摘要
目的初步探讨赖氨大黄酸(RHL)对肾性压力负荷性心肌纤维化模型大鼠Smad7表达的影响。方法将32只大鼠随机分为对照组、模型组、赖氨酸组及RHL组,每组8只,用"两肾一夹"法建立肾性压力负荷性心肌纤维化模型,通过测量鼠尾动脉收缩压及左心室质量指数评价造模效果,通过Masson染色观察大鼠心肌纤维化病变程度,采用免疫组织化学法及实时荧光定量聚合酶链反应在蛋白及mRNA水平检测Smad7表达情况。结果与模型组相比,经RHL治疗后肾性压力负荷性心肌纤维化大鼠心肌组织中Smad7蛋白及mRNA表达均明显升高,差异有统计学意义(P<0.05)。结论 RHL可有效抑制肾性压力负荷性大鼠心肌纤维化进程,其机制与上调Smad7表达,靶向拮抗TGF-β/Smads信号传导通路有关。
Objective To preliminarily explore the effect of rhein lysine （RHL） on the expression of Smad7 in renal pressure-loaded myocardial fibrosis model rats. Methods Thirty-two rats were randomly assigned to the control group,model group,lysine group and RHL group,8 cases in each group.The renal pressure-loaded myocardial fibrosis model was established by the method of two kidney one clip.The effect of constructing model was evaluated by measuring the artery systolic pressure of rat tail and left ventricular mass index.The degree of myocardial fibrosis lesion was observed by Masson staining;the expression situation of Smad7 in protein and mRNA level was detected by adopting the immunohistochemical method and real-time fluorescent quantitative PCR. Results Compared with the model group,the myocardial tissue Smad7 protein and mRNA after RHL treatment in the rats with renal pressure-loaded myocardial fibrosis were significantly increased,the difference was statistically significant （ P 〈0.05）. Conclusion RHL can effectively inhibit the progression of myocardial fibrosis in renal pressure-loaded rats,its mechanism is related with up-regulating Smad7 expression and targeted antagonism on the TGF-β/Smads signal transduction pathway.
作者
赵鹏
刘志勇
ZHAO Peng;LIU Zhiyong(Department of Thoracic and Cardiovascular Surgery,Affiliated Hospital of North China Universityof Science and Technology,Tangshan,Hebei 063000,China)
出处
《检验医学与临床》
CAS
2018年第19期2845-2847,2851,共4页
Laboratory Medicine and Clinic
基金
国家自然科学基金资助项目(81201281)
河北省自然科学基金资助项目(H2013209180
C2012401037
H2013209040)
