摘要
目的探讨绿原酸(CGA)通过基因编码基质相互作用分子1(Stim1)/钙释放激活钙调节蛋白1(Orai1)通路改善糖尿病小鼠动脉粥样硬化(AS)的机制。方法将30只C57BL/6J雄性小鼠随机分为对照组、模型组、CGA组,每组各10只。采用高脂饲料饲养加腹腔注射50 mg/kg的链脲佐霉素(STZ)建立糖尿病AS小鼠模型,对照组采用普通饲料+等量生理盐水,CGA组建立模型后给予CGA干预,模型组给予等量生理盐水。HE染色、油红O染色观察动脉斑块情况;CCK-8检测主动脉血管平滑肌细胞(VSMCs)增殖活力;qPCR检测Stim1、Orai1表达水平。结果CGA组、模型组的斑块沉积面积大于对照组,差异有统计学意义(P<0.05);而CGA组的斑块沉积面积小于模型组,差异有统计学意义(P<0.05)。模型组、CGA组的VSMCs增殖率高于对照组,差异有统计学意义(P<0.05);而CGA组的VSMCs增殖率低于模型组,差异有统计学意义(P<0.05)。模型组、CGA组的Stim1、Orai1水平高于对照组,差异有统计学意义(P<0.05);而CGA组的Stim1、Orai1水平低于模型组,差异有统计学意义(P<0.05)。结论CGA能够改善糖尿病AS及VSMCs增殖,其机制可能与调节Stim1/Orai1通路有关。
Objective To investigate the mechanism of chlorogenic acid(CGA)in improving atherosclerosis(AS)in diabetic mice by stromal interaction molecule 1(Stim1)/calcium release-activated calcium modulator 1(Ora1)pathrray.Methods A total of 30 C57BL/6J male mice were randomly divided into control group,model group and CGA group,with 10 mice in each group.The diabetic AS mouse model was established by feeding high-fat diet plus intrabitoneal injection of 50 mg/kg streptozocin(STZ).The control group was given ordinary diet plus equal amount of normal saline,the CGA group was given CGA intervention after establishing the model,and the model group was given equal amount of normal saline.Arterial plaque was observed by HE staining and oil red O staining.The proliferative activity of aortic vascular smooth muscle cells(VSMCs)was detected by CCK-8.The expression levels of Stim1 and Orai1 were detected by qPCR.Results The plaque deposition area of CGA group and model group was larger than that of control group,and the difference was statistically significant(P<0.05).The plaque deposition area of CGA group was smaller than that of model group,and the difference was statistically significant(P<0.05).The proliferation rate of VSMCs in model group and CGA group was higher than that in control group,the difference was statistically significant(P<0.05).The proliferation rate of VSMCs in CGA group was lower than that in model group,and the difference was statistically significant(P<0.05).Stim1 and Orai1 levels in model group and CGA group were higher than those in control group,and the differences were statistically significant(P<0.05).The levels of Stim1 and Orai1 in CGA group were lower than those in model group,and the differences were statistically significant(P<0.05).Conclusion CGA can improve diabetic atherosclerosis and VSMCs proliferation,and its mechanism may be related to the regulation of Stim1/Orai1 pathway.
作者
杨得奖
李新明
龚欢
谭彧
周凤
YANG Dejiang;LI Xinming;GONG Huan;TAN Yu;ZHOU Feng(Department of Neurology,Nanchang First Hospital,Jiangxi Province,Nanchang330008,China;Department of Cadre Health Care,Nanchang First Hospital,Jiangxi Province,Nanchang330008,China;Department of Neurology,the Fifth Affiliated Hospital of Sun Yat-sen University,Guangdong Province,Zhuhai519000,China)
出处
《中国当代医药》
CAS
2024年第20期9-13,共5页
China Modern Medicine
基金
江西省中医药管理局科技计划项目(2020A0336)。
