Application of caffeoyl butanediamine in preparation of medicine, health care product or functional food for preventing and treating atherosclerosis

Abstract

The invention belongs to the technical field of biological medicines, and particularly relates to application of caffeoyl butanediamine in preparation of medicines, health-care products or functional foods for preventing and treating atherosclerosis. According to the invention, the caffeoyl butanediamine is found for the first time, and experiments prove that the caffeoyl butanediamine can be used for preventing and treating atherosclerosis and can be used for remarkably reducing the area of ApoE- / -mouse atherosclerotic plaque induced by high homocysteine (HCY); meanwhile, the levels of HCY and four items (TG, TC, LDL-C and HDL-C) of blood fat in serum of the atherosclerotic mice and the levels of inflammatory factors such as IL-6, IL-1beta, TNF-alpha, MCP-1 and CRP can be remarkably called back. The compound caffeoyl butanediamine provided by the invention can be used for preventing and treating cardiovascular system diseases such as atherosclerosis.

Description

Technical Field

[0001] The present invention belongs to the technical field of biomedicine, and more specifically relates to the application of caffeoyl succinamide in the preparation of drugs, health products or functional foods for preventing and treating atherosclerosis. Background Art

[0002] Atherosclerosis is a systemic and progressive vascular disease, and its characteristic pathological changes include intimal lipid deposition, fibrous plaque formation and progressive vascular wall sclerosis, which is the core pathological basis of cardiovascular and cerebrovascular diseases. As the main pathological basis of cardiovascular and cerebrovascular diseases, the pathogenesis of this disease involves multiple pathological links such as vascular endothelial dysfunction, oxidation modification of low-density lipoprotein, macrophage infiltration, foam cell formation and abnormal proliferation of vascular smooth muscle cells. These complex pathophysiological processes ultimately lead to stenosis of the arterial lumen, limited blood flow and even complete occlusion. The clinical hazards of this disease are not only manifested as local vascular dysfunction, but also can cause ischemic damage to multiple organ systems, which is the fundamental cause of fatal cardiovascular and cerebrovascular events such as myocardial infarction and ischemic stroke. Given its high incidence, severe disability rate and significantly increased mortality rate, atherosclerosis has become a major challenge in the global public health field, bringing a heavy burden to the medical system and social economy.

[0003] At present, the clinical drug treatment of atherosclerosis mainly includes three categories: lipid-lowering drugs, antiplatelet drugs, and anti-inflammatory and plaque-stabilizing drugs. However, these chemically synthesized drugs generally have limitations such as more adverse reactions, easy generation of drug resistance and drug dependence after long-term use. It is worth noting that in recent years, breakthrough progress has been made in the field of natural drug research. A large number of experimental studies have shown that a variety of active monomer components of traditional Chinese medicine, including tetrahydropalmatine, berberine and neferine, have shown significant efficacy in preventing and treating the pathological process of atherosclerosis through multiple mechanisms such as regulating lipid metabolism, inhibiting inflammatory reactions and improving endothelial function. These important findings have not only opened up new research directions for the prevention and treatment of cardiovascular diseases, but also made the screening and development of monomer components with anti-atherosclerotic activity from the treasure house of natural drugs become the current frontier hot spot in drug research. Compared with chemically synthesized drugs, these natural active components show great clinical application potential in the prevention and treatment of cardiovascular diseases due to their unique multi-target synergistic action mechanism, good biocompatibility and low toxicity and side effects.

[0004] At present, there are few research reports on the biological activity of caffeoyl succinamide, and there is no relevant record of caffeoyl succinamide being used for preventing and treating atherosclerosis. Summary of the Invention

[0005] In view of this, the present invention provides the application of caffeoylbutanediamide in the preparation of medicaments, health products or functional foods for preventing and treating atherosclerosis. Through previous animal experiments, the present invention found that caffeoylbutanediamide has a significant effect on alleviating atherosclerosis. Further, developing it into a drug that can be used to prevent and treat atherosclerosis, or a health product or functional food that can prevent and treat atherosclerosis, will have great clinical application value.

[0006] Caffeoylbutanediamide, with the molecular formula C 13 H 18 N2O3, the English name is N-(4-aminobutyl)-3-(3,4-dihydroxyphenyl)propenamide, the English abbreviation is N-caffeoylputrescine or Caffeoylputrescine, the molecular weight is 250.14, and its chemical structural formula is shown in Formula (1):

[0007] Formula (1) In order to achieve the above object, the present invention adopts the following technical solutions: The application of caffeoylbutanediamide in the preparation of medicaments for preventing and treating atherosclerosis, or in the preparation of health products or functional foods for preventing and treating atherosclerosis.

[0008] Further, caffeoylbutanediamide can significantly reduce the plaque area in the aorta of atherosclerotic mice.

[0009] Further, it can reduce the level of homocysteine (HCY) in the serum.

[0010] Further, it can adjust back the levels of the four lipid items in the serum, including TG, TC, LDL-C, and HDL-C.

[0011] Further, it can adjust back the levels of inflammatory factors such as IL-6, IL-1β, TNF-α, MCP-1, and CRP in the serum.

[0012] A medicament for preventing and treating atherosclerosis, characterized by comprising caffeoylbutanediamide.

[0013] Further, the dosage form is an oral dosage form, an external patch or an injection dosage form permitted in pharmacy.

[0014] Further, the single application dose of caffeoylbutanediamide is 10 - 25 mg / kg.

[0015] A health product for preventing and treating atherosclerosis, comprising caffeoylbutanediamide.

[0016] A functional food for preventing and treating atherosclerosis, comprising cafoyl succinamide.

[0017] As can be seen from the above technical solutions, compared with the prior art, the beneficial effects achieved by the present invention are as follows: within the dose range of 10-25 mg / kg administered to experimental animals, cafoyl succinamide can significantly reduce the atherosclerotic plaque area in ApoE- / - mice induced by HCY, and at the same time can significantly reverse the HCY level, the levels of the four lipid items (TG, TC, LDL-C, HDL-C), and the levels of inflammatory factors such as IL-6, IL-1β, TNF-α, MCP-1, CRP in the serum of atherosclerotic mice. The above all confirm that cafoyl succinamide has the effect of preventing and treating atherosclerosis and can be used for the prevention and treatment of cardiovascular system diseases such as atherosclerosis. Description of the Drawings

[0018] In order to more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the following will briefly introduce the drawings required for the description of the embodiments or the prior art. Obviously, the drawings in the following description are only the embodiments of the present invention. For those of ordinary skill in the art, without creative efforts, other drawings can also be obtained according to the provided drawings.

[0019] Appendix Figure 1 Shows the effect of cafoyl succinamide on the plaque area in the aorta of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinamide group, NCP-L is the low-dose cafoyl succinamide group; compared with the normal group, ### p<0.001; compared with the model group, *** p<0.001).

[0020] Appendix Figure 2 Shows the effect of cafoyl succinamide on the HCY level in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinamide group, NCP-L is the low-dose cafoyl succinamide group; compared with the normal group, ### p<0.001; compared with the model group, * p<0.05, *** p<0.001).

[0021] Appendix Figure 3 Shows the effect of cafoyl succinamide on the TG level in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinamide group, NCP-L is the low-dose cafoyl succinamide group; compared with the normal group,### p < 0.001; compared with the model group, *** p < 0.001).

[0022] Appendix Figure 4 This shows the effect of cafoylputrescine on the TC level in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoylputrescine group, NCP-L is the low-dose cafoylputrescine group; compared with the normal group, ## p < 0.01; compared with the model group, ** p < 0.01, *** p < 0.001).

[0023] Appendix Figure 5 This shows the effect of cafoylputrescine on the LDL-C level in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoylputrescine group, NCP-L is the low-dose cafoylputrescine group; compared with the normal group, ### p < 0.001; compared with the model group, *** p < 0.001).

[0024] Appendix Figure 6 This shows the effect of cafoylputrescine on the HDL-C level in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoylputrescine group, NCP-L is the low-dose cafoylputrescine group; compared with the normal group, ## p < 0.01; compared with the model group, ns > 0.05, ** p < 0.01, *** p < 0.001).

[0025] Appendix Figure 7 This shows the effect of cafoylputrescine on the IL-6 level of inflammatory factors in the serum of mice in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoylputrescine group, NCP-L is the low-dose cafoylputrescine group; compared with the normal group, ### p < 0.001; compared with the model group, ** p < 0.01, *** p < 0.001).

[0026] Appendix Figure 8Effect of cafoyl succinyl diamine on the level of inflammatory factor IL-1β in mouse serum in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinyl diamine group, NCP-L is the low-dose cafoyl succinyl diamine group; compared with the normal group, ### p < 0.001; compared with the model group, *** p < 0.001).

[0027] Appendix Figure 9 Effect of cafoyl succinyl diamine on the level of inflammatory factor TNF-α in mouse serum in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinyl diamine group, NCP-L is the low-dose cafoyl succinyl diamine group; compared with the normal group, ### p < 0.001; compared with the model group, *** p < 0.001).

[0028] Appendix Figure 10 Effect of cafoyl succinyl diamine on the level of inflammatory factor MCP-1 in mouse serum in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinyl diamine group, NCP-L is the low-dose cafoyl succinyl diamine group; compared with the normal group, ### p < 0.001; compared with the model group, ** p < 0.01, *** p < 0.001).

[0029] Appendix Figure 11 Effect of cafoyl succinyl diamine on the level of inflammatory factor CRP in mouse serum in Experiment 1 of the present invention (C is the normal group, M is the model group, Y is the positive drug atorvastatin group, NCP-H is the high-dose cafoyl succinyl diamine group, NCP-L is the low-dose cafoyl succinyl diamine group; compared with the normal group, ### p < 0.001; compared with the model group, ns > 0.05, * p < 0.05, *** p < 0.001). Detailed implementation manners

[0030] Next, the technical solutions in the embodiments of the present invention will be clearly and completely described in conjunction with the accompanying drawings in the embodiments of the present invention. Obviously, the described embodiments are only a part of the embodiments of the present invention, rather than all the embodiments. All other embodiments obtained by those of ordinary skill in the art based on the embodiments of the present invention without creative efforts shall fall within the protection scope of the present invention.

[0031] The caffeoyl succinyl diamine used in the following examples is the compound shown in the above formula (1), which can be obtained through commercial purchase or experimental self - preparation.

[0032] The medicaments required for this invention are conventional experimental medicaments, purchased from commercial channels; the experimental methods not mentioned are conventional experimental methods and will not be elaborated one by one here. Example 1

[0033] A drug for preventing and treating atherosclerosis, in oral dosage form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 10 mg / kg. Example 2

[0034] A drug for preventing and treating atherosclerosis, in oral dosage form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 25 mg / kg. Example 3

[0035] A health product for preventing and treating atherosclerosis, in oral health - product form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 25 mg / kg. Example 4

[0036] A functional food for preventing and treating atherosclerosis, in oral form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 10 mg / kg. Example 5

[0037] A drug for preventing and treating atherosclerosis, in injection dosage form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 10 mg / kg. Example 6

[0038] A drug for preventing and treating atherosclerosis, in external patch dosage form, including caffeoyl succinyl diamine, wherein the single - dose application of caffeoyl succinyl diamine is 25 mg / kg.

[0039] Experiment 1 The following animal experiments further illustrate the effects of Examples 1 - 6 above: I. Animal experiment design An ApoE - / - mouse atherosclerosis model induced by HCY was used. After intragastric administration of caffeoyl succinyl diamine, the preventive and therapeutic effects of caffeoyl succinyl diamine on atherosclerotic mice were evaluated by the area of aortic plaques in mice, serum HCY levels, four - item blood lipid levels (TG, TC, LDL - C, HDL - C), and levels of inflammatory factors (IL - 6, IL - 1β, TNF - α, MCP - 1, CRP).

[0040] II. Experimental Procedures 1. Experimental Animals Healthy SPF-grade male ApoE- / - mice (6 - 8 weeks old) were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Laboratory Animal License No. SCXK (Jing) 2021 - 0006). They were adaptively fed in an SPF-grade standard laboratory, and the feeding conditions for each group of animals were the same: environmental temperature (25°C), relative humidity (50% - 60%). They had free access to food and water.

[0041] 2. Experimental Methods ApoE- / - mice were adaptively fed for 3 days before modeling. One day before modeling, they were randomly divided into 5 groups: a normal group, a model group, a positive drug group (atorvastatin), and caffeoyl succinamide groups (low-dose group at 10 mg / kg and high-dose group at 25 mg / kg), with 8 mice in each group. After adaptive feeding, continuous modeling was carried out for 8 weeks. The normal group was fed with ordinary feed, and the other groups were fed with a special feed containing 1.7% high methionine. Administration started in the 9th week. The normal group and the model group were given normal saline (0.1 mL / 10g / d), the positive drug group was given atorvastatin (10 mg / kg / d), and the low-dose and high-dose caffeoyl succinamide groups were given doses of 10 mg / kg / d and 25 mg / kg / d respectively. Each group of mice was intragastrically administered in turn from 8:00 to 12:00 every morning for 10 consecutive weeks.

[0042] 3. Aortic Plaque Area After 10 weeks of administration, the mice were fasted and water-deprived for 12 h. After blood was collected by eye puncture, they were sacrificed by cervical dislocation. The whole aorta was removed after perfusion. Subsequently, gross Oil Red O staining was performed, and the red areas were the plaques.

[0043] 4. Determination of HCY Level The blood samples were centrifuged at 3000 r for 10 min at 4°C, and then the supernatant was centrifuged at 10000 r for 5 min. The supernatant was collected, and the level of HCY in the serum was detected by ELISA.

[0044] 5. Determination of Four Lipid Levels The blood samples were centrifuged at 3000 r for 10 min at 4°C, and then the supernatant was centrifuged at 10000 r for 5 min. The supernatant was collected, and the levels of TG, TC, LDL-C, and HDL-C in the serum were detected by ELISA.

[0045] 6. Determination of Inflammatory Factor Levels The blood samples were centrifuged at 3000 r for 10 min at 4°C, and then the supernatant was centrifuged at 10000 r for 5 min. The supernatant was collected, and the levels of IL-6, IL-1β, TNF-α, MCP-1, and CRP in the serum were detected by ELISA.

[0046] 7. Data Processing For data processing in this invention, ImageJ and Graphpad Prism 9.5 were used for data analysis and statistics. The obtained results were all expressed as mean ± standard deviation (X±S). One-way ANOVA was used for data processing of the inter-group difference comparison, and p<0.05 was used as the standard for statistical significance of the difference.

[0047] III. Experimental Results 1. Effect on the Aortic Plaque Area of Mice The results of the effect of caffeoylbutanediamine on the aortic plaque area of mice are shown in Figure 1 the figure. Compared with the normal control group (7.32±0.17%), the area of aortic plaque in the model group mice (18.03±0.78%) increased significantly (p<0.001), indicating that the HCY-induced atherosclerotic mouse model was successful. Compared with the model group, the area of plaque in the positive drug group mice (8.93±1.39%) decreased significantly (p<0.001), and the area of plaque in the aortic of caffeoylbutanediamine at each dose group mice decreased significantly (p<0.001), showing a certain positive correlation with the dose, that is, the larger the administration dose, the smaller the plaque area.

[0048] In summary, atherosclerosis significantly increased the area of plaque in the aorta. Each dose group of caffeoylbutanediamine could reduce the area of plaque in the aorta of mice to varying degrees.

[0049] 2. Effect on the HCY Level in the Serum of Mice The results of the effect of caffeoylbutanediamine on the HCY level in the serum of mice are shown in Figure 2 the figure. Compared with the normal control group (7.30±1.34 μmol / L), the content of HCY in the serum of model mice (28.27±5.03 μmol / L) increased significantly (p<0.001), indicating that the content of HCY in the serum of HCY-induced atherosclerotic mice increased. Compared with the model group, the content of HCY in the serum of positive drug group mice (14.59±0.53 μmol / L) decreased significantly (p<0.001), and the content of HCY in the serum of caffeoylbutanediamine at each dose group mice decreased significantly (p<0.05).

[0050] In summary, the content of HCY in the serum of the HCY-induced atherosclerotic mouse model increased significantly, and each dose group of caffeoylbutanediamine could reduce the content of HCY in the serum of mice to varying degrees.

[0051] 3. Effect on the Four Serum Lipid Levels of Mice The results of the effects of caffeoyl succinamide on the levels of four blood lipids (TG, TC, LDL-C, HDL-C) in the serum of mice are shown in Figure 3 , 4 , 5, and 6. Compared with the normal control group (8.40 ± 0.95 mmol / L), the content of TG (17.62 ± 3.17 mmol / L) in the serum of mice in the model group was significantly increased (p < 0.001), indicating that the content of TG in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of TG (11.35 ± 1.35 mmol / L) in the serum of mice in the positive drug group was significantly decreased (p < 0.001), and the content of TG in the serum of mice in each dose group of caffeoyl succinamide was significantly decreased (p < 0.001).

[0052] Compared with the normal control group (1.26 ± 0.14 mmol / L), the content of TC (1.69 ± 0.17 mmol / L) in the serum of mice in the model group was significantly increased (p < 0.01), indicating that the content of TC in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of TC (1.14 ± 0.21 mmol / L) in the serum of mice in the positive drug group was decreased (p < 0.001), and the content of TC in the serum of mice in each dose group of caffeoyl succinamide was significantly decreased (p < 0.01).

[0053] Compared with the normal control group (9.33 ± 2.10 mmol / L), the content of LDL-C (16.95 ± 3.20 mmol / L) in the serum of mice in the model group was significantly increased (p < 0.001), indicating that the content of LDL-C in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of LDL-C (10.97 ± 0.84 mmol / L) in the serum of mice in the positive drug group was decreased (p < 0.001), and the content of LDL-C in the serum of mice in each dose group of caffeoyl succinamide was significantly decreased (p < 0.001).

[0054] Compared with the normal control group (1.87 ± 0.08 mmol / L), the content of HDL-C (1.44 ± 0.11 mmol / L) in the serum of mice in the model group was significantly decreased (p < 0.01), indicating that the content of HDL-C in the serum of HCY-induced atherosclerotic mice was decreased. Compared with the model group, the content of HDL-C (2.10 ± 0.07 mmol / L) in the serum of mice in the positive drug group was significantly increased (p < 0.001). The content of HDL-C (1.52 ± 0.26 mmol / L) in the serum of mice in the low-dose group of caffeoyl succinamide was increased, but there was no significant difference. The content of HDL-C (1.89 ± 0.17 mmol / L) in the serum of mice in the high-dose group of caffeoyl succinamide was significantly increased (p < 0.01).

[0055] In summary, in the serum of the HCY-induced atherosclerotic mouse model, the contents of TG, TC, and LDL-C were significantly increased, and each dose group of cafestol butanediamide could reduce the contents of TG, TC, and LDL-C in the mouse serum to varying degrees. In the serum of the HCY-induced atherosclerotic mouse model, the content of HDL-C was significantly decreased, and each dose group of cafestol butanediamide could increase the content of HDL-C in the mouse serum to varying degrees.

[0056] 4. Effects on the levels of inflammatory factors in mouse serum The results of the effects of cafestol butanediamide on the levels of inflammatory factors (IL-6, IL-1β, TNF-α, MCP-1, CRP) in mouse serum are shown in Figure 7 , 8 , 9, 10, 11. Compared with the normal control group (28.67 ± 6.31 pg / mL), the content of IL-6 (100.22 ± 5.12 pg / mL) in the serum of the model group mice was significantly increased (p < 0.001), indicating that the content of IL-6 in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of IL-6 (48.67 ± 20.18 pg / mL) in the serum of the positive drug group mice was decreased (p < 0.001), and the content of IL-6 in the serum of each dose group of cafestol butanediamide was significantly decreased (p < 0.01).

[0057] Compared with the normal control group (34.55 ± 1.62 pg / mL), the content of IL-1β (65.26 ± 6.09 pg / mL) in the serum of the model group mice was significantly increased (p < 0.001), indicating that the content of IL-1β in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of IL-1β (40.09 ± 4.22 pg / mL) in the serum of the positive drug group mice was significantly decreased (p < 0.001), and the content of IL-1β in the serum of each dose group of cafestol butanediamide was significantly decreased (p < 0.001).

[0058] Compared with the normal control group (40.06 ± 3.53 pg / mL), the content of TNF-α (105.90 ± 4.50 pg / mL) in the serum of the model group mice was significantly increased (p < 0.001), indicating that the content of TNF-α in the serum of HCY-induced atherosclerotic mice was increased. Compared with the model group, the content of TNF-α (50.90 ± 5.62 pg / mL) in the serum of the positive drug group mice was significantly decreased (p < 0.001), and the content of TNF-α in the serum of each dose group of cafestol butanediamide was significantly decreased (p < 0.001).

[0059] Compared with the normal control group (75.87 ± 3.43 pg / mL), the content of MCP-1 in the serum of mice in the model group (113.45 ± 16.16 pg / mL) increased significantly (p < 0.001), indicating that the content of MCP-1 in the serum of HCY-induced atherosclerotic mice increased. Compared with the model group, the content of MCP-1 in the serum of mice in the positive drug group (89.55 ± 8.22 pg / mL) decreased significantly (p < 0.01), and the content of MCP-1 in the serum of mice in each dose group of caffeoylbutanediamine decreased significantly (p < 0.01).

[0060] Compared with the normal control group (1.56 ± 0.18 ng / mL), the content of CRP in the serum of mice in the model group (2.83 ± 0.75 ng / mL) increased significantly (p < 0.001), indicating that the content of CRP in the serum of HCY-induced atherosclerotic mice increased. Compared with the model group, the content of CRP in the serum of mice in the positive drug group (1.56 ± 0.21 ng / mL) decreased significantly (p < 0.001). The content of CRP in the serum of mice in the low-dose group of caffeoylbutanediamine (2.59 ± 0.41 ng / mL) decreased, but there was no significant difference. The content of CRP in the serum of mice in the high-dose group of caffeoylbutanediamine (1.98 ± 0.06 ng / mL) decreased significantly (p < 0.05).

[0061] In summary, the contents of IL-6, IL-1β, TNF-α, MCP-1, and CRP in the serum of the HCY-induced atherosclerotic mouse model increased significantly, and each dose group of caffeoylbutanediamine could reduce the contents of IL-6, IL-1β, TNF-α, MCP-1, and CRP in the serum of mice to varying degrees.

[0062] During the whole process of animal administration, no mice died, and there were no abnormal conditions in the appearance and behavior of the mice.

[0063] Each embodiment in this specification is described in a progressive manner. The key point of each embodiment is to illustrate the differences from other embodiments. The same or similar parts among the embodiments can be referred to each other.

[0064] The above description of the disclosed embodiments enables those skilled in the art to implement or use the present invention. Various modifications to these embodiments will be obvious to those skilled in the art. The general principles defined herein can be implemented in other embodiments without departing from the spirit or scope of the present invention. Therefore, the present invention will not be limited to these embodiments shown herein, but will conform to the widest scope consistent with the principles and novel features disclosed herein.

Claims

1. Use of caffeoylbutanediamide in the preparation of medicines for preventing and treating atherosclerosis, or in the preparation of health products or functional foods for preventing and treating atherosclerosis.

2. The use according to claim 1, characterized in that Caffeine can reduce the plaque area in the aorta of atherosclerotic mice.

3. The use according to claim 1, characterized in that Caffeine can reduce serum homocysteine ​​levels.

4. The use according to claim 1, characterized in that Caffeine can lower the levels of four blood lipids in serum, including TG, TC, LDL-C, and HDL-C.

5. The use according to claim 1, characterized in that Caffeine can adjust the levels of inflammatory factors such as IL-6, IL-1β, TNF-α, MCP-1, and CRP in serum.

6. A drug for preventing and treating atherosclerosis, characterized in that: Includes caffeine.

7. The drug according to claim 6, characterized in that The dosage form is a pharmaceutically acceptable oral dosage form, external patch or injection dosage form.

8. A health product for preventing and treating atherosclerosis, characterized in that: Includes caffeine.

9. A functional food for preventing and treating atherosclerosis, characterized in that: Includes caffeine.

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