, including activation of endoplasmic reticulum stress and inhibition of AKT / mTOR signaling pathways, which may be related to its anti-proliferative activity and ability to induce cancer cell death. Recent studies have shown that α-solanine has a neuroprotective effect, but whether α-solanine can inhibit apoptosis by regulating microglial autophagy and thus delay the progression of Alzheimer's disease has not been reported.

[0005] Therefore, exploring the effects and mechanisms of α-solanine on Alzheimer's disease by regulating microglial autophagy is expected to provide a potential drug basis and theoretical basis for the prevention and treatment of neurodegenerative diseases such as Alzheimer's disease, and also has important scientific value and good prospects for clinical transformation. Summary of the invention

[0006] In view of the deficiencies in the prior art, the present invention provides the use of α-solanine in the preparation of a drug for treating Alzheimer's disease.

[0007] The technical solution of the present invention is as follows: Application of α-solanine in the preparation of drugs for treating Alzheimer's disease.

[0008] Preferably according to the present invention, the structural formula of α-solanine is as follows: .

[0009] Preferably, according to the present invention, the α-solanine is used in the preparation of a drug for inhibiting apoptosis of microglia in brain tissue of patients with Alzheimer's disease.

[0010] Preferably, according to the present invention, the α-solanine is used in the preparation of a drug for inhibiting the expression of Aβ protein in the hippocampal tissue of patients with Alzheimer's disease.

[0011] Preferably according to the present invention, in the drug for treating Alzheimer's disease, α-solanine is the only active ingredient.

[0012] Preferably according to the present invention, the drug for treating Alzheimer's disease comprises α-solanine and a pharmaceutically acceptable carrier.

[0013] Preferably according to the present invention, the dosage form of the drug for treating Alzheimer's disease is granules, tablets, capsules, pills or oral liquid preparations.

[0014] Beneficial effects: 1. The present invention discloses for the first time a new use of α-solanine in the preparation of drugs for the treatment of Alzheimer's disease. First, based on 5xFAD model mice, the present invention found that α-solanine can improve the cognitive function of Alzheimer's disease model mice and alleviate related pathological phenotypes. Secondly, the present invention uses in vitro primary microglia to illustrate that α-solanine promotes microglial autophagy, inhibits microglial apoptosis, and plays a role in treating Alzheimer's disease by regulating microglial autophagy. These results all show that α-solanine can significantly reduce or increase the relevant pathological indicators of Alzheimer's disease, and α-solanine can be used to prepare drugs for the treatment of Alzheimer's disease, which is of great significance in the research and development of drugs for the treatment of Alzheimer's disease.

[0015] 2. Existing drugs for treating Alzheimer's disease face bottlenecks due to their single target and complex pathological mechanisms, while α-solanine has the advantages of low toxicity and multiple targets from natural products, as well as the characteristics of focusing on regulating the activation of microglial autophagy. The present invention provides a new medicinal use for α-solanine, shortens the time for the development of new drugs for treating Alzheimer's disease, and provides new ideas for the development of new drugs for treating Alzheimer's disease. BRIEF DESCRIPTION OF THE DRAWINGS

[0016] Figure 1 It is the cognitive and memory function assessment of each group of mice in the water maze test; In the figure, A and B are the evaluation results of each group of mice in the adaptive training stage; C and D are the evaluation results of each group of mice in the positioning navigation experiment stage; E and F are the evaluation indicators of each group of mice in the space exploration stage.

[0017] Figure 2 It is the staining conditions and statistical results of different indicators of brain tissue sections of mice in each group; In the figure, A is the HE staining result of brain tissue sections of mice in each group; B is the Nissl staining result of brain tissue sections of mice in each group; C is the statistical result of the number of neurons after brain tissue staining of mice in each group; D is the result of immunohistochemical staining of Aβ protein expression in brain tissue sections of mice in each group; E is the statistical result of Aβ protein expression in brain tissues of mice in each group; F is the result of immunofluorescence staining of brain tissue sections of mice in each group; G is the statistical result of Pearson correlation coefficient after immunofluorescence staining of brain tissues of mice in each group.

[0018] Figure 3 is the detection result of apoptosis-related protein expression in each group of mice; In the figure, A is the staining result of Cleaved-caspase3 (C-Cas3), an apoptosis-related indicator in the hippocampus of each group of mice evaluated by immunohistochemical staining; B is the staining result of Cleaved-caspase9 (C-Cas9), an apoptosis-related indicator in the hippocampus of each group of mice evaluated by immunohistochemical staining; C is the expression result of C-Cas3, an apoptosis-related indicator in the hippocampus of each group of mice; D is the expression result of C-Cas9, an apoptosis-related indicator in the hippocampus of each group of mice; E is the activity result of apoptosis protein Caspsae3 in the hippocampus of each group of mice; F is the activity result of apoptosis protein Caspsae9 in the hippocampus of each group of mice; GK is the expression result of apoptosis-related proteins in primary microglia of each group of mice.

[0019] Figure 4 This is a study on the effect of α-solanine in promoting microglial autophagy and inhibiting apoptosis; In the figure, A is the result of KEGG functional enrichment analysis; BD is the detection of autophagy-related proteins in primary microglia of each group of mice; E and F are the observation of autophagy flow by immunofluorescence staining; GK is the detection of apoptosis-related proteins in primary microglia of each group of mice; L and M are the detection of apoptosis protein activity in primary microglia.

[0020] Figure 5 α-Solanine promotes microglial autophagy and delays disease progression in Alzheimer's disease model mice.

[0021] In the figure, A is HE staining to evaluate the neuronal structure of each group of mice; B and C are Nissl staining to evaluate the situation and quantity statistics of Nissl bodies in each group of mice; D and E are Aβ protein expression and statistical results; FH are the evaluation results of water maze experiments in each group of mice. DETAILED DESCRIPTION

[0022] The technical solution of the present invention is further described below in conjunction with the embodiments, but the protection scope of the present invention is not limited thereto. The reagents and materials involved in the embodiments are all common commercially available products unless otherwise specified.

[0023] The α-solanine used in the examples was purchased from MCE, AβO was purchased from Sigma, and the autophagy inhibitor 3MA was purchased from Selleck.

[0024] The C57BL6J mice used in the examples were purchased from Shanghai Model Organisms Technology Co., Ltd.

[0025] The apoptosis protein activity detection kits Caspase3 colorimetric assay kit and Caspase9 colorimetric assay kit used in the examples were purchased from Beijing Solebow Technology Co., Ltd.

[0026] The collection and detection of mouse brain tissue specimens used in the examples were approved by the Animal Ethics Committee of Shandong University.

[0027] The autophagy double-labeled adenovirus mRFP-GFP-LC3 was purchased from Hanheng Biotechnology Co., Ltd.

[0028] Example 1: Effects of α-solanine on cognitive and memory functions in Alzheimer's disease model mice 1. Animal Preparation C57BL / 6 mice were taken and the amyloid precursor protein gene on chromosome 21 (APP, K670N / M671L, I716V, V717I) and the presenilin 1 (PSEN1, M146L, L286V) on chromosome 14 were mutated according to the existing method. The genes were expressed under the drive of a neuron-specific promoter, which synergistically accelerated the formation of Aβ plaques. 5xFAD mice were constructed and raised for 5 months to obtain Alzheimer's disease model mice.

[0029] 2. Drug preparation and injection The solvent was obtained by mixing dimethyl sulfoxide (DMSO) and PBS buffer at a ratio of 5:95 (volume ratio); α-solanine was added to the solvent and mixed evenly to obtain an α-solanine solution. The mice were then divided into three groups. The first group was given an intraperitoneal injection of 200 μl of normal saline to wild-type mice every other day, recorded as the wild control group (WT group); the second group was given an intraperitoneal injection of 200 μl of normal saline to 5xFAD mice every other day, recorded as the Alzheimer's disease group (AD group); the third group was given an intraperitoneal injection of 200 μl of α-solanine to 5xFAD mice every other day at a dose of 5 mg / kg, recorded as the Alzheimer's disease + α-solanine group (AD + α-solanine group). The above groups were treated continuously for 1 month.

[0030] 3. Cognitive and memory function assessment The water maze test was performed on the above three groups of mice. The specific steps are as follows: (1) Adaptive training: Each mouse was tested four times a day. The platform was placed in the same position for the first two and last two experiments. The mice were placed on both sides of the quadrant opposite to the platform. For example, if the platform was at position N, the mice were placed at positions 2 and 4. When placing the mice, they faced the wall of the pool and were placed gently in the water to avoid choking. The evaluation results of the adaptive training phase for each group of mice are shown in the figure below. Figure 1 As shown in A and B.

[0031] (2) Navigation test: Place the platform underwater to make it invisible. Place mice in water from four different entry points every day and record the time it takes for the mice to find the hidden platform. If the mice fail to find the platform within 60 seconds, guide them to the platform and record the maximum latency. Train four times a day, with a 20-minute interval between training sessions, for five consecutive days. The evaluation results of mice in each group during the navigation test are as follows: Figure 1 As shown in C and D.

[0032] (3) Spatial exploration experiment: On the second day after the last acquisition training, the platform was removed and a 60-second exploration training was started. The mice were placed in the water from the opposite side of the original platform quadrant. The time the mice spent in the target quadrant (the quadrant where the platform was originally placed) and the number of times they entered the target quadrant were recorded. The evaluation results of each group of mice in the spatial exploration stage are as follows: Figure 1 As shown in E and F.

[0033] Depend on Figure 1 As can be seen from A and B in the figure, compared with the Alzheimer's disease group mice, the Alzheimer's disease + α-solanine group mice significantly shortened the escape latency, while not affecting the swimming speed.

[0034] Depend on Figure 1As shown in C and D, compared with the Alzheimer's disease group mice, the Alzheimer's disease + α-solanine group mice significantly shortened the time to find the platform and the distance to reach the target.

[0035] Depend on Figure 1 As shown in Figures E and F, compared with the Alzheimer's disease group mice, the Alzheimer's disease + α-solanine group mice significantly increased the number of times they crossed the platform and the time they stayed in the target quadrant.

[0036] From the above results, it can be seen that α-solanine can significantly improve the behavior and memory of Alzheimer's disease model mice.

[0037] Example 2: Effect of α-solanine on pathological phenotypes of Alzheimer's disease model mice Brain tissues of the WT group, AD group, and AD+α-solanine group of mice constructed in Example 1 were taken, and then paraffin-embedded and sectioned, and then subjected to hematoxylin-eosin staining, Nissl body staining, immunohistochemistry, and immunofluorescence experiments, respectively. The results are as follows: Figure 2 The experimental data were analyzed using GraphPad Prism 9 software, and the t-test was used to analyze the differences between different groups. P <0.05,** P <0.01,*** P <0.001, and the results are expressed as mean ± SD. The hematoxylin-eosin staining, Nissl body staining, immunohistochemistry and immunofluorescence experiments are all conventional techniques and can be performed according to existing methods.

[0038] Depend on Figure 2 As shown in A, compared with the wild-type control mice, the cell contour clarity, nuclear structure prominence and cytoplasm transparency of neurons in the dentate gyrus (DG), hippocampal CA3 region (CA3) and hippocampal CA1 region (CA1) of the Alzheimer's disease group mice were significantly reduced, while the Alzheimer's disease + α-solanine group improved the decreased cell contour clarity, nuclear structure prominence and cytoplasm transparency of neurons in the Alzheimer's disease mice, indicating that α-solanine can significantly reverse this phenomenon.

[0039] Depend on Figure 2 As shown in B, compared with the wild-type control mice, the cell bodies and Nissl bodies of neurons in the dentate gyrus (DG), hippocampal CA3 region (CA3) and hippocampal CA1 region (CA1) of the brains of the Alzheimer's disease group mice were incomplete, while the Alzheimer's disease + α-solanine group improved the incompleteness of the neuronal cell bodies and Nissl bodies of the Alzheimer's disease mice, indicating that α-solanine can also significantly reverse the pathological phenotypes related to neurodegenerative diseases.

[0040] Depend on Figure 2As can be seen from C, the number of neurons in the Alzheimer's disease + α-solanine group mice increased significantly compared with that in the Alzheimer's disease group mice.

[0041] Depend on Figure 2 As shown in D and E, compared with the Alzheimer's disease group mice, the expression level of Aβ protein in the Alzheimer's disease + α-solanine group mice was decreased, indicating that α-solanine can inhibit the expression of Aβ protein in the hippocampus of the brain.

[0042] Depend on Figure 2 As shown in F and G, the co-localization of IBA1 and IL-6 in the hippocampus of the brain in the Alzheimer's disease + α-solanine group mice was reduced compared with that in the Alzheimer's disease group mice.

[0043] The above results show that α-solanine can alleviate the Alzheimer's disease-related pathological phenotypes produced in the Alzheimer's disease group mice.

[0044] Example 3: Effect of α-solanine on inhibiting microglial apoptosis in Alzheimer's disease model mice Brain tissues of the WT group, AD group, and AD+α-solanine group of mice constructed in Example 1 were paraffin-embedded and sectioned. First, the expression of apoptosis-related indicators in the hippocampus of the brain of each group of mice was evaluated by immunohistochemical staining; secondly, the apoptosis protein activity detection kit (Caspase3 colorimetric assay kit and Caspase9 colorimetric assay kit, immunoturbidimetric method) was used to detect the activity of apoptosis proteins in primary microglia of each group of mice; finally, primary microglia of each group of mice were extracted, and the expression of apoptosis-related proteins was detected by Western Blot.

[0045] Among them, the apoptosis staining related indicators are caspase 3 splicing form (C-Cas3) and caspase 9 splicing form (C-Cas9); the apoptosis related proteins are Bax, Bcl2, C-Cas3 and C-Cas9; the apoptosis protein activity detection is to detect the activity of Caspase3 and Caspase9.

[0046] Depend on Figure 3It can be seen from the AD in that compared with the wild-type control group, the expression of C-Cas3 protein and C-Cas9 protein in the brain tissue of mice in the Alzheimer's disease group and the activity of Caspase3 and Caspase9 were significantly increased. Compared with the Alzheimer's disease group, the expression of C-Cas3 protein and C-Cas9 protein in the brain tissue of mice in the Alzheimer's disease + α-solanine group and the expression and activity of Caspase3 and Caspase9 were significantly reduced. This shows that α-solanine can significantly reverse the phenomenon of increased expression and activity of apoptotic proteins in the hippocampus.

[0047] Depend on Figure 3 As shown in Figures E and F, compared with the Alzheimer's disease group mice, the activity of apoptotic proteins in the brain tissue of the Alzheimer's disease + α-solanine group mice was significantly reduced, indicating that α-solanine can significantly reduce the activity of apoptotic proteins in AD mice.

[0048] Depend on Figure 3 GK in the results showed that compared with the wild-type control mice, the expression of apoptosis-related proteins Bax, C-Cas3 and C-Cas9 in the brain tissue of the Alzheimer's disease group mice was significantly increased, and the expression of Bcl-2 protein was significantly decreased. Compared with the Alzheimer's disease group, the expression of apoptosis-related proteins Bax, C-Cas3 and C-Cas9 in the brain tissue of the Alzheimer's disease + α-solanine group mice was significantly decreased, and the expression of Bcl-2 protein was significantly increased, indicating that α-solanine can significantly reverse this trend.

[0049] The above results show that α-solanine inhibits microglial apoptosis.

[0050] Example 4: Effect of α-solanine on promoting microglial autophagy and inhibiting apoptosis 1. Transcriptome sequencing of primary mouse microglia: C57BL / 6 mice were raised, primary microglia were extracted from mouse brain tissue, and primary microglia were pretreated with Aβo (final concentration 5μM) for 9 hours. Then they were divided into two groups and treated with PBS buffer and α-solanine (final concentration 5μM) for 3 hours respectively. Then, cell transcriptome sequencing and KEGG functional enrichment analysis were performed. The results are as follows: Figure 4 As shown in A.

[0051] 2. Detection of autophagy indexes in primary microglia: Brain tissues of the WT group, AD group, and AD+α-solanine group of mice constructed in Example 1 were taken to extract primary microglia from the brain tissues of mice. The expression of autophagy-related indexes in primary microglia in the brains of the three groups of mice (WT group, AD group, and AD+α-solanine group) was detected by Western Blot. The results are as follows: Figure 4 As shown in BD.

[0052] Among them, the autophagy-related indicators are autophagy-related gene 5 (Autophagy-Related Gene 5, Atg5) and chelate body 1 (Sequestosome 1, SQSTM1).

[0053] 3. Autophagy double-labeled adenovirus mRFP-GFP-LC3 transfection: The autophagy double-labeled adenovirus mRFP-GFP-LC was transfected at a titer of 1×10 10 PFU / mL calculation, take 30µL to 270µL and add to regular culture medium for dilution to get 1×10 9 PFU / mL titer of autophagy double-labeled adenovirus mRFP-GFP-LC3. Primary microglia in logarithmic phase were selected and inoculated into 6-well plates. DMSO and α-solanine (final concentration 5 μM) were added respectively and cultured at 37°C overnight. 50 μL of autophagy double-labeled adenovirus mRFP-GFP-LC3 (titer 1×10 9 After adding 1000 PFU / mL) to the cell culture dish, seal it, put it into a flat-angle centrifuge, and centrifuge it at low speed (1200×g) for 1 hour. Then, aspirate the cells and virus solution and transfer them to the culture dish to continue virus infection until 2 hours later, and then change the solution. 36-48 hours after infection, EGFP and mCherry expression began to be observed. The expression of autophagosomes (yellow) and autophagolysosomes (red) was detected using an autophagy double-labeled adenovirus fluorescent probe. The strength of the autophagic flow can be clearly seen by counting spots of different colors. The results are shown in the figure. Figure 4 As shown in E and F.

[0054] 4. Detection of apoptosis indicators of primary microglial cells: Primary microglial cells from wild-type mice were extracted and divided into Control group, α-solanine group and α-solanine + 3MA group, where 3MA is a specific autophagy inhibitor. The above three groups of cells were stimulated with Aβo (final concentration 5μM) for 9 hours, and then the α-solanine group was treated with α-solanine (final concentration 5μM) for 3 hours; the α-solanine + 3MA group was treated with α-solanine (final concentration 5μM) and the specific autophagy inhibitor 3-MA (final concentration 2.5mM) was continued for 2 hours; the Control group was treated with an equal amount of PBS buffer for 3 hours. Western Blot was used to detect apoptosis-related proteins, and the apoptosis protein activity detection kit (immunoturbidimetric method) was used to detect the activity of apoptotic proteins in primary microglia. The results are as follows Figure 4 As shown in GM.

[0055] Among them, apoptosis-related proteins are Bax, Bcl2, C-Cas3 and C-Cas9; apoptosis protein activity detection is to detect the activity of Caspase3 and Caspase9.

[0056] Depend on Figure 4 As shown in A, α-solanine mainly regulates the autophagy function of microglia.

[0057] Depend on Figure 4 It can be seen from the BD in the figure that the expression of Atg5 and P62 in the brain tissue of the Alzheimer's disease group mice was significantly inhibited, and the expression of autophagy-related proteins in the Alzheimer's disease + α-solanine group mice was significantly promoted, which proves that α-solanine can promote autophagy of microglia in AD mice.

[0058] Depend on Figure 4 As shown in E and F, α-solanine can promote the occurrence of autophagic flux, proving that α-solanine can promote microglial autophagy.

[0059] Depend on Figure 4 It can be seen from the GM in α-solanine that the expression of Bax, Bcl-2, C-Cas3 and C-Cas9 was inhibited, and the expression of apoptosis-related proteins was significantly increased after pretreatment with the autophagy inhibitor 3-MA ( Figure 4 GK in the sample); and immunoturbidimetric assay revealed that α-solanine inhibited the activity of Caspase3 and Caspase9 apoptotic proteins, and that the activity of apoptotic proteins increased significantly after 3-MA was used to inhibit autophagy ( Figure 4 L and M in the diagram).

[0060] The above results show that α-solanine inhibits apoptosis by promoting microglial autophagy.

[0061] Example 5: Effect of α-solanine in promoting microglial autophagy and delaying disease progression in AD model mice 1. Wild-type mice and 5xFAD mice were raised and divided into a wild-type control group and an Alzheimer's disease group. The Alzheimer's disease group was treated with α-solanine and α-solanine + 3MA, respectively. The mice in the Alzheimer's disease group were injected intraperitoneally with α-solanine (5 mg / kg) once every other day for a total of 4 weeks; the mice in the Alzheimer's disease + α-solanine + 3MA group were injected intraperitoneally with 3MA (15 mg / kg) in addition to α-solanine (5 mg / kg) once every other day for a total of 4 weeks.

[0062] 2. Tissue staining: For the above three groups of mice, brain tissues were collected at the same time, embedded in paraffin, and sliced. HE staining, Nissl staining, and immunohistochemical staining were performed using conventional methods. The results are as follows: Figure 5 As shown in A~E.

[0063] 3. Evaluation of cognitive and memory functions: According to the functional evaluation method in Example 1, a water maze test was performed to observe the behavior and memory of the three groups of mice at different stages, including the escape latency, the number of platform crossings, and the residence time in the target quadrant during the spatial exploration stage. The results are as follows: Figure 5 As shown in F~H.

[0064] Depend on Figure 5 As shown in A, the structure of neurons in the hippocampus of mice in the α-solanine + 3MA group was more incomplete than that in the α-solanine group.

[0065] Depend on Figure 5 As shown in Figures B and C, the structure of Nissl bodies in the hippocampus of the mice in the α-solanine + 3MA group was worse and the number was smaller than that in the α-solanine group.

[0066] Depend on Figure 5 As shown in D and E, compared with the α-solanine group, the Aβ expression in the hippocampus of the mice in the α-solanine+3MA group was significantly increased, further indicating that α-solanine delays the deposition of Aβ in the hippocampus of the mice by promoting autophagy of primary microglia.

[0067] Depend on Figure 5 From the FH in Figure 3, we can see that compared with the α-solanine group mice, the escape latency of the α-solanine+3MA group mice was significantly prolonged, and the number of times they crossed the platform and the time they stayed in the target quadrant were less, indicating that α-solanine delays the development of Alzheimer's disease in mice by promoting autophagy in primary microglia of mice to delay autophagy.

[0068] The above results show that α-solanine delays the development of Alzheimer's disease in mice by promoting autophagy in primary microglia.

[0069] In summary, α-solanine can improve the behavior and memory of Alzheimer's disease model mice, and promote the structure of neurons and the integrity of Nissl bodies in the hippocampus of mice, thereby delaying the progression of Alzheimer's disease. From a mechanistic perspective, α-solanine inhibits apoptosis by promoting microglial autophagy, thereby playing a role in treating Alzheimer's disease. Therefore, α-solanine can be used to prepare drugs for the treatment of Alzheimer's disease, which is of great significance in the future clinical treatment of Alzheimer's disease.

[0070] The above-described embodiments are only preferred specific implementation schemes of the present invention and are not intended to limit the present invention. Any modifications, equivalent substitutions and improvements made within the spirit and principles of the present invention should be included in the protection scope of the present invention.

Claims

1. The use of α-solanine in the preparation of a drug for treating Alzheimer's disease, characterized in that: The structural formula of α-solanine is shown below: 。 2. The use of α-solanine as claimed in claim 1 in the preparation of a drug for treating Alzheimer's disease, characterized in that: The α-solanine is used in the preparation of a drug for inhibiting apoptosis of microglia in brain tissue of patients with Alzheimer's disease.

3. The use of α-solanine in the preparation of a drug for treating Alzheimer's disease according to claim 1, characterized in that: The α-solanine is used in the preparation of a drug for inhibiting the expression of Aβ protein in the hippocampal tissue of patients with Alzheimer's disease.

4. The use of α-solanine in the preparation of a drug for treating Alzheimer's disease according to claim 1, characterized in that: In the drug for treating Alzheimer's disease, α-solanine is the only active ingredient.

5. The use of α-solanine in the preparation of a drug for treating Alzheimer's disease according to claim 1, characterized in that: The drug for treating Alzheimer's disease comprises α-solanine and a pharmaceutically acceptable carrier.

6. The use of α-solanine in the preparation of a drug for treating Alzheimer's disease according to claim 1, characterized in that: The dosage form of the drug for treating Alzheimer's disease is granules, tablets, capsules, pills or oral liquid preparations.

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