LncRNA PFL通过AMPK-PPARα信号通路改善心肌纤维化  

LncRNA PFL improves myocardial fibrosis by activating AMPK-αsignaling pathway

作　　者：李庆勇[1] 汤宝鹏[2] 牛锁成 申文祥[1] 周贤惠[2] 芦颜美[2] LI Qing-Yong;TANG Bao-Peng;NIU Suo-Cheng(First Department of Cardiology,Puyang People's Hospital,Puyang 457000,Henan,China)

机构地区：[1]濮阳市人民医院心内一科,河南濮阳457000 [2]新疆医科大学一附院起搏电生理科

出　　处：《中国老年学杂志》2023年第9期2181-2185,共5页Chinese Journal of Gerontology

基　　金：国家自然科学基金(81570297)。

摘　　要：目的研究促纤维化长链非编码RNA(LncRNA PFL)改善压力负荷诱导的心肌纤维化同腺苷酸活化蛋白激酶(AMPK)-过氧化物酶增殖激活的α亚型受体(PPAR)α信号通路的激活是否相关。方法将60只大鼠随机分为A(假手术)组、B(压力负荷诱导的心肌纤维化模型)组、C(压力负荷诱导的心肌纤维化模型+LncRNA PFL抑制剂)组。采用苏木素-伊红(HE)染色检测心肌组织的病理形态和纤维化程度,羟脯氨酸(HYP)检测心肌质量,Western印迹测定心肌组织中AMPK、PPARα蛋白水平。结果与A组比较,B组和C组心脏重量指数(HWI)和左心室重量指数(LVWI)均显著升高(P<0.01);与B组比较,C组显著下降(P<0.01)。HE染色结果:与A组比较,B组和C组心肌细胞的炎症浸润和细胞间胶原纤维均显著增加,神经元细胞损伤程度加重(P<0.05);与B相比,C组显著好转(P<0.05)。免疫荧光结果:B组AMPK及PPARα蛋白水平明显低于A组和C组,且C组明显低于A组。RT-qPCR及Western印迹结果:B组心肌组织中AMPK和PPARαmRNA及蛋白表达显著低于A组和C组,且C组显著高于A组(P<0.05)。结论LncRNA PFL表达下调改善压力负荷诱导的心肌纤维化与激活AMPK-α信号通路有关。Objective To investigate whether fibrosis-promoting long noncoding RNA(LncRNA PEL)on myocardial fibrosis induced by pressure overload by activating adenosine monophosphate activated protein kinase(AMPK)-peroxisome proliferator-activated receptor(PPAR)-αsignaling pathway.Methods Sixty rats were randomly divided into A(fake surgery team)group,B(pressure-induced myocardial fibrosis model)group and C(stress load induced myocardial fibrosis model+LncRNA PFL inhibitor)group.Htoxylin eosin(HE)staining was used to detect the pathological morphology and degree of fibrosis in myocardium tissue,hydroxyproline(HYP)was used to detect myocardial mass,and Western blot was used to detect the levels of AMPK and PPARαprotein in myocardium.Results Compared with A group,the heart weight index(HWI)and left ventricle weight index(LVWI)of B and C groups were significantly increased(P<0.01);compared with B group,above index in C group were significantly decreased(P<0.01).The result of HE staining showed that compared with A group,the inflammatory infiltration and intercellular collagen of myocardial cells in B and C groups were significantly increased,and the degrees of neuronal cell damage were significantly increased(P<0.05);compared with B group,above index in C group were significantly improved(P<0.05).The immunofluorescence result showed that the levels of AMPK and PPARαprotein in B group were significantly lower than those in A and C groups,and the protein levels of C group were significantly lower than those in A group.RT-qPCR and Western blot results showed that the levels of AMPK and PPARαmRNA and protein expression in myocardial tissue in B group were significantly lower than those in A and C groups,and the levels of C group were significantly higher than those in A group(P<0.05).Conclusions The downregulated expression of LncRNA PEL improves myocardial fibrosis induced by pressure overload which should be related to activation of AMPK-αsignaling pathway.

关 键 词：促纤维化长链非编码RNA(LncRNA PFL) 腺苷酸活化蛋白激酶(AMPK)-过氧化物酶增殖激活的α亚型受体(PPAR)α信号通路 压力负荷 心肌纤维化 

分 类 号：R43[医药卫生—临床医学]