幽门螺杆菌诱导蒙古沙鼠胃上皮细胞凋亡可能涉及线粒体途径  

Apoptosis of gastric epithelial cells of Mongolian gerbils induced by Helicobacter pylori involved in the mitochondrial pathway

作　　者：兰春慧 房殿春 邹全明[2] 

机构地区：[1]第三军区大学西南医院全军消化专科中心,重庆400038 [2]第三军医大学微生物及免疫学教研室

出　　处：《中华消化杂志》2006年第6期390-392,共3页Chinese Journal of Digestion

摘　　要：目的建立幽门螺杆菌(Hp)感染蒙古沙鼠模型,探讨线粒体途径在Hp诱导胃上皮细胞凋亡中的作用。方法 48只雄性蒙古沙鼠均分为Hp感染组和对照组,每组分别于1、3和6个月3个时相点各处死8只动物,取胃黏膜行组织学检查:用Warthin-Starry银染、PCR和快速尿素酶法检测 Hp;通过H-E染色,光镜下观察胃黏膜病理变化;流式细胞仪测定细胞凋亡、线粒体膜电位及胞内游离 Ca2+含量。结果 Hp感染蒙古沙鼠后,胃黏膜出现慢性胃炎、肠化生及异型增生改变,而对照组胃黏膜基本正常,Hp感染组肠化生及异型增生发生率明显高于对照组(P<0．05)。Hp感染胃上皮细胞1、3、 6个月后的凋亡率分别为(16．71±3．30)％、(5．90±0．82)％、(5．69±0．70)％,而对照组的凋亡率分别为(4．20±0．94)％、(3．17±0．43)％、(4．70±0．55)％。其中Hp感染1个月后胃上皮细胞的凋亡率高于其他各组(P<0．05)。Hp感染胃上皮细胞1、3、6个月后的线粒体膜电位分别为43．10±17．62、 71．19±38．03、80．56±32．90,而对照组分别为84．70±23．50、84．39±37．51、79．54±30．24,其中Hp 感染1个月后胃上皮细胞的线粒体膜电位低于其他各组(P<0．05);Hp感染1、3、6个月后胃上皮细胞内游离Ca2+含量分别为18．60±9．32、5．18±2．06、4．94±3．25,而对照组分别为4．82±3．70、6．86 ±2．34、5．28±3．13,Hp感染1个月后胃上皮细胞内游离Ca2+含量高于其他各组(P<0．05)。结论 Hp诱导蒙古沙鼠胃上皮细胞凋亡主要发生在Hp感染早期;线粒体膜电位的下降和胞内游离Ca2+含量的升高参与了Hp诱发蒙古沙鼠胃上皮细胞凋亡的过程。Objective To evaluate the role of mitochondrial pathway in the apoptosis of gastric epithelial cells induced by H. pylori in Mongolian gerbils. Methods A total of 48 Mongolian gerbils were randomly divided into H. pylori infection and without H. pylori infection groups. Eight animals from each group were killed at 1, 3 and 6 months, and histopathological changes in their stomachs were examined. A flow cytometry was used to measure apoptosis, mitochondrial membrane potential and intracellular free Ca^2＋ . Results The incidences of intestinal metaplasia and dysplasia in the gastric mucosa with H. pylori infection were significantly higher than those without H. pylori infection （P d0.05）. The apoptosis rates at 1 ,3 and 6 months were （16.71±3.30）%, （5.90--/-_0.82） ~ and （5.69＋_0.70） ~ in the gastric mucosa with H. pylori infection, and （4.20--/-_0.94） %, （ 3.17--/-_0.43 ） % and（4.70±0.55）in the group without H. pylori infection. The apoptositics frequencies and the level of intracellular free Ca^2＋ after infected with H. pylori for one month were significantly higher than those in the other groups （P〈0.05）. On the contrary, the mitochondrial membrane potential after infected with H. pylori for one month was significantly lower than that in the other groups （P〈0.05）. Conclusions H. pylori can induce the apoptosis of gastric epithelial cells via the mitochondrial pathway in Mongolian gerbils.

关 键 词：幽门螺杆菌 凋亡 线粒体 动物模型 

分 类 号：R573[医药卫生—消化系统]