CN108498521A - Application of the cycloastragenol in preparing the drug for inhibiting abdominal aneurvsm - Google Patents

Abstract

The invention discloses the application of cycloastragenol in the preparation of medicine for inhibiting abdominal aortic aneurysm. The present invention provides an application of cycloastragenol for the following (a1) and/or (a2): (a1) preparing a product for preventing and/or treating abdominal aortic aneurysm; (a2) preventing and/or treating Abdominal aortic aneurysm. The invention also protects a medicine for preventing and/or treating abdominal aortic aneurysm, the active ingredient of which is cycloastragenol. The drug for inhibiting abdominal aortic aneurysm provided by the present invention is safe, low in toxicity, and has strong pharmacological effects; its raw material has a wide range of sources and is cheap, and can be obtained by hydrolyzing astragaloside IV, an extract of the medicinal material Astragalus membranaceus; its treatment cost is low, its process is simple, and its yield is high ; And the curative effect is exact. The invention provides a new drug source for the prevention, diagnosis, detection, protection, treatment and research of abdominal aortic aneurysm disease, is easy to popularize and apply, and can generate huge social and economic benefits in a relatively short period of time.

Description

Application of cycloastragenol in the preparation of drugs for inhibiting abdominal aortic aneurysm

technical field

The invention relates to the application of cycloastragenol in the preparation of medicine for inhibiting abdominal aortic aneurysm.

Background technique

Abdominal aortic aneurysm (AAA) is a severe progressive degenerative disease characterized by dilation of the abdominal aorta, accompanied by degradation of the extracellular matrix of the arterial wall and the occurrence of chronic inflammation. The incidence rate of AAA among elderly men over 65 years old is as high as 8%, and the incidence rate of AAA is slightly higher than that of women. It is the 13th cause of death in our country. Smoking, advanced age and atherosclerosis have been proven to be the most important risk factors for AAA. Most AAA patients have no obvious clinical symptoms except occasional abdominal pain, and a small number of patients have ruptured tumors when they are discovered. The mortality rate after rupture is as high as 80%, which is a serious hazard to human health and life.

Clinically, when the diameter of the abdominal aorta exceeds 50% of the normal diameter or the diameter of the abdominal aorta is >3.0cm, it is considered that AAA has occurred. When the tumor diameter is > 5.5cm, it is a large AAA, and when the tumor diameter is between 3.0-5.5cm, it is a small AAA. At present, the clinical treatment of AAA depends on its diameter. When the diameter is larger than 5.5cm, surgical treatment is adopted, and such large AAAs only account for about 10%. Most AAAs are small AAAs, and routine B-ultrasound monitoring is recommended clinically. However, these small AAAs continue to expand at a rate of 4 mm per year, and will eventually reach about 5 cm in 3-5 years, and may even rupture, causing death of the patient. Therefore, the treatment of small AAAs is an important research topic. Finding ways to inhibit small AAAs Effective drugs for dilation have very important clinical significance in reducing the risk of rupture and mortality in patients.

Studies have shown that the pathogenesis of AAA is related to chronic transmural inflammation of the arterial wall, degradation of extracellular matrix, and reduction and apoptosis of smooth muscle cells. Among them, the occurrence of inflammation is considered to be the initiating factor of the occurrence and development of AAA. Inflammatory cells, mainly macrophages, infiltrate and activate the arterial wall, and then secrete a large amount of pro-inflammatory cytokines, aggravating the inflammatory response of the arterial wall. In addition, macrophages also secrete matrix metalloproteinases to degrade the extracellular matrix of the arterial wall and reduce the elasticity of the arterial wall. At the same time, inflammation will cause the apoptosis of smooth muscle cells in the arterial wall, and the apoptotic smooth muscle cells will secrete pro-inflammatory cytokines and monocyte chemoattractant proteins, etc., triggering an inflammatory cascade reaction, further recruiting inflammatory cell infiltration and inducing matrix metalloproteinases secretion. This creates a vicious cycle that eventually leads to progressive degradation of the extracellular matrix of the arterial wall. In addition, oxidative stress and inflammation synergistically aggravate the occurrence and development of AAA.

From the perspective of the pathogenesis of AAA, the targets of drug treatment mainly focus on anti-inflammation, anti-oxidation and inhibition of matrix metalloproteinase activity. In recent years, the drugs clinically used to treat AAA mainly include statins represented by simvastatin, antihypertensive drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, and antibiotics represented by doxycycline. Wait. However, studies have reported that these drugs have uncertain curative effects or have certain toxic and side effects. Therefore, there is still a lack of effective clinical drugs for the prevention and treatment of small abdominal aortic aneurysms, and the development of new drugs with definite curative effects and less side effects will have great clinical significance for the prevention and treatment of abdominal aortic aneurysms.

Cycloastragenol (CAG) is the active aglycon of astragaloside IV. Studies have shown that cycloastragenol has a wide range of anti-inflammatory, anti-oxidative stress, inhibition of endoplasmic reticulum stress, anti-aging, anti-virus and anti-hyperlipidemia etc. effect. There are currently no reports on the anti-AAA activity of cycloastragenol.

Contents of the invention

The purpose of the present invention is to provide an application of cycloastragenol in the preparation of medicine for inhibiting abdominal aortic aneurysm.

The present invention provides the application of cycloastragenol, which is as follows (a1) and/or (a2):

(a1) Preparation of products for the prevention and/or treatment of abdominal aortic aneurysms;

(a2) Prevention and/or treatment of abdominal aortic aneurysm.

The present invention also protects the application of cycloastragenol, which is at least one of the following (b1)-(b12):

(b1) preparing a product for inhibiting the rupture of the elastic plate of the abdominal aorta;

(b2) preparing a product for inhibiting adventitia thickening of the abdominal aorta;

(b3) preparing a product for inhibiting abdominal aortic vasodilation;

(b4) preparing a product for inhibiting the rupture of the elastic plate of the abdominal aorta in patients with abdominal aortic aneurysm;

(b5) preparing a product for inhibiting adventitial thickening of the abdominal aorta in patients with abdominal aortic aneurysm;

(b6) preparing a product for inhibiting abdominal aortic vasodilation in patients with abdominal aortic aneurysm;

(b7) inhibiting the fracture of the elastic plate of the abdominal aorta;

(b8) inhibition of abdominal aortic adventitia thickening;

(b9) inhibit abdominal aorta vasodilation;

(b10) Inhibit the rupture of the abdominal aortic elastic plate in patients with abdominal aortic aneurysm;

(b11) inhibition of abdominal aortic adventitia thickening in patients with abdominal aortic aneurysm;

(b12) inhibits abdominal aortic vasodilation in patients with abdominal aortic aneurysm.

The present invention also protects the application of cycloastragenol, which is at least one of the following (c1)-(c16):

(c1) preparing a product for inhibiting oxidative stress in vascular smooth muscle cells;

(c2) preparing a product for inhibiting the inflammatory response of vascular smooth muscle cells;

(c3) preparing a product for inhibiting oxidative stress in the abdominal aorta;

(c4) preparing a product for inhibiting the inflammatory response of the abdominal aorta;

(c5) preparing products for inhibiting oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysms;

(c6) preparing a product for inhibiting the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm;

(c7) preparing a product for inhibiting oxidative stress in the abdominal aorta of patients with abdominal aortic aneurysm;

(c8) preparing a product for inhibiting the inflammatory response of the abdominal aorta in patients with abdominal aortic aneurysm;

(c9) inhibiting oxidative stress in vascular smooth muscle cells;

(c10) inhibiting the inflammatory response of vascular smooth muscle cells;

(c11) inhibits oxidative stress in the abdominal aorta;

(c12) inhibiting abdominal aorta inflammatory response;

(c13) inhibits oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysm;

(c14) inhibits the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm;

(c15) inhibits oxidative stress in abdominal aorta in patients with abdominal aortic aneurysm;

(c16) inhibits the inflammatory response of abdominal aorta in patients with abdominal aortic aneurysm.

The present invention also protects the application of cycloastragenol, which is at least one of the following (d1)-(d8):

(d1) preparing a product for promoting the synthesis of elastin in vascular smooth muscle cells;

(d2) preparing a product for promoting the synthesis of abdominal aortic elastin;

(d3) preparing a product for promoting the synthesis of elastin in vascular smooth muscle cells of patients with abdominal aortic aneurysm;

(d4) preparing a product for promoting the synthesis of elastin in the abdominal aorta of patients with abdominal aortic aneurysm;

(d5) Promote the synthesis of elastin in vascular smooth muscle cells;

(d6) Promote the synthesis of elastin in the abdominal aorta;

(d7) Promote elastin synthesis in vascular smooth muscle cells of patients with abdominal aortic aneurysm;

(d8) Promoting elastin synthesis in abdominal aorta in patients with abdominal aortic aneurysm.

The invention also protects a product whose active ingredient is cycloastragenol; the use of the product is to prevent and/or treat abdominal aortic aneurysm.

The present invention also protects a product whose active ingredient is cycloastragenol; the use of the product is at least one of the following (e1)-(e6):

(e1) inhibiting the rupture of the elastic plate of the abdominal aorta;

(e2) inhibition of abdominal aortic adventitia thickening;

(e3) inhibition of abdominal aortic vasodilation;

(e4) inhibit the rupture of the elastic plate of the abdominal aorta in patients with abdominal aortic aneurysm;

(e5) inhibit abdominal aortic adventitia thickening in patients with abdominal aortic aneurysm;

(e6) Inhibition of abdominal aortic vasodilation in patients with abdominal aortic aneurysm.

The present invention also protects a product whose active ingredient is cycloastragenol; the use of the product is at least one of the following (f1)-(f8):

(f1) inhibit oxidative stress in vascular smooth muscle cells;

(f2) inhibiting the inflammatory response of vascular smooth muscle cells;

(f3) inhibit abdominal aorta oxidative stress;

(f4) inhibit abdominal aorta inflammatory response;

(f5) inhibit oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysm;

(f6) inhibit the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm;

(f7) inhibit abdominal aortic oxidative stress in patients with abdominal aortic aneurysm;

(f8) Inhibition of abdominal aortic inflammatory response in patients with abdominal aortic aneurysm.

The present invention also protects a product whose active ingredient is cycloastragenol; the use of the product is at least one of the following (g1)-(g4):

(g1) Promote the synthesis of elastin in vascular smooth muscle cells;

(g2) Promote the synthesis of elastin in the abdominal aorta;

(g3) Promote elastin synthesis in vascular smooth muscle cells of patients with abdominal aortic aneurysm;

(g4) promotes elastin synthesis in abdominal aorta in patients with abdominal aortic aneurysm.

Any of the above-mentioned products can specifically be medicine, food or health care product.

The invention also protects a medicine for preventing abdominal aortic aneurysm, the active ingredient of which is cycloastragenol.

The invention also protects a medicine for treating abdominal aortic aneurysm, the active ingredient of which is cycloastragenol.

Any of the above drugs can be introduced into the body such as muscle, intradermal, subcutaneous, vein, mucosal tissue by injection, spray, nasal drop, eye drop, penetration, absorption, physical or chemical mediated methods. It can also be introduced into the body by mixing with other substances or being wrapped by other substances. When necessary, one or more pharmaceutically acceptable carriers can also be added to any of the above drugs. The carrier includes conventional diluents, excipients, fillers, binders, wetting agents, disintegrants, absorption promoters, surfactants, adsorption carriers, lubricants and the like in the pharmaceutical field. Any of the above-mentioned medicines can be made into various forms such as injection, suspension, powder, tablet, and granule. The above-mentioned medicines in various dosage forms can be prepared according to conventional methods in the field of pharmacy.

The invention provides an application of cycloastragenol in the preparation of medicine for inhibiting abdominal aortic aneurysm. The present invention adopts a clinically relevant abdominal aortic aneurysm disease model: the abdominal aortic aneurysms of C57BL/6J mice locally induced by incubating the abdominal aorta with elastase (2U) are used for experiments. Experiments have shown that oral gavage of cycloastragenol can significantly inhibit the development of elastase-induced abdominal aortic aneurysms in mice, and can be used to inhibit abdominal aortic aneurysms. The in vitro abdominal aortic aneurysm microenvironment cell model adopted in the present invention is: 100ng/mL tumor necrosis factor-α incubation of rat vascular smooth muscle cells caused cell damage, and incubation of cycloastragenol can significantly inhibit the damage of vascular smooth muscle cells, thereby inhibiting abdominal aortic aneurysm. development of aortic aneurysm.

The drug for inhibiting abdominal aortic aneurysm provided by the invention is safe, low in toxicity, and has strong pharmacological effects; its raw material has a wide range of sources and is cheap, and can be obtained by hydrolyzing astragaloside IV, an extract of the medicinal material Astragalus; it has low cost of treatment, simple process, and high yield ; And the curative effect is exact. The invention provides a new drug source for the prevention, diagnosis, detection, protection, treatment and research of abdominal aortic aneurysm disease, is easy to popularize and apply, and can generate huge social and economic benefits in a relatively short period of time.

Description of drawings

Fig. 1 is the result of the experiment on animals administered with cycloastragenol in Example 1.

Fig. 2 is the result of the experiment on animals administered with cycloastragenol in Example 2.

Figure 3 shows the expression of HO-1 gene, NOX-4 gene, Fibulin-5 gene and MCP-1 gene in Example 3.

Detailed ways

The following examples facilitate a better understanding of the present invention, but do not limit the present invention. The experimental methods in the following examples are conventional methods unless otherwise specified. The test materials used in the following examples, unless otherwise specified, were purchased from conventional biochemical reagent stores. Quantitative experiments in the following examples were all set up to repeat the experiments three times, and the results were averaged.

C57BL/6J mice: Sibeifu (Beijing) Biotechnology Co., Ltd.

SD rats: Department of Experimental Animal Science, Peking University Health Science Center.

Elastase: Sigma-Aldrich company, product number is E1250.

Cycloastragenol: Chengdu Jintaihe Pharmaceutical Chemical Technology Co., Ltd., batch number: 160618; the molecular formula of cycloastragenol is C ₃₀ H ₅₀ O ₅ , CAS number: 78574-94-4, and the structural formula is as follows:

Embodiment 1, the application of cycloastragenol in the prevention of abdominal aortic aneurysm

1. Mouse infrarenal aorta incubated with elastase to induce abdominal aortic aneurysm model

Experimental animals: 10-week-old male C57BL/6J mice (average body weight 23 g).

The experimental animals were divided into model group and sham operation group (12 in the model group and 3 in the sham operation group).

1. Experimental animals were anesthetized by intraperitoneal injection of 5% chloral hydrate (injection according to body weight, 8 μL/g).

2. After completing the anesthesia in step 1, the infrarenal abdominal aorta was separated, and a section of the abdominal aorta (about 1 cm in length) with no branches on the anterior wall and side wall was taken below the plane of the renal artery, and fixed with threading marks. In the model group, gauze soaked with 2U elastase was wrapped around the exposed abdominal aorta. After 50 min, the gauze and silk thread were taken out, and the abdomen was closed and the skin was sutured. In the sham operation group, gauze soaked with saline was wrapped around the exposed abdominal aorta, and the gauze and silk thread were taken out after 50 min, and the abdomen was closed and the skin was sutured.

2. Oral administration of cycloastragenol

1. After completing step 1, the mice in the model group were randomly divided into a normal saline group and a cycloastragenol group (6 mice in each group). In M PBS solution, the intragastric dosage is 50 mg cycloastragenol/kg body weight), the mice in the normal saline group were intragastrically administered with normal saline (200 μL/only), and the mice in the sham operation group were intragastrically administered with normal saline (200 μL/only) every day. ) for 14 days.

2. After completing step 1, the mice in each group were perfused with 0.01M PBS buffer solution in vivo to remove the blood in the circulation, and then the abdominal aorta tissue was fixed and dehydrated. The fat and connective tissue around the infrarenal abdominal aorta were peeled off, the heart was cut off, photographed against a black background, the largest diameter of the infrarenal aorta was measured, the incidence of abdominal aortic aneurysms in mice was counted, and the infrarenal aorta was taken for HE staining Paraffin sections and aldehyde fuchsin-stained paraffin sections.

The photographic results of the infrarenal abdominal aorta are shown in Figure 1A. The largest diameter of the infrarenal abdominal aorta is shown in Figure 1B. The statistical results of the incidence of abdominal aortic aneurysm are shown in Figure 1C (abdominal aortic aneurysm was considered to have occurred if the maximum diameter of the abdominal aorta in mice was greater than 50% of the normal maximum diameter). The results of HE staining are shown in Figure 1D. The results of aldehyde fuchsin staining are shown in Figure 1E.

The results showed that, compared with the mice in the sham operation group, the blood vessels in the infrarenal part of the mice in the normal saline group had obvious swelling, and the arteries were obviously dilated, and intragastric administration of cycloastragenol could reduce the incidence and degree of arterial dilation. Compared with the mice in the sham operation group, incubation with elastase can significantly increase the diameter of blood vessels in the mouse subrenal, but daily oral administration of cycloastragenol can significantly reduce the vasodilation caused by incubation with elastase. Compared with the mice in the sham operation group, incubation with elastase significantly increased the infiltration of inflammatory cells, the thickening of the adventitia and the rupture of the elastic plate in the infrarenal artery of the mice, and intragastric administration of cycloastragenol could inhibit the above pathological changes .

Example 2. Intragastric administration of cycloastragenol to treat abdominal aortic aneurysm induced by infrarenal artery of C57BL/6J mice incubated with elastase

1. Mouse infrarenal aorta incubated with elastase to induce abdominal aortic aneurysm model

Same as Step 1 of Example 1.

2. Oral administration of cycloastragenol

1. After 14 days of completing step 1, the mice in the model group were randomly divided into a normal saline group and a cycloastragenol group (6 mice in each group), and the cycloastragenol group mice were intragastrically administered with cycloastragenol every day (cycloastragelol dissolved In 0.01M PBS solution, the intragastric administration dose is 125mg cycloastragenol/kg body weight), the mice in the normal saline group were intragastrically administered with normal saline (200 μL/only), and the mice in the sham operation group were intragastrically administered with normal saline (200 μL/only). /piece) for 28 days.

2. After completing step 1, the mice in each group were perfused and washed with 0.01M PBS buffer, and the abdominal aorta tissue was fixed and dehydrated. The heart was stripped and cut off, photographed against a black background, the largest diameter of the infrarenal abdominal aorta was measured, and the infrarenal abdominal aorta was taken to make HE-stained paraffin sections and aldehyde fuchsin-stained paraffin sections.

The photographic results of the infrarenal abdominal aorta are shown in Figure 2A. The maximum diameter of the infrarenal abdominal aorta is shown in Figure 2B. The statistical results of the incidence of abdominal aortic aneurysm are shown in Figure 2C (abdominal aortic aneurysm was considered to have occurred if the maximum diameter of the abdominal aorta in mice was greater than 50% of the normal maximum diameter). The results of HE staining are shown in Figure 2D. The results of aldehyde fuchsin staining are shown in Figure 2E.

The results showed that, compared with the mice in the sham operation group, the blood vessels in the infrarenal part of the mice in the normal saline group had obvious swelling, and the arteries were obviously dilated, and intragastric administration of cycloastragenol could reduce the incidence and degree of arterial dilation. Compared with the mice in the sham operation group, incubation with elastase can significantly increase the diameter of the infrarenal blood vessels in mice, but intragastric administration of cycloastragenol can significantly reduce the vasodilation caused by incubation with elastase. Compared with the mice in the sham operation group, incubation with elastase significantly increased the infiltration of inflammatory cells, the thickening of the adventitia and the rupture of the elastic plate in the infrarenal artery of the mice, and intragastric administration of cycloastragenol could inhibit the above pathological changes .

Example 3, cycloastragenol inhibits the injury of rat vascular smooth muscle cells induced by TNF-α

1. Preparation of rat vascular smooth muscle cells

SD rats (body weight about 100 g) were anesthetized with 10% chloral hydrate, soaked in 75% alcohol for 2 min for disinfection. The chest cavity and abdominal cavity were opened, the organs were pushed aside, the heart and aorta were exposed, and the blood was sucked away with gauze. Carefully cut the full length of the heart and aorta up to the bifurcation of the abdominal aorta, and immediately put it in 0.01M PBS buffer. The adipose tissue and connective tissue were separated, and the heart was carefully cut off, during which the heart was washed three times with 0.01M PBS buffer. The separated transparent aorta was washed once in DMEM containing 0.05g/100ml amphotericin B. The aorta was then cut longitudinally, the intima was scraped off, and the aorta was minced. Transfer the cut aortic tissue pieces to a 3.5 cm Petri dish covered with 0.1% gelatin with tweezers, add 1 mL of DMEM medium (containing 20% FBS, 100 U/mL penicillin and 100 μg/mL streptomycin), and incubate at 37°C Cultured in the incubator, the medium was changed and passaged. Cells were cultured to 4-6 passages for experiments.

2. Inoculate the smooth muscle cells prepared in step 1 in a 6-well plate (1.5×10 ⁵ cells per well), using DMEM medium (containing 10% FBS, 100 U/mL penicillin and 100 μg/mL streptomycin), 37 ℃, 5% CO ₂ incubator to grow to 80%.

3. After completing step 2, take the 6-well plate, replace the DMEM medium (containing 5% FBS, 100 U/mL penicillin and 100 μg/mL streptomycin), cultivate for 12 hours, and perform the following grouping treatment:

Control group: cultivated for 24 hours.

TNF-α group: add 100ng/mL TNF-α to each well and culture for 24h.

TNF-α+ cycloastragenol group: add 100ng/mL TNF-α and 31.25μg/mL cycloastragenol to each well and incubate for 24h.

4. After completing step 3, collect cells from each group, extract total RNA and reverse transcribe it into eDNA. Using the eDNA as a template, the expression of HO-1 gene, NOX-4 gene, Fibulin-5 gene and MCP-1 gene is detected. The GAPDH gene was used as an internal reference gene.

The primer sequences used to detect the HO-1 gene are as follows:

HO-1-F: 5'-ACAGAAGAGGCTAAGACCG-3';

HO-1-R: 5'-CAGGCATTCTCCTTCCATT-3'.

The primer sequences used to detect the NOX-4 gene are as follows:

NOX-4-F: 5'-CCAGATGTTGGGCCTAGGATT-3';

NOX-4-R: 5'-ACTGATACAGCCAGGAGGGT-3'.

The primer sequences for the Fibulin-5 gene are as follows:

Fibulin-5-F: 5'-GTTAAGCGAAACCAGGTGCC-3';

Fibulin-5-R: 5'-TCGTCCACATCCACACACTG-3'.

The primer sequences used to detect the MCP-1 gene are as follows:

MCP-1-F: 5'-AATGAGTCGGCTGGAGAA-3';

MCP-1-R: 5'-GTGCTTGAGGTGGTTGTG-3'.

The primer sequences used to detect the GAPDH gene are as follows:

GAPDH-F: 5'-TGATGACATCAAGAAGGTGGTGAAG-3';

GAPDH-R: 5'-TCCTTGGAGGCCATGTAGGCCAT-3'.

The result is shown in Figure 3. The results showed that, compared with the control group, after TNF-α incubation for 24 hours, the expression level of HO-1 mRNA in the cells was significantly reduced, and the level of NADPH oxidase (NADPH peroxidase, NOX)-4 mRNA was significantly increased, causing oxidative stress in cells; The expression level of Fibulin-5mRNA in the cells was significantly reduced, which affected the synthesis of elastin; it caused the expression level of monocyte chemoattractant protein (MCP)-1mRNA in the cells to increase, which promoted the inflammatory response of cells; and the incubation of cycloastragenol could Significantly inhibit the changes of the above cytokines caused by TNF-α, reduce the oxidative stress and inflammatory response of cells, and promote the synthesis of elastin.

Claims (10)

1. The application of cycloastragenol is as follows (a1) and/or (a2): (a1) Preparation of products for the prevention and/or treatment of abdominal aortic aneurysms; (a2) Prevention and/or treatment of abdominal aortic aneurysm. 2. The application of cycloastragenol is at least one of the following (b1)-(b12): (b1) preparing a product for inhibiting the rupture of the elastic plate of the abdominal aorta; (b2) preparing a product for inhibiting adventitia thickening of the abdominal aorta; (b3) preparing a product for inhibiting abdominal aortic vasodilation; (b4) preparing a product for inhibiting the rupture of the elastic plate of the abdominal aorta in patients with abdominal aortic aneurysm; (b5) preparing a product for inhibiting adventitial thickening of the abdominal aorta in patients with abdominal aortic aneurysm; (b6) preparing a product for inhibiting abdominal aortic vasodilation in patients with abdominal aortic aneurysm; (b7) inhibiting the fracture of the elastic plate of the abdominal aorta; (b8) inhibition of abdominal aortic adventitia thickening; (b9) inhibit abdominal aorta vasodilation; (b10) Inhibit the rupture of the abdominal aortic elastic plate in patients with abdominal aortic aneurysm; (b11) inhibition of abdominal aortic adventitia thickening in patients with abdominal aortic aneurysm; (b12) inhibits abdominal aortic vasodilation in patients with abdominal aortic aneurysm. 3. The application of cycloastragenol is at least one of the following (c1)-(c16): (c1) preparing a product for inhibiting oxidative stress in vascular smooth muscle cells; (c2) preparing a product for inhibiting the inflammatory response of vascular smooth muscle cells; (c3) preparing a product for inhibiting oxidative stress in the abdominal aorta; (c4) preparing a product for inhibiting the inflammatory response of the abdominal aorta; (c5) preparing products for inhibiting oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysms; (c6) preparing a product for inhibiting the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm; (c7) preparing a product for inhibiting oxidative stress in the abdominal aorta of patients with abdominal aortic aneurysm; (c8) preparing a product for inhibiting the inflammatory response of the abdominal aorta in patients with abdominal aortic aneurysm; (c9) inhibiting oxidative stress in vascular smooth muscle cells; (c10) inhibiting the inflammatory response of vascular smooth muscle cells; (c11) inhibits oxidative stress in the abdominal aorta; (c12) inhibiting abdominal aorta inflammatory response; (c13) inhibits oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysm; (c14) inhibits the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm; (c15) inhibits oxidative stress in abdominal aorta in patients with abdominal aortic aneurysm; (c16) inhibits the inflammatory response of abdominal aorta in patients with abdominal aortic aneurysm. 4. The application of cycloastragenol, which is at least one of the following (d1)-(d8): (d1) preparing a product for promoting the synthesis of elastin in vascular smooth muscle cells; (d2) preparing a product for promoting the synthesis of abdominal aortic elastin; (d3) preparing a product for promoting the synthesis of elastin in vascular smooth muscle cells of patients with abdominal aortic aneurysm; (d4) preparing a product for promoting the synthesis of elastin in the abdominal aorta of patients with abdominal aortic aneurysm; (d5) Promote the synthesis of elastin in vascular smooth muscle cells; (d6) Promote the synthesis of elastin in the abdominal aorta; (d7) Promote elastin synthesis in vascular smooth muscle cells of patients with abdominal aortic aneurysm; (d8) Promoting elastin synthesis in abdominal aorta in patients with abdominal aortic aneurysm. 5. A product whose active ingredient is cycloastragenol; the purpose of said product is to prevent and/or treat abdominal aortic aneurysm. 6. A product whose active ingredient is cycloastragenol; the purposes of the product are at least one of the following (e1)-(e6): (e1) inhibiting the rupture of the elastic plate of the abdominal aorta; (e2) inhibition of abdominal aortic adventitia thickening; (e3) inhibition of abdominal aortic vasodilation; (e4) inhibit the rupture of the elastic plate of the abdominal aorta in patients with abdominal aortic aneurysm; (e5) inhibit abdominal aortic adventitia thickening in patients with abdominal aortic aneurysm; (e6) Inhibition of abdominal aortic vasodilation in patients with abdominal aortic aneurysm. 7. A product whose active ingredient is cycloastragenol; the use of the product is at least one of the following (f1)-(f8): (f1) inhibit oxidative stress in vascular smooth muscle cells; (f2) inhibiting the inflammatory response of vascular smooth muscle cells; (f3) inhibit abdominal aorta oxidative stress; (f4) inhibit abdominal aorta inflammatory response; (f5) inhibit oxidative stress in vascular smooth muscle cells of patients with abdominal aortic aneurysm; (f6) inhibit the inflammatory response of vascular smooth muscle cells in patients with abdominal aortic aneurysm; (f7) inhibit abdominal aortic oxidative stress in patients with abdominal aortic aneurysm; (f8) Inhibition of abdominal aortic inflammatory response in patients with abdominal aortic aneurysm. 8. A product whose active ingredient is cycloastragenol; the use of the product is at least one of the following (g1)-(g4): (g1) Promote the synthesis of elastin in vascular smooth muscle cells; (g2) Promote the synthesis of elastin in the abdominal aorta; (g3) Promote elastin synthesis in vascular smooth muscle cells of patients with abdominal aortic aneurysm; (g4) promotes elastin synthesis in abdominal aorta in patients with abdominal aortic aneurysm. 9. A medicine for preventing abdominal aortic aneurysm, the active ingredient of which is cycloastragenol. 10. A medicine for treating abdominal aortic aneurysm, the active ingredient of which is cycloastragenol.