汪德坤 魏汉维 彭戬（湖北省武汉市东湖医院，湖北武汉430074）

·综述·

丹参酮ⅡA对脓毒症大鼠心肌细胞高迁移率族蛋白-1、肿瘤坏死因子-α表达的影响及机制*

汪德坤 魏汉维 彭戬
（湖北省武汉市东湖医院，湖北武汉430074）

目的观察丹参酮ⅡA对高迁移率族蛋白B1（HMGB-I）、肿瘤坏死因子-α（TNF-α）在脓毒症大鼠心肌细胞的表达的影响。方法雄性SD大鼠45只随机分为正常组（A组）、脓毒症组（B组）及丹参酮ⅡA+脓毒症组（C组），采用HE染色和ELISA法测定心肌组织中的TNF-α含量，Western blot法检测心肌组织中HMGB-1的表达。结果HE染色显示B组大鼠心肌纤维水肿、疏松，间质充血水肿，胶原纤维增多，可见部分心内膜内皮细胞水肿脱落，而C组心肌病理改变较B组轻。ELISA法测定心肌组织TNF-α含量，Western blot法检测心肌组织中HMGB-1的表达，B组都较C组明显增加（P＜0.05），心肌凋亡指数B组与C组也有明显差异（P＜0.05）。且以上改变C组与A组也存在差异（P＜0.05）。结论丹参酮ⅡA可以减少脓毒症大鼠心肌组织TNF-α及HMGB-I的表达，对脓毒症心肌抑制有保护作用。

脓毒症丹参酮ⅡA高迁移率族蛋白-1肿瘤坏死因子-α

【Abstract】Objective:To observe the influence and mechanism of tanshinoneⅡA on the expression of HMGB-I and TNF-αof cardiomyocyte in ratswith sepsis.M ethods:45male SD ratswere random ly divided into 3 groups：the normal group（group A），sepsis group（group B），tanshinoneⅡA+sepsis group（group C），using HE staining and ELISA method to determine the contentof TNF-αinmyocardial tissue，Western blotmethod to detect the expression of HMGB-1 in myocardial tissue.Results:HE staining showed that in group B，there were myocardial fibers edema，osteoporosis，interstitial hyperemia and edema，increased collagen fibers，the visible part of the endocardial endothelial edema，and myocardial pathological changes compared with group B and group C.Group B was significantly increased compared with the group C in ELISA method to determine content of TNF-αin myocardial tissue and Western blotmethod to detect the expression of HMGB-1 inmyocardial tissue（P《0.05），and myocardial apoptosis index of group B and group C also had obvious difference（P《0.05）.And the changes above and the differences also existed in the comparison between group A and group C（P《0.05）.Conclusion:TanshinoneⅡA can reduce the expression of TNF-αand HMGB-Iofmyocardial tissue of rat in sepsis，has a protective effect tomyocardial inhibition in sepsis.

【Key words】Sepsis；TanshinoneⅡA；Highmobility group protein 1；Tumor necrosis factor alpha

心功能不全是脓毒症的常见并发症之一，近50%的脓毒症患者可出现不同程度的心肌抑制，病死率高达70%～90%［1］。心肌细胞凋亡是引起脓毒症心肌抑制的重要因素［2］。炎症早期的重要炎性因子肿瘤坏死因子-α（TNF-α）可促进心肌凋亡，TNF-α通常在脂多糖刺激几分钟内即开始释放，在2 h左右达高峰，并在随后2 h内迅速下降至无法测出［3］，而且利用TNF-α拮抗剂治疗脓毒症也多以失败告终，提示在脓毒症后期的病理生理过程中有其他晚期炎症介质参与。……