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作 者:司林杰[1] 许晶[1] 易晨龙 徐晓晗[1] 张杨杨[1] 张郁青[2] 王晓伟[1]
机构地区:[1]南京医科大学第一附属医院胸心外科,江苏南京210029 [2]南京医科大学附属江宁医院心血管内科,江苏南京210029
出 处:《南京医科大学学报(自然科学版)》2014年第9期1168-1172,共5页Journal of Nanjing Medical University(Natural Sciences)
基 金:江苏省教育厅自然科学基金(12KJB320003);江苏省中医药局科技基(lz13217);南京市科技局科技发展基金(201303036)
摘 要:目的:观察积雪草酸(asiatic acid,AA)对小鼠主动脉弓缩窄术后心肌肥厚的保护作用并探讨其可能的机制。方法:采用主动脉弓缩窄(transverse aortic constriction,TAC)法建立小鼠心肌肥厚模型。实验分为5组:假手术组(Sham组)、手术组(TAC组)、TAC+AA1[25 mg/(kg·d)]组、TAC+AA2[50 mg/(kg·d)组、TAC+AA3[100 mg/(kg·d)]组。TAC术后2周,心脏超声检测心功能,Western blot法检测心肌组织中转化生长因子(transforming growth factor,TGF)-β1、p-p38、p38、p-ERK1/2以及ERK1/2蛋白的表达,real-time PCR法检测心肌组织中ANP和TGF-β1基因的表达。结果:AA可显著抑制TAC诱导的心肌肥厚,改善心功能,降低TGF-β1基因和蛋白表达,并抑制p38和ERK1/2磷酸化。结论:AA治疗可抑制心肌肥厚,其机制可能与AA抑制TGF-β1-p38/ERK1/2信号通路有关。Objective:To determine the protective effects and molecular mechanisms of asiatic acid (AA) on postoperative cardiac hypertrophy induced by transverse aortic constriction in mice. Methods:Transverse aortic constriction(TAC) was performed to establish the mice model of myocardial hypertrophy. C57BL/6 mice were divided into five groups:the Sham group,the TAC group,the TAC+AA1 [25 mg/(kg·day)] group;the TAC+AA2 [50 mg/(kg·day)1 group and the TAC+AA3 [ 100 mg/(kg·day)] group. After 2 weeks of TAC, echocardiography was performed to measure the hypertrophic criteria of the hearts. The protein expressions of TGF-β1, p-p38,p38,p-ERKl/2 and ERK1/2 were detected by Western blot. The mRNA expressions of ANP and TGF-β1 were detected by real-time PCR. Results:AA significantly inhibited cardiac hypertrophy induced by TAC,improved cardiac function,reduced the mRNA and protein expression of TGF-β1,as well as the phosphorylation of p38 and ERK1/2. Conclusion:AA attenuates TAC- induced cardiac hypertrophy. The protective mechanisms of AA may through inhibiting TGF-β1-p38/ERK1/2 signaling pathway.
关 键 词:积雪草酸 心肌肥厚 转化生长因子Β1 丝裂原激活蛋白激酶
分 类 号:R541[医药卫生—心血管疾病]
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