论文部分内容阅读
目的:探讨米诺环素预处理对大鼠心肌缺血再灌注损伤的保护作用及其可能的机制。方法:成年雄性SD大鼠缺血前1h给予米诺环素(45mg/kg,ip),结扎冠脉前降支缺血30min后,恢复灌注4h;应用2,3,5-氯化三苯基四氮(TTC)法检测心肌梗死面积;试剂盒检测乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA)和超氧化物歧化酶(SOD);采用原位脱氧糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)法检测心肌细胞的凋亡;Western blot检测高迁移率族蛋B1(HMGB1)表达。结果:与对照组相比,米诺环素预处理显著减小了心肌梗死面积,降低了心肌细胞凋亡和LDH、CK等血清心肌坏死标记物的表达(P<0.05)。米诺环素预处理也显著降低了MDA的表达,抑制了SOD的减少(P<0.05)。同时,米诺环素预处理抑制了缺血再灌注引起的HMGB1的表达(P<0.05)。结论:米诺环素预处理能够减轻心肌缺血再灌注损伤并抑制心肌细胞凋亡,这种保护作用可能与其抑制缺血再灌注诱导的HMGB1的表达有关。
Objective: To investigate the protective effect of minocycline preconditioning on myocardial ischemia-reperfusion injury in rats and its possible mechanism. METHODS: Adult male Sprague-Dawley rats were treated with minocycline (45 mg / kg, ip) 1 h before ischemia and ligation of the anterior descending coronary artery for 30 min followed by 4 h reperfusion. 2,3,5-trichlorobenzene The area of myocardial infarction was detected by TTC method. The contents of lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA) and superoxide dismutase (SOD) The apoptosis of cardiomyocytes was detected by TUNEL method and the expression of HMGB1 was detected by Western blot. Results: Compared with the control group, minocycline preconditioning significantly reduced the area of myocardial infarction and decreased the apoptosis of myocardial cells and the expression of LDH, CK and other markers of myocardial necrosis (P <0.05). Minocycline preconditioning also significantly reduced the expression of MDA and inhibited the decrease of SOD (P <0.05). Meanwhile, minocycline preconditioning inhibited HMGB1 expression induced by ischemia-reperfusion (P <0.05). CONCLUSION: Minocycline preconditioning can reduce myocardial ischemia-reperfusion injury and inhibit cardiomyocyte apoptosis, which may be related to the inhibition of HMGB1 expression induced by ischemia-reperfusion.