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目的检测内质网应激蛋白Grp78及Grp94在糖尿病心肌损伤大鼠中表达的变化,探讨内质网应激在糖尿病心肌损伤中发挥的作用。方法 Wistar大鼠随机分为正常对照(A)组及糖尿病模型(B)组,B组腹腔注射STZ 35mg/kg制备。两组均饲养至20周龄时取大鼠尾静脉血测FPG、FIns,并计算胰岛素抵抗指数(HOMA-IR)。取大鼠心肌组织检测肌酸激酶(CK)、乳酸脱氢酶(LDH)活力。心肌组织HE染色,免疫组化法检测Grp78及Grp94表达变化,RT-PCR测定Grp78mRNA、Grp94mRNA的表达。结果 B组FPG、FIns、HOMA-IR、CK和LDH均高于A组(P均<0.05)。B组心肌纤维肥大,走形较为紊乱,出现核固缩、裂解及丢失现象,心肌细胞变性、坏死,横纹肌消失;B组Grp78和Grp94免疫组化阳性指数(IPI)高于A组(P均<0.01);RT-PCR产物琼脂糖凝胶电泳显示,B组Grp78mRNA及Grp94mRNA条带较A组变粗变亮,Grp78mRNA、Grp94mRNA表达量增加(P均<0.01)。结论内质网应激蛋白Grp78及Grp94在糖尿病心肌损伤大鼠中表达比正常大鼠增加,内质网应激可能在糖尿病心肌损伤中发挥作用。
Objective To investigate the changes of endoplasmic reticulum stress protein Grp78 and Grp94 in diabetic rats with myocardial injury and to explore the role of endoplasmic reticulum stress in myocardial injury in diabetic rats. Methods Wistar rats were randomly divided into normal control group (A) and diabetic model group (B). Group B was injected intraperitoneally with STZ 35 mg / kg. Rats in both groups were fed until the age of 20 weeks to measure the FPG and FIns in the tail vein of the rats, and the insulin resistance index (HOMA-IR) was calculated. Myocardial tissue was taken for determination of creatine kinase (CK) and lactate dehydrogenase (LDH) activity. Myocardial tissue HE staining, immunohistochemistry Grp78 and Grp94 expression changes, RT-PCR determination Grp78mRNA, Grp94mRNA expression. Results The FPG, FIns, HOMA-IR, CK and LDH in group B were higher than those in group A (all P <0.05). In group B, cardiac fibrosis was hypertrophy and the pathological changes were disorderly. Nuclear condensation, lysis and loss were observed. Cardiomyocytes degeneration, necrosis and rhabdomyolysis disappeared. The positive expression of Grp78 and Grp94 in group B was higher than that in group A <0.01). The agarose gel electrophoresis of RT-PCR products showed that Grp78mRNA and Grp94mRNA bands of group B were thicker and brighter than group A, Grp78mRNA and Grp94mRNA increased (all P <0.01). Conclusion The expression of endoplasmic reticulum stress protein Grp78 and Grp94 in diabetic rats with myocardial injury increased compared with normal rats, and endoplasmic reticulum stress may play a role in myocardial injury.