Rho激酶抑制剂DL0805-0对大鼠离体胸主动脉的舒张作用及机制研究

目的探讨Rho激酶抑制剂DL0805-0对离体大鼠胸主动脉的舒张作用及作用机制。方法采用大鼠胸主动脉环张力测定法,观察DL0805-0对内皮完整或剔除的大鼠胸主动脉环的影响。应用法舒地尔、左旋硝基精氨酸甲醋(LNAME)、亚甲蓝、吲哚美辛、四乙胺(TEA)、格列本脲和4-氨基吡啶(4-AP)等工具药,研究DL0805-0舒张血管的作用机制。结果 DL0805-0能剂量依赖性的舒张KCl(60 mmol·L-1)和NE(0.1μmol·L-1)预收缩的大鼠胸主动脉环。LNAME可明显抑制DL0805-0对NE收缩血管的舒张作用,而亚甲蓝和吲哚美辛无明显影响。TEA可明显抑制DL0805-0对NE收缩血管的舒张作用,而格列本脲和4-AP无明显影响。DL0805-0能够明显抑制NE在无钙K-H液中引起的血管收缩和复钙诱导的外钙依赖性血管收缩。结论 DL0805-0具有明显的舒张血管作用,其作用可能依赖于血管内皮功能,另外开放血管平滑肌细胞上钙激活的钾离子通道以及阻滞钙离子通道可能也是作用机制之一。     

薰衣草花水煎液对大鼠离体胸主动脉舒张作用机制研究

目的观察薰衣草花提液对大鼠胸主动脉的血管环舒张作用及可能的机制。方法采用离体大鼠胸主动脉环张力测定法。结果①100.0～700.0mg/L的薰衣草花水煎液对内皮完整的血管环的基础张力没有影响。②100.0~700.0mg/L薰衣草花水煎液对KCl(60mmol/L)所致血管收缩没有明显影响,100.0～500.0mg/L的薰衣草花水煎液对去甲肾上腺素(NE,10μmol/L)预收缩的内皮完整血管环产生舒张作用,100.0～700.0mg/L的薰衣草花水煎液对去甲肾上腺素(NE,10μmol/L)预收缩的去内皮血管环产生舒张作用,一氧化氮合酶抑制剂左旋硝基精氨酸甲酯L-NAME(0.1mmol/L)、鸟苷酸环化酶抑制剂亚甲蓝(10μmol/L)预处理后均可明显抑制薰衣草花水煎液的血管舒张作用,环氧化酶抑制剂吲哚美辛(10μmol/L)预处理后不能抑制薰衣草花水煎液的血管舒张作用。③薰衣草花水煎液预处理去除内皮血管环后,能够明显抑制细胞外钙内流所致的血管收缩,但对细胞内钙释放引起的血管收缩没有影响。结论薰衣草花水煎液对血管舒张的作用是部分依赖内皮,部分不依赖内皮,一方面可通过内皮依赖性的NO-cGMP通路产生血管舒张作用,另一方面通过抑制血管平滑肌细胞膜上受体依赖性钙通道产生血管舒张作用。     

新结构Rho激酶抑制剂对离体胸主动脉血管环舒张作用及机制研究

目的评价2个全新结构小分子Rho激酶抑制剂J35242和J35243对离体大鼠胸主动脉血管环的舒张作用,并探讨其作用机制。方法利用离体大鼠胸主动脉血管环模型,分别用高浓度KCl和去甲肾上腺素(norepinephrine,NE)预刺激,评价化合物的舒张血管活性;通过各种工具药干预,观察化合物舒张血管作用的内皮相关机制、钾通道相关机制和钙离子相关机制。结果 J35242和J35243可以剂量依赖性舒张高浓度KCl和NE预收缩的血管环,并呈现一定的内皮依赖性;L-NAME和亚甲蓝可在一定程度上影响其舒张作用;化合物还明显抑制由细胞内钙释放和外钙内流引起的血管收缩,说明其可能通过阻断钙离子通道发挥舒张血管作用;另外两个化合物可能不是通过开放钾离子通道发挥舒张血管作用。结论 J35242和J35243在体外具有一定的舒张血管作用,并且J35242的作用要强于J35243,其机制可能依赖于血管内皮功能,另外可能与抑制平滑肌细胞钙离子通道,降低细胞内钙离子浓度相关。     

山楂总黄酮对大鼠离体血管功能的影响及其机制

目的研究山楂总黄酮对大鼠离体血管功能的影响,并初步探讨其作用机制。方法采用大鼠离体血管灌流模型,观察山楂总黄酮对大鼠离体血管舒张和收缩功能的影响。结果山楂总黄酮时大鼠离体血管具有浓度依赖性地舒张作用,还可浓度依赖性地抑制苯肾上腺素、CaCl2：引起的血管收缩,对无钙液中肾上腺素引起的血管收缩也有抑制作用。非选择性钾通道抑制剂、内向整流钾通道抑制剂可部分阻断山楂总黄酮引起的血管舒张作用。结论山楂总黄酮对大鼠离体血管具有舒张作用,该作用主要是通过抑制细胞外Ca＾2＋内流,抑制细胞内贮Ca＾2＋释放,以及激活非选择性钾通道和内向整流钾通道来实现的。     

黄芪的内皮依赖性血管舒缩作用及其机制

目的　黄芪有一定的治疗高血压作用 ,本研究观察其对大鼠离体胸主动脉环舒缩的影响 ,并探讨其可能机制。方法　采用大鼠离体主动脉环灌流模型 ,观察累积浓度黄芪 (0 .0 1～ 10 0g·L- 1)对基础状态、KCl预收缩和去氧肾上腺素 (PE)预收缩的血管环的作用。结果　黄芪 (0 .0 1～ 10 0g·L- 1)对基础状态或KCl预收缩的内皮完整血管环张力无影响。对PE预收缩的内皮完整血管环 ,黄芪在低浓度 (0 .0 1～ 3.0g·L- 1)时呈浓度依赖性舒张作用 ,此作用可被一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(0 .1mmol·L- 1)或鸟苷酸环化酶抑制剂亚甲蓝 (10μmol·L- 1)预处理所抑制 ;而在高浓度 (10～ 10 0g·L- 1)时呈短暂的收缩作用 ,可被内皮素转换酶抑制剂磷阿米酮 (5 μmol·L- 1)预处理所抑制。黄芪对PE预收缩的去除内皮血管环仅呈微弱的浓度依赖性舒张作用。结论　黄芪对主动脉具有内皮依赖性舒缩双相作用。其舒张机制可能为激活血管内皮细胞一氧化氮 鸟苷酸环化酶途径 ;而其收缩机制可能为促进血管内皮合成内皮素。     

黄芩苷对离体大鼠胸主动脉的舒张作用及机制

研究黄芩苷对大鼠离体胸主动脉环的舒张作用并探讨其可能的机制。记录去甲肾上腺素(NE)和KCl预收缩的大鼠离体主动脉环张力变化,观察黄芩苷的舒血管作用及不同工具药对其影响。实验发现黄芩苷对NE和KCl引起的去内皮和内皮完整大鼠胸主动脉环的收缩均有舒张作用;L-硝基精氨酸甲酯、亚甲蓝不能抑制黄芩苷对大鼠胸主动脉环的舒张作用,吲哚美辛能显著抑制;钾离子通道阻断剂4-氨基吡啶、四乙基胺、BaCl2不能抑制黄芩苷对胸主动脉环的舒张作用,格列苯脲能抑制黄芩苷的舒张作用;无钙环境下,黄芩苷预处理对NE收缩有明显抑制作用。因此,黄芩苷具有浓度依赖性血管舒张作用,此作用具有内皮依赖性和非内皮依赖性特点,内皮依赖性收缩可能与前列环素途径有关,非内皮依赖机制可能与KATP通道及钙离子通道有关。     

MS23对大鼠的不同器官血管环收缩的影响

目的研究MS23对不同激动剂所致不同部位血管收缩的对抗作用或舒张作用。方法大鼠主动脉环和小动脉环的张力舒缩状态分别采用PowerLab和DMT系统记录。结果MS23浓度依赖性抑制去甲肾上腺(NA)引起的主动脉环收缩,使NA浓度-效应曲线非平行性右移,并抑制最大反应,使最大效应下降74.7%。MS23和氨茶碱对高钾和NA引起的大鼠主动脉环预收缩均表现出浓度依赖性舒张效应。去内皮和一氧化氮合酶抑制剂L-NAME对MS23的血管舒张作用无明显影响。小动脉环实验结果为,MS23和氨茶碱浓度依赖性舒张高钾所致大鼠冠状动脉、大脑中动脉、肾动脉和肠系膜动脉环的收缩,此4脏器的小动脉对此二药舒张作用的敏感程度差异均无显著性。结论MS23对多种刺激引起的血管环收缩具有对抗或舒张作用,对血管来源和刺激剂无明显的选择性。其血管舒张作用与NO产生及血管内皮是否存在无关。     

盐酸关附甲素对大鼠血管舒缩功能的影响及其机制

目的研究盐酸关附甲素(guanfu base-A,GFA)对大鼠离体胸主动脉舒缩功能的影响,并探讨其可能机制。方法将SD大鼠胸主动脉分离并制成血管环,分成内皮完整组和去内皮组,采用离体血管环实验,观察GFA对基础状态,氯化钾(KCl)预收缩及苯肾上腺素(phenylephrine,PE)预收缩的血管舒张功能的影响,并结合不同抑制剂及无钙液处理,探讨其舒张血管的可能机制。结果累积浓度的GFA(10-8～10-4mol·L-1)对基础状态或KCl预收缩的有无内皮的血管环的张力均无明显影响(P>0.05);对PE(10-6mol·L-1)预收缩内皮完整的血管有浓度依赖性舒张作用,而与PE预收缩的去内皮组相比,从10-7mol·L-1开始差异有显著性(P<0.01)。一氧化氮合酶抑制剂L-NAME、鸟苷酸环化酶抑制剂亚甲蓝及环氧合酶抑制剂吲哚美辛孵育后,均能明显抑制GFA的扩血管作用(P<0.01);经无钙液及GFA处理后,胸主动脉对PE的反应性降低(P<0.01)。结论 GFA对大鼠胸主动脉的舒张作用主要通过两种途径:内皮依赖性舒张作用的机制主要与NO-GC-cGMP途径及激活环氧合酶有关;非内皮依赖性舒张机制主要与抑制内钙释放有关,与门控钙通道引起的外钙内流无关。     

黄芪甲苷对急性心衰犬心脏舒缩功能的影响

黄芪是传统中药,不但对正常和心功能受抑制的心脏有正性肌力作用,而且对收缩和舒张功能均有改善作用[1～2].黄芪甲苷是从黄芪中提取的有效成分,有正性肌力作用[1].为进一步确定黄芪甲苷对心力衰竭的作用,我们用戊巴比妥钠造成急性心衰犬模型,观察黄芪甲苷对实验性心力衰竭的影响.     

黄芪甲苷对黑色素瘤细胞生长和迁移的影响

目的研究黄芪甲苷对黑色素瘤A375细胞生长和迁移的作用。方法通过MTT试验检测不同浓度的黄芪甲苷对A375细胞增殖的影响,应用流式细胞术对黄芪甲苷作用后的A375细胞周期进行分析。通过Annexin V-FITC/PI双染色法观察经黄芪甲苷处理的A375细胞的凋亡情况,transwell实验分析黄芪甲苷对A375细胞迁移的作用。通过Western Blot验证黄芪甲苷对CDK4/CDK6,caspase 3和MMP2的作用。结果不同浓度的黄芪甲苷对A375细胞的增殖均有一定的抑制作用。黄芪甲苷作用后细胞周期阻滞于G1期,细胞凋亡增加,迁移能力减弱。黄芪甲苷通过抑制细胞CDK4/CDK6,caspase 3和MMP2的表达来抑制细胞增殖和迁移,促进细胞凋亡。结论黄芪甲苷能够抑制A375细胞的增殖,促进其凋亡并且抑制其迁移作用,可考虑用于黑色素瘤的预防和治疗。     

Mechanisms underlying vasorelaxant action of astragaloside IV in isolated rat aortic rings

1. Astragaloside IV is a component from the widely used traditional Chinese herb Astragalus membranaceus and its effect on rat aortic ring contraction and relaxation were investigated. 2. The aorta from male Sprague-Dawley rats was isolated in an organ bath and ring tension was recorded with or without endothelium. Cumulative effects of astragaloside IV on vessel contraction and relaxation were observed in the presence of various antagonists related to vessel activity. 3. Astragaloside IV showed concentration-dependent inhibition of vessel contraction induced by phenylephrine and potassium chloride. The amount of calcium released from intracellular stores sensitive to phenylephrine was also markedly reduced by astragaloside IV. There was dose-dependent vasorelaxation in endothelium-intact rings, which was partly inhibited by pre-incubation with nitric oxide (NO) synthase (NOS) Nomega-nitro-L-arginine methyl ester and guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazolo [4,3-alpha] quinoxalin-1-one. Astragaloside IV also induced a significant increase in aortic tissue content of guanosine 3",5"-cyclic monophosphate (cGMP) both in vivo and in vitro. Endothelial NOS inhibitor Nomega-nitro-L-arginine prevented vasodilatation, whereas neuronal NOS inhibitor 7-nitroindazole did not show significant influence on the vessel relaxation of astragaloside IV. 4. In conclusion, astragaloside IV inhibited vessel contraction through blocking calcium influx and intracellular calcium release. The endothelium-dependent vessel dilation of astragaloside IV was attributed mainly to the endothelium-dependent NO-cGMP pathway.     

Astragaloside IV dilates aortic vessels from normal and spontaneously hypertensive rats through endothelium-dependent and endothelium-independent ways

The major active constituent of Astragalus membranaceus, astragaloside IV, has been found to have properties of increasing coronary flow and cardioprotection. In this study, we examined the direct effects of astragaloside IV on vessel dilatation and contraction in isolated aortic rings from both normal and stroke-prone spontaneously hypertensive rats (SHR-SP) in vitro. The results demonstrated that astragaloside IV could antagonize vessel contractions induced by phenylephrine and potassium chloride in a concentration-dependent way. Astragaloside IV reduced CaCl2-induced contractions in Ca2+-free solution. Astragaloside IV also dilated aortic vessels in a dose-dependent manner, which was partially endothelium-dependent through the nitric oxide (NO) and cGMP pathways. The aorta from 6-month-old SHR-SP rats showed impaired endothelium function, and astragaloside IV dilated the vessels from the hypertensive rats to a lesser extent as compared with normal control rats. In the presence of perivascular fat tissue, the contractile responses induced by angiotensin II and phenylephrine were also attenuated by astragaloside IV. Collectively, this study provides functional evidence that astragaloside IV exerts vessel dilatation properties through the endothelium-dependent NO-cGMP pathway in normal and hypertensive rats. It blocks extracellular calcium influx and participates in vessel relaxation partly through phenylephrine and angiotensin II inhibition when perivascular fat is present.     

Astragaloside IV attenuates myocardial fibrosis by inhibiting TGF-β1 signaling in coxsackievirus B3-induced cardiomyopathy

Myocardial fibrosis plays an important role in coxsackievirus B3 (CVB3) induced dilated cardiomyopathy. Excessive transforming growth factor (TGF)-β1 contributes to a pathologic excess of tissue fibrosis. We investigated the effect of astragaloside IV on myocardial fibrosis in CVB3-induced dilated cardiomyopathy. BALB/c mice were inoculated with CVB3 to induce acute viral myocarditis on day 7 (acute VMC group), monthly for 3 months to induce chronic myocarditis (chronic VMC group), and monthly for 9 months to induce dilated cardiomyopathy (DCM group). The same method was used for the DCM+Astra group as that of the DCM group, but former group was given with astragaloside IV-containing drinking water. Compared to DCM group, astragaloside IV treatment significantly increased the survival rate. Histological findings and the collagen volume fraction showed that astragaloside IV decreased fibrosis in heart tissues. Astragaloside IV decreased the level of the serum carboxy-terminal propeptide of procollagen type I (PICP) and the ratio of PICP/ N-terminal type I procollagen propeptide (PINP). Ameliorated myocardial fibrosis was consistent with the downregulated expression of TGF-β1 and its downstream pSmad2/3 and Smad4 in the myocardium of the DCM+Astra group compared to the DCM group. The level of type I collagen was lower in the DCM+Astra group than the DCM group. The same effect was found in the in vitro study. These findings showed that astragaloside IV had a potent preventive effect on myocardial fibrosis in CVB3-induced dilated cardiomyopathy that might be due to downregulation of TGF-β1-Smad signaling.     

黄芪静脉输液中黄芪甲苷和黄芪多糖的含量测定

目的建立黄芪静脉输液中黄芪甲苷和黄芪多糖的含量测定方法。方法用高效液相色谱法测定黄芪甲苷的含量,用碘量法测定黄芪多糖的含量。结果黄芪甲苷和黄芪多糖的平均回收率分别为9751%、9918%,相对标准差分别为248%、191%。结论本文建立的方法准确可靠、灵敏度高、重现性好,可作为黄芪静脉输液质量控制的有效方法。     

黄芪甲苷调控自噬减轻氧糖剥夺/复氧复糖PC12细胞氧化应激损伤研究

目的观察黄芪甲苷对氧糖剥夺/复氧复糖PC12细胞自噬和氧化应激的影响。方法将PC12细胞分为正常组、模型组(即氧糖剥夺/复氧复糖组)、黄芪甲苷组、自噬抑制剂+黄芪甲苷组。用CCK-8法检测细胞活性;ELISA法检测MDA含量、SOD和GSH-Px活性;透射电镜和MDC荧光染色检测自噬小体;Western blot检测Beclin1蛋白表达。结果与正常组相比,模型组细胞活性降低(P<0.05),MDA含量增多、SOD和GSH-Px活性下降(P<0.05),可见自噬小体,Beclin1表达增多(P<0.05);与模型组相比,黄芪甲苷组细胞活性升高(P<0.05),MDA含量减少、SOD和GSH-Px活性升高(P<0.05),自噬小体数量增多(P<0.05),Beclin1表达增多(P<0.05);当给予自噬抑制剂处理时,自噬抑制剂在减轻自噬的同时,可明显拮抗黄芪甲苷的抗氧化作用。结论黄芪甲苷可通过上调自噬减轻氧糖剥夺/复氧复糖诱导的PC12细胞氧化应激损伤,发挥保护作用。     

Astragaloside IV from Astragalus membranaceus shows cardioprotection during myocardial ischemia in vivo and in vitro

Astragaloside IV is the major active constituent of Astragalus membranaceus, which has been widely used for the treatment of cardiovascular diseases in China. However, the effects of astragaloside IV on myocardial ischemia and its mechanisms of action remain largely unknown. In this study, we have examined the effects of astragaloside IV on myocardial infarction and coronary flow in vivo and in vitro. The possible roles of its antioxidative and nitric oxide-inducing properties were also explored. Astragaloside IV significantly reduced infarct size in dogs subjected to coronary ligation in vivo. Astragaloside IV also improved post-ischemic heart function and ameliorated reperfusion arrhythmias in rat hearts in vitro. The cardioprotection of astragaloside IV was accompanied by a significant increase in coronary flow both in vivo and in vitro. The nitric oxide synthase inhibitor, Nomega-nitro- L-arginine methyl ester partially abrogated astragaloside IV's protective effect on heart function. Myocardial antioxidative enzyme superoxide dismutase activity increased with astragaloside IV administration. These data suggest the potential roles of antioxidative and nitric oxide-inducing properties of astragaloside IV in its protection from myocardial ischemia.     

Astragaloside IV inhibits adenovirus replication and apoptosis in A549 cells in vitro

Objectives Astragaloside IV, purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge and Astragalus caspicus Bieb, is an important natural product with multiple pharmacological actions. This study investigated the anti‐ADVs effect of astragaloside IV on HAdV‐3 (human adenovirus type 3) in A549 cell. Methods CPE, MTT, quantitative real‐time PCR (qPCR), flow cytometry (FCM) and Western blot were apply to detect the cytotoxicity, the inhibition and the mechanisms of astragaloside IV on HAdV‐3. Key findings TC₀ of astragaloside IV was 116.8 µm , the virus inhibition rate from 15.98% to 65.68% positively was correlated with the concentration of astragaloside IV from 1.25 µm to 80 µm , IC50 (the medium inhibitory concentration) was 23.85 µm , LC50 (lethal dose 50% concentration) was 865.26 µm and the TI (therapeutic index) was 36.28. qPCR result showed astragaloside IV inhibited the replication of HAdV‐3. Flow FCM analysis demonstrated that the anti‐HAdV‐3 effect was associated with apoptosis. Astragaloside IV was further detected to reduce the protein expressions of Bax and Caspase‐3 and increasing the protein expressions of Bcl‐2 using western blotting, which improved the anti‐apoptosis mechanism of astragaloside IV on HAdV‐3. Conclusions Our findings suggested that astragaloside IV possessed anti‐HAdV‐3 capabilities and the underlying mechanisms might involve inhibiting HAdV‐3 replication and HAdV‐3‐induced apoptosis.     

Astragaloside IV improved intracellular calcium handling in hypoxia-reoxygenated cardiomyocytes via the sarcoplasmic reticulum Ca-ATPase

Although astragaloside IV, a saponin isolated from Astragalus membranaceus, has been shown to protect the myocardium against ischemia/reperfusion injury, its effect on the status of sarcoplasmic reticulum (SR) Ca2+ transport in the injured myocardium remains largely unknown. In this study, we investigated whether in cultured cardiomyocytes subjected to hypoxia and reoxygenation (H/R) administration of astragaloside IV during H/R attenuates the myocardial cell injury and prevents changes in Ca2+ handling activities and gene expression of SR Ca2+ pump. Cultured cardiomyocytes from neonatal rats were exposed to 6 h of hypoxia followed by 3 h of reoxygenation. Myocyte injury was determined by the release of cardiac troponin I in supernatant. Astragaloside IV significantly inhibited cardiac troponin I release after H/R in a dose-dependent manner. The diastolic [Ca2+]i measured with Fura-2/AM was significantly increased after reoxygenation. Astragaloside IV prevented the rise of diastolic [Ca2+]i and the depression of caffeine-induced Ca2+ transients caused by H/R. Furthermore, the observed depressions in SR Ca2+-ATPase activity as well as the mRNA and protein expression of SR Ca2+-ATPase in hypoxic-reoxygenated cardiomyocytes were attenuated by astragaloside IV treatment. These results suggest that the beneficial effect of astragaloside IV in H/R-induced injury may be related to normalization of SR Ca2+ pump expression and, thus, may prevent the depression in SR Ca2+ handling.     

氨基胍改善高果糖对大鼠主动脉内皮依赖性舒张功能损伤的保护作用及机制

目的探讨氨基胍对高果糖致大鼠离体胸主动脉环内皮依赖性舒张反应损伤的保护作用及机制。方法用离体血管环灌流装置,观察不同浓度氨基胍对高果糖引起血管内皮依赖性舒张反应损伤的保护作用;并分析血管壁中NO含量以及eNOS、Akt和ERK1/2蛋白磷酸化的表达。结果高果糖抑制乙酰胆碱诱导的内皮依赖性舒张,降低血管壁中NO的含量和eNOS活性,并促进ERK1/2磷酸化水平上调,但对Akt磷酸化无显著影响;用氨基胍与高果糖共同孵育后,明显改善高果糖对内皮依赖性舒张反应的损伤并恢复血管壁NO含量和eNOS活性,同时降低ERK1/2磷酸化水平。结论氨基胍能改善高果糖对离体胸主动脉环内皮依赖舒张反应的损伤作用。其保护机制与抑制ERK1/2磷酸化和恢复eNOS活性有关,而与AKT磷酸化活性无关。     

Astragaloside IV inhibits proliferation and promotes apoptosis in rat vascular smooth muscle cells under high glucose concentration in vitro

Astragaloside IV is one of the main active ingredients of Radix astragali, which is a herbal remedy widely used in traditional Chinese medicine for the treatment of diabetes and cardiovascular diseases. However, its effects on vascular smooth muscle cell (VSMC), which plays a key role in the development of diabetic vascular complications, were not well studied. The present study was performed to examine the effects of astragaloside IV on proliferation, apoptosis and phenotypic modulation of VSMC under high D-glucose (25 mM). Application of astragaloside IV inhibited the proliferation and the rise of the proliferation index (PI) of VSMC induced by high glucose in a dose-dependent manner. Astragaloside IV induced apoptosis in VSMC under high glucose conditions, accompanied with typical morphological alterations and loss of mitochondrial membrane potential (Delta Psim). In addition, Western blot analysis revealed that astragaloside IV increased the expression of alpha-smooth muscle actin, an important phenotypic modulation marker. In conclusion, astragaloside IV could inhibit high glucose-induced VSMC proliferation through intervention with the cell cycle, promoting apoptosis and regulating phenotypic modulation of VSMC, which strongly suggest that astragaloside IV could hinder the process of pathological vascular remodeling in diabetic patients.