论文部分内容阅读
目的研究外源性H2S吸入对大鼠双下肢缺血/再灌注后心肌损伤的保护作用。方法雄性Wistar大鼠23只,随机分为三组:①正常对照组(C组,8只);②缺血/再灌注组(I/R组,8只):应用止血带结扎构建大鼠双下肢缺血/再灌注模型,缺血4 h再灌注4 h。③H2S吸入组(H2S组,7只):大鼠双下肢缺血4 h,再灌注时给予含80 ppm H2S的合成空气持续吸入4 h。观察各组大鼠心肌病理、血浆H2S、肌酸激酶同工酶(CK-MB)、肌钙蛋白-T(TnT)、髓过氧化物酶(MPO)、肿瘤坏死因子-α(TNF-α)水平的变化及心肌胱硫醚-γ-裂解酶(CSE)活性、MPO、TNF-α水平的变化。以免疫组化法观察心肌细胞TNF-α的表达。结果与C组比较,I/R组血浆CK-MB、TnT、MPO、TNF-α及心肌MPO、TNF-α水平明显上升(P<0.05),血浆H2S及心肌CSE活性明显下降(P<0.05),H2S吸入后血浆H2S及心肌CSE活性明显升高;同时,血浆CK-MB、TnT、MPO、TNF-α及心肌MPO、TNF-α水平明显降低(P<0.05)。心肌病理提示I/R组心肌明显肿胀、血管充血,心肌细胞间可见明显分叶核粒细胞浸润,红细胞漏出增多,H2S吸入后心肌损伤明显减轻。心肌TNF-α免疫组化提示I/R组心肌胞浆棕色染色颗粒较C组明显增多,H2S吸入后心肌胞浆棕色染色颗粒明显减少。结论外源性H2S吸入可以通过降低炎细胞浸润及炎性细胞因子激活而对骨骼肌缺血/再灌注的心肌损伤发挥保护作用。
Objective To study the protective effect of exogenous H2S inhalation on myocardial injury after ischemia / reperfusion in both lower limbs of rats. Methods Twenty-three male Wistar rats were randomly divided into three groups: ① normal control group (C group, 8 rats); ② ischemia / reperfusion group (I / R group, 8 rats) The model of bilateral lower extremity ischemia / reperfusion was reperfusion 4 h after ischemia. ② H2S inhalation group (H2S group, 7 rats): The rats were subjected to ischemia for 4 h and reperfused with 80 ppm H2S for 4 h. The changes of myocardial pathology, plasma H2S, CK-MB, TnT, MPO, TNF-α ) Levels and changes of myocardial cystathionine-γ-lyase (CSE) activity, MPO, TNF-α levels. The expression of TNF-αin cardiomyocytes was observed by immunohistochemistry. Results Compared with group C, the levels of CK-MB, TnT, MPO, TNF-α and the levels of MPO and TNF-α in plasma of I / R group were significantly increased (P < ), And the activities of H2S and CSE in plasma after H2S inhalation were significantly increased. At the same time, the levels of CK-MB, TnT, MPO, TNF-α and MPO and TNF-α in plasma significantly decreased (P <0.05). Myocardial pathology showed that the myocardium of I / R group was obviously swollen, vascular congestion was observed, obvious mitochondrial infiltration of erythrocytes was observed among myocardial cells, and the leakage of erythrocytes was increased. Myocardial injury was remarkably alleviated after inhaling H2S. Myocardial TNF-α immunohistochemistry suggested that I / R group of myocardial cytoplasm brown stained particles increased significantly than the C group, H2S inhalation myocardial cytoplasm brown stained particles was significantly reduced. Conclusions Exogenous H2S inhalation can protect myocardium from ischemia / reperfusion injury of skeletal muscle by decreasing inflammatory cell infiltration and activation of inflammatory cytokines.