CAJ | 학술논문

目的观察抑制Ppif基因的表达对缺血再灌注损伤肾脏的保护作用,并探讨其作用机制.方法建立大鼠肾缺血再灌注模型,将实验动物随机分为3组:空白对照组、阴性对照组、治疗组(各20只).治疗组大鼠给Ppif基因靶向RNA干扰(RNAi)慢病毒载体(4μg)0.3 ml,阴性对照组再灌注时给予0.3 ml含体积分数0.01二甲基亚砜(DMSO)的生理盐水,空白对照组不夹闭肾蒂,余处理同阴性对照组.分别检测各组血肌酐(Cr)含量、尿素氮(BUN)含量、细胞凋亡指数(AI)、苏木素-伊红(HE)染色组织病理学分析.结果治疗组与阴性对照组比较,血Cr和BUN均明显降低,AI明显下降,差异均有统计学意义(P＜0.05),HE染色组织病理学分析结果显示治疗组较另外2组缺血明显减轻.结论 Ppif基因靶向RNAi慢病毒载体能抑制大鼠Ppif基因的表达,从而抑制线粒体的凋亡,减轻肾脏缺血再灌注损伤.
목적 관찰억제Ppif기인적표체대결혈재관주손상신장적보호작용,병탐토기작용궤제.방법 건립대서신결혈재관주모형,장실험동물수궤분위3조:공백대조조、음성대조조、치료조(각20지).치료조대서급Ppif기인파향RNA간우(RNAi)만병독재체(4μg)0.3 ml,음성대조조재관주시급여0.3 ml함체적분수0.01이갑기아풍(DMSO)적생리염수,공백대조조불협폐신체,여처리동음성대조조.분별검측각조혈기항(Cr)함량、뇨소담(BUN)함량、세포조망지수(AI)、소목소-이홍(HE)염색조직병이학분석.결과 치료조여음성대조조비교,혈Cr화BUN균명현강저,AI명현하강,차이균유통계학의의(P＜0.05),HE염색조직병이학분석결과현시치료조교령외2조결혈명현감경.결론 Ppif기인파향RNAi만병독재체능억제대서Ppif기인적표체,종이억제선립체적조망,감경신장결혈재관주손상.
Objective To study the protective effect of Ppif gene inhibitor on renal ischemiareperfusion injury and the action mechansim. Methods A renal ischemia-reperfusion model was made in 60 rats, and the rats were evenly divided into three groups: control group (CON group), negative control group (NC group), and Ppif gene inhibitor group (treated group). The blood urea nitrogen (BUN) and creatinine (Cr), and renal cell apoptosis index (AI) were measured. Histopathological analysis was performed by using HE staining. Results A comparison between treated group and NC group showed that for treated group, the levels of both Cr and BUN were decreased, and AI decreased in the treated group as compared with the NC group (P ＜ 0. 05 ). Histolopathological analysis revealed that the ischemia in the treated group was significantly alleviated as compared with other two groups. Conclusion Ppif gene-targeted RNA interference ( RNAi ) lentiviral vector could inhibit the expression of Ppif gene in rats, thereby inhibiting the mitochondrial apoptosis and alleviating renal ischemia-reperfusion injury.