Objective To observe the expression of TNF - α on myocardium tissue of mice to explore the mechanisms by Agkistrodon snake venom - mediated myocardial injury. Methods The 96 male mice were divided into 12 groups(n = 8) randomly and snake venom was divided into three groups: normal saline ( control group) , venomous snake venom and saline ( experimental group) , venomous snake venom and TNF - α inhibitors (intervention group). Poisoning time to set up four levels: 1 h, 12 h, 24 h, 48 h. The level of serum cTnT were detected by ELISA and pathological changes of myocardial were observed and TNF - α protein expression of myocardial tissue were detected by immunohistochemistry. Linear correlation analysis were performed in myocardial histopathologic scores, serum cTnT levels and TNF - α expression. Results Myocardial histopathologic scores and the expression of TNF - α protein in myocardium at each time point in experimental group were higher than intervention group and intervention group were higher than control group (P < 0. 05 ) , 48 h group were higher than 24 h group, and 24 h group were higher than 12 h group, and 12 h group were higher than lh group, and, and these differences in experimental group and intervention group were statistically significant(P <0. 05) ; besides lh group, serum cTnT levels at each time point in experimental group were higher than intervention group and and intervention group were higher than control group ( P < 0. 05) , 48 h group were higher than 24 h group, and 24 h group were higher than 12 h group, and 12 h group were higher than 1 h group, and, and these differences in experimental group and intervention group were statistically significant P < 0. 05 ) ; myocardial histopathologic scores was significant positive correlation with the expression of TNF - α protein in myocardium ( r = 0. 728 , P < 0. 05 ) ; serum cTnT levels was significant positive correlation with the expression of TNF - α protein in myocardium ( r = 0.666, P < 0. 05 ). Conclusion Agkistrodon snake venom can lead to acute myocardial injury of mice, and with the extension of time, the more severe myocardial injury, the higher the expression of TNF - α protein increased significantly. TNF - α inhibitors can reduce the degree of Agkistrodon snake venom - mediated myocardial injury, the expression of TNF - α protein in myocardium and serum cTnT. Over - expression of TNF - α may be one of the mechanisms that agkistrodon snake venom - mediated myocardial injury.%目的 观察蝮蛇毒介导的心肌损伤与TNF-α的表达,探讨蝮蛇毒介导的心肌损伤的机制.方法 96只小鼠随机分成12组(n=8),共设3个组:生理盐水(对照组)、蝮蛇毒+生理盐水(实验组)、蝮蛇毒+TNF-α抑制剂(干预组);分4个时相点:1 h、12 h、24 h和48 h.ELISA检测血清cTnT水平,观察心肌组织病变,免疫组化检测心肌组织TNF-α蛋白的表达.对心肌病变积分、血清cTnT水平与心肌TNF-α表达行直线相关分析.结果 实验组各时相点心肌病变积分和心肌TNF-α蛋白表达均高于干预组和对照组(P＜0.05),干预组各时相点均高对照组(P＜0.05),实验组和干预组48 h＞24 h＞12 h＞1 h(P＜0.05);除1 h组外,实验组各时相点血清cTnT水平均高于干预组及对照组(P＜0.05),干预组各时相点高于对照组(P＜0.05),实验组和干预组48 h＞24 h＞12 h＞1 h(P＜0.05);小鼠心肌病变积分与心肌TNF-α表达呈显著正相关(r＝0.728,P＜0.05),小鼠血清cTnT水平与心肌TNF-α表达呈显著正相关(r＝0.666,P＜0.05).结论 蝮蛇毒可致小鼠急性心肌损伤,随时间的延长,心肌损伤越严重.TNF-α抑制剂能降低蝮蛇毒介导的心肌损伤程度、血清cTnT水平及心肌TNF-α蛋白的表达.TNF-α的过度表达可能是蝮蛇毒介导心肌损伤的机制之一.
展开▼
