| Objective:Observe serum NT-proBNP level and the expression of TNF-α on myocardiumtissue of mice to explore the mechanisms by Agkistrodon snake venom-mediatedmyocardial injury.Methods:1. The96male mice were divided into12groups(n=8) randomly and snake venomwas divided into three groups: normal saline(control group), venomous snakevenom and saline (experimental group), venomous snake venom and TNF-αinhibitors (intervention group). Poisoning time to set up four levels:1hours,12hours,24hours,48hours.2. Collected serum and detected the level of serum cTnT and NT-proBNP byELISA.3. Collected myocardial specimens and observed pathological changes ofmyocardial and detected TNF-α protein expression of myocardial tissue byimmunohistochemistry.4. Linear correlation analysis were performed in myocardial histopathologic scores,serum cTnT levels, serum NT-proBNP levels and TNF-α expression.Results:1. Myocardial histopathologic scores at each time point in experimental group werehigher than intervention group and control group(P＜0.05);12h group werehigher than1h group, and24h group were higher than12h group, and48h group were higher than12h group, and these differences in experimental group andintervention group were statistically significant(P＜0.05).2. The expression of TNF-α protein in myocardium at each time point inexperimental group were higher than intervention group and control group(P＜0.05);the expression of TNF-protein in myocardium at each time point inintervention group were higher than control group(P＜0.05);12h group werehigher than1h group, and24h group were higher than12h group, and48h groupwere higher than12h group, and these differences in experimental group andintervention group were statistically significant (P＜0.05).3. Besides1h group, serum cTnT levels at each time point in experimental groupwere higher than intervention group and control group(P＜0.05), serum cTnTlevels at each time point in intervention group were higher than control group(P＜0.05);12h group were higher than1h group, and24h group were higher than12h group, and48h group were higher than12h group, and these differences inexperimental group and intervention group were statistically significant(P＜0.05).4. Serum NT-ProBNP levels at each time point in experimental group were higherthan intervention group and control group(P＜0.05)，serum cTnT levels at eachtime point in intervention group were higher than control group(P＜0.05);12hgroup were higher than1h group, and24h group were higher than12h group, and48h group were higher than12h group, and these differences in experimentalgroup and intervention group were statistically significant(P＜0.05).5. Correlation analysis: myocardial histopathologic scores was significant positivecorrelation with the expression of TNF-α protein in myocardium and serumNT-ProBNP levels respectively(r＝0.728and r＝0.647, P＜0.05); serum cTnTlevels was significant positive correlation with the expression of TNF-α protein inmyocardium and serum NT-ProBNP levels respectively(r＝0.666and r＝0.529, P＜0.05); the expression of TNF-α protein in myocardium was significant positivecorrelation with serum NT-ProBNP levels(r＝0.575, P＜0.05). Conclusions:1. Agkistrodon snake venom can lead to acute myocardial injury of mice, elevatedTNF-α protein in myocardium, increased the level of serum cTnT andNT-ProBNP, and with the extension of time, the more severe myocardial injury,the higher its expression increased significantly.2. TNF-α inhibitors can reduce the degree of Agkistrodon snake venom-mediatedmyocardial injury, the expression of TNF-α protein in myocardium, serum cTnTand NT-ProBNP level.3. Over-expression of TNF-α may be one of the mechanisms that agkistrodon snakevenom-mediated myocardial injury and increased synthesis and release ofNT-ProBNP. |
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