摘要
目的:研究内质网应激是否在高脂血症大鼠诱导心肌细胞凋亡中起作用。方法:通过建立高脂血症大鼠模型,全自动化生化仪检测血清甘油三酯(Triglycercide,TG)及胆固醇(Cholesterol,TC)水平;HE染色观察心肌组织的病理学变化;TUNEL法检测心肌细胞凋亡;免疫组化法及RT-PCR技术检测心肌细胞内质网应激(Endoplasmic reticulum stress,ERS)信号通路分子GRP78的表达变化。结果:喂养12周时模型组大鼠血清TC、TG含量明显高于对照组(P<0.01);大鼠模型组较正常组心肌组织排列紊乱、边界不清、心肌纤维断裂、部分细胞核溶解消失;模型组大鼠心肌细胞凋亡率明显高于正常组(P<0.05);大鼠心肌GRP78mRNA及蛋白的表达量,模型组均较对照组明显升高(P<0.05)。结论:ERS途径可能在高脂血症诱导心肌细胞凋亡中起到重要作用。
Objective：To investigate the mechanism of effects of endoplasmic reticulum stress on apoptosis of cardiomyocyte in hyperlipidemia rats. Methods：Rat model of established with fatty dieting.After twelve weaks,the serum triglycerides（TG）and cholesterol （TC）were oberserved by completely automatic biochemistry meter;The pathological changes of myocardial tissue were detected by HE staining;The apoptosis of cardiomyocyte were tested by TUNEL. The expression of endoplasmic reticulum stress associated molecular glucose regulated protein 78 in myocardial tissue were tested byimmunohistochemistry and RT-PCR. Results ：The levels of TC and TG in blood sera of control group did not change after 12 weeks , while TC and TG in model group significantly increased along with the te mporal prolongation compared with those in control group （ P 0.01 ） . The expression of GRP78 mRNA and protein in myocardiocyte of rats in model group significantly increased with those in control group （ P0.05 ） . Enhanced expression of GRP78 could be induced by fatty diet. Couclusion：The hyperlipidemia maybe can induce myocardiocyte apoptosis through endoplasmic reticulum pathways.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2010年第10期1509-1512,共4页
Journal of Chongqing Medical University
关键词
高脂血症
内质网应激
心肌细胞
凋亡
Hyperlipidemia
Endoplasmic reticulum stress
Cardiomycyte
Apoptosis
