瑞舒伐他汀后处理通过抑制高迁移率族蛋白表达减轻心肌缺血再灌注损伤的研究

摘要

Objective To investigate whether rosuvastatin post-condition could reduce myocardial I/R injury via inhibiting the expression of HMGB1.Methods Rats were randomly divided into 3 groups which were sham operate group (SO,n=10),ischemia/reperfusion group (I/R,n=15),post-condition with rosuvastatin + ischmia/reper-fusion group (RS+I/R,n=15).Serum Lactate dehydrogenase (LDH),creatine kinase (CK),myocardial tissue infarct size,superoxide dismutase (SOD)activities,malondialdehyde (MDA)levels and high mobility group box 1 protein (HMGB1)expression were tested.Results Infarct size in myocardial tissue(28.9±3.7 vs.52.8±4.4%)and the activities of LDH and CK in serum were significantly reduced by rosuvastatin post-condition(LDH(U/L)was 1389.4±103.7 vs 2301.6±117.4,CK(U/L)was 1390.5±96.5 vs 2402.3±130.2,and All P <0.05),the same with the MDA production(5.84±0.36 vs 10.98±0.83)SOD activity (157.1±9.51 vs 90.12±4.48)and HMGB1 expression (0.267±0.024 vs 0.927±0.117)in myocardial tissue (all P<0.05).Conclusion Rosuvastatin can re-duce myocardial I/R injury via inhibiting the expression of HMGB1.%目的：研究瑞舒伐他汀（RS）后处理是否可以通过抑制高迁移率族蛋白（HMGB1）的表达减轻心肌缺血再灌注损伤（I／R）。方法使用 SD 大鼠缺血再灌注模型，缺血30 min，再灌4 h。将大鼠随机分为假手术组（n＝10）、缺血再灌注组（n＝15）和 RS 后处理组（n＝15）三组，检测血清中乳酸脱氢酶（LDH）水平和肌酸激酶（CK）活性、心肌组织中超氧化物歧化酶（SOD）活性和丙二醛（MDA）水平及心肌梗死面积和心肌中 HMGB1的表达水平。结果 RS 后处理能明显减少梗死面积（P ＜0．05）及 LDH、CK 活性（P 均＜0．05）；明显抑制 MDA 的升高和 SOD 的活性（P 均＜0．05）；明显抑制 HMGB1的表达（P ＜0．05）。结论 RS 后处理对心肌 I／R 的保护作用与抑制 HMGB1的表达有关。