CAJ | 학술논문

目的研究参附注射液(简称参附)对大鼠肠缺血再灌注期间黏膜上皮细胞凋亡的影响,并探讨其可能机制.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(C组)、缺血再灌注组(I/R组)和参附治疗组(SF组),SF组于阻断前30 min静注SF液2 mL/100g.再灌注2 h检测回肠黏膜上皮细胞Cas-pase-3,Bcl-2蛋白的表达及细胞凋亡;同时观察小肠黏膜病理形态学改变.结果凋亡细胞检测显示:I/R组凋亡细胞显著增多,SF组凋亡细胞数较I/R组显著减少而多于C组(均P＜0.05);Caspase-3,Bcl-2蛋白的表达:Caspase-3表达I/R组显著多于SF组和C组(P＜0.01),SF组与C组无明显差异;Bcl-2表达SF组显著高于I/R组(P＜0.05),后者显著低于C组(P＜0.05);SF组小肠黏膜病理损伤程度明显减轻I/R组(P＜0.01).结论参附注射液通过抑制Caspase-3表达和促进Bcl-2基因表达减少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.
목적연구삼부주사액(간칭삼부)대대서장결혈재관주기간점막상피세포조망적영향,병탐토기가능궤제.방법채용대서장결혈재관주모형.24지대서수궤분위대조조(C조)、결혈재관주조(I/R조)화삼부치료조(SF조),SF조우조단전30 min정주SF액2 mL/100g.재관주2 h검측회장점막상피세포Cas-pase-3,Bcl-2단백적표체급세포조망;동시관찰소장점막병리형태학개변.결과조망세포검측현시:I/R조조망세포현저증다,SF조조망세포수교I/R조현저감소이다우C조(균P＜0.05);Caspase-3,Bcl-2단백적표체:Caspase-3표체I/R조현저다우SF조화C조(P＜0.01),SF조여C조무명현차이;Bcl-2표체SF조현저고우I/R조(P＜0.05),후자현저저우C조(P＜0.05);SF조소장점막병리손상정도명현감경I/R조(P＜0.01).결론삼부주사액통과억제Caspase-3표체화촉진Bcl-2기인표체감소결혈재관주기간장점막상피세포적조망,종이감경장점막결혈재관주손상.
[Objective] To investigate effects of ShenFu injection on apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats. and discuss the mechanisms. [Methods] Ischemia-reperfusion model was established with rats, twenty-four rats were divided randomly into control group (C group), ischemia-reperfusion group(I/R group) and ShenFu injection (SF group). At choiced time rat guts were cut to sections for HE, Tunnel staining and caspase-3, Bcl-2 protein immunohistochemical staining. [Results] In the detection of apoptosis cells the number increased more notably in I/R group, it was decreased more in SF group than I/R group and it had increased more than C group (P ＜0.05). The expression of caspase-3 in I/R group was increased more notably than C group and SF group (P ＜0.01), it hadn't distinct difference between C group and SF group; the expression of Bcl-2in SF group increased more markedly than I/R group (P ＜0.05), the expression in I/R group was less than C group (P＜0.01) . The injury of intestinal mucosal in SF group alleviated more than I/R group. [Conclusions] Shenfu injection can reduce the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of caspase-3 gene and accelerating the expression of Bcl-2 gene, thus to alleviate the injury of intestinal mucosal epithelial cells during ischemia-reperfusion.