丹参酮对大鼠缺血再灌注期间肠黏膜保护作用及机制

Mechanism of Protective Effects of TanshinoneⅡ-A(TanⅡ-A)on Intestine in Rats with Ischemia/Reperfusion Injury

目的研究丹参酮Ⅱ-A磺酸钠注射液对缺血再灌注期间大鼠肠黏膜的保护作用及机制。方法采用大鼠肠缺血再灌注模型,24只大鼠随机分为对照组、模型组和丹参酮组。丹参酮组于阻断前30min于股静脉静注丹参酮Ⅱ-A 2mL/100g。再灌注2h检测回肠黏膜内pH(pHi)、血清内双胺氧化酶(DAO)活性,同时观察回肠黏膜组织肿瘤坏死因子α(TNF-α)水平及病理形态学改变。结果丹参酮组再灌注2h时pHi明显高于模型组;丹参酮组血清DAO水平显著低于模型组;模型组TNF-α的表达显著高于对照组和丹参酮组,丹参酮组与对照组无明显差异;丹参酮组小肠黏膜病理损伤程度明显轻于模型组。结论丹参酮Ⅱ-A通过增加黏膜血流量及氧合,清除氧自由基及抑制缺血再灌注期间肠黏膜上皮细胞的凋亡,从而减轻肠黏膜缺血再灌注损伤,对休克期的肠黏膜有良好的保护作用。

Objective： To investigate the protective effects and mechanism of tanshinone Ⅱ-A（TanⅡ-A） on intestine in rats with ischemia /reperfusion injury.Methods： 24 SD rats weighing225 ～ 275g were divided into three groups with eight animals in each group including the sham-operation group,the control group and the tanshinone group.The TanⅡ-A were injected in 30 minutes before occlusion.The pH,the DAO and the TNF-αwere detected in 2h reperfusion.Results： After as long as 2 hours of reperfusion,the levels of PH value in membrane in expremental group were significantly higher than those in control group.The DAO content in expremental group was much lower than that in control group.The expression level of TNF-α in control group was significantly higher than that in control group and that in sham-operation group.The intestine pathology damage was less serious in expremental group that in control group.Conclusion： TanshinoneⅡ-A could protect intestine against ischemic reperfusion injury because of oxygen free radicals scavenging and repressing apoptosis of leal mucous cells by increasing intestinal blood flow and improving intestinal oxygenation