摘要
目的揭示糖尿病胃轻瘫(DGP)发病机制。方法SD大鼠随机分为对照组和模型组,造模10周后,模型检测;流式细胞术测细胞凋亡与Δψm;免疫组化测CytC。结果与对照组相比:(1)模型组造模后均出现多尿、多饮、多食症状,体重减轻;血糖浓度显著增高(P<0.01);胃内色素残留率显著降低(P<0.01)。(2)模型组胃平滑肌细胞凋亡率显著增高(P<0.01),Δψm显著降低(P<0.01),胞质CytC显著增加。结论线粒体介导了糖尿病大鼠胃平滑肌细胞凋亡,后者在糖尿病胃轻瘫发病机制中扮演了一定角色。
Objective To investigate the pathogenesis of gastroparesis in diabetic rats. Methods SD rats were randomly divided into control group and diabetes group. Ten weeks later, gastroparesis model was established. The apoptosis rate and mitochondrial membrane potential of the gastric smooth muscle cells were detected by flow cytometry. Cytochrome C was detected by immunohistochemistry. Results Compared with rats in control group : (1) Typical symptoms of diabetes mellitus appeared; The rate of gastric residual pigment was significantly higher ( P 〈0.01). (2) Apoptosis rate was significantly higher( P 〈 0. 01 ) ; Mitochondrial membrane potential was signifi- cantly lower( P 〈 0. 01 ) ; Cytochrome C was significantly higher ( P 〈 0. 05 ). Conclusion Mitochondrion mediates smooth muscle cell apoptosis,which paly a potential role in diabetic gastroparesis.
出处
《基础医学与临床》
CSCD
北大核心
2009年第10期1083-1086,共4页
Basic and Clinical Medicine
关键词
糖尿病
胃轻瘫
细胞凋亡
线粒体膜电位
细胞色素C
diabetes
gastroparesis
apoptosis
mitochondrial membrane potential
cytochorome C