Hu Lei, Cai Na, Jia Hui
Department of Clinical Laboratory, Northwest Women and Children's Hospital, Xi'an, Shaanxi 710061, P.R. China.
Department of Medical Genetics, Northwest Women and Children's Hospital, Xi'an, Shaanxi 710061, P.R. China.
Exp Ther Med. 2017 Dec;14(6):5509-5514. doi: 10.3892/etm.2017.5246. Epub 2017 Oct 2.
The current study aimed to evaluate the cardioprotective effects of pterostilbene (PTB) on myocardial ischemia-reperfusion (I/R) injury in rats and identify its possible underlying mechanisms of action. A rat I/R model was established by ligating the left anterior descending coronary artery for 30 min and releasing the ligature to induce reperfusion for 120 min. Serum creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) levels were measured using CK-MB and LDH assay kits and myeloperoxidase (MPO) activity in the myocardium was evaluated using an MPO assay kit. Tumor necrosis factor-α, interleukin (IL)-6 and IL-8 levels were assayed using ELISA kits. Cardiomyocyte apoptosis was measured using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Levels of protein kinase B (Akt) and phosphorylated Akt (p-Akt) were measured using western blotting. The results demonstrated that treatment with PTB significantly reduced cardiomyocyte apoptosis, significantly increased Bcl-2 and p-Akt levels and decreased Bax expression in the hearts of rats subjected to I/R injury. However, the protective effects induced by PTB were attenuated by LY294002, which inhibits Akt activation. The results of the current study suggest that PTB treatment may reduce the I/R injury-induced apoptosis of cardiomyocytes, which is mediated by the phosphoinositide 3-kinase/Akt signaling pathway.
本研究旨在评估紫檀芪(PTB)对大鼠心肌缺血再灌注(I/R)损伤的心脏保护作用,并确定其可能的潜在作用机制。通过结扎左冠状动脉前降支30分钟,然后松开结扎线诱导再灌注120分钟,建立大鼠I/R模型。使用肌酸激酶同工酶MB(CK-MB)和乳酸脱氢酶(LDH)检测试剂盒测量血清CK-MB和LDH水平,并使用髓过氧化物酶(MPO)检测试剂盒评估心肌中的MPO活性。使用酶联免疫吸附测定(ELISA)试剂盒检测肿瘤坏死因子-α、白细胞介素(IL)-6和IL-8水平。使用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记染色法检测心肌细胞凋亡。使用蛋白质免疫印迹法测量蛋白激酶B(Akt)和磷酸化Akt(p-Akt)的水平。结果表明,PTB处理可显著减少I/R损伤大鼠心脏中的心肌细胞凋亡,显著增加Bcl-2和p-Akt水平,并降低Bax表达。然而,抑制Akt激活的LY294002减弱了PTB诱导的保护作用。本研究结果表明,PTB处理可能减少I/R损伤诱导的心肌细胞凋亡,这是由磷脂酰肌醇3-激酶/Akt信号通路介导的。