ABSTRACT
Objective To study the role of gastric mitochondrial DNA cytochrome C oxidases (COX) subunit Ⅱ gene and its expression in diabetic gastric motility dysfunction. Methods Seventy Wister rats were randomly divided into 2 groups: diabetic group (STZ 60mg/Kg intraperitonealy) and control group. The changes in expressions of COX protein were assayed by Westernblot. Mitochondrial DNA COX mRNA was assayed with reverse-transcriptional polymerase chain reaction(RT-PCR). Cytochrome C oxidase activity was determined by ultraviolet spectrophotometer. Results Gastricelectric dysrythmia was more frequently delected in diabetic rats, and the COX activity in diabetic rats was 0.41?0.21/min, which was significantly lower than that in normal rats (0.78?0.37/min). The expression of gastrointestinal COX protein and COX gene in diabetic gastroparesis rats were markedly decreased compared with normal rats. Conclusion Cytochrome C oxidases activity was greatly reduced in diabetic rats. Diabetic gastroparesis was associated with down-regulation of the expression of gastrointestinal mtDNA encoding COX gene and protein. These changes might play a key role in pathogenesis of diabetic gastroparesis
ABSTRACT
Objective To study the expression and effect of hepatocyte mitochondrial DNA cytochrome c oxidase subunitsⅠ (COXⅠ) gene in rat nonalcoholic fatty liver model. Methods Forty Wistar rats were randomly divided into control group and high-fat diet group, and the high-fat diet group was subsequently divided into 4 subgroups (2, 4, 8 and 12 week) with 8 rats in each. Cytochrome c oxidase activity was determined by ultraviolet spectrophotometer. Meanwhile,the expression of hepatocyte COXⅠ antigen in rat nonalcoholic steatosis model induced by high fat diet were detected by Western blotting. Mitochondrial DNA COXⅠ mRNA were assayed by reversetranscription polymerase chain reaction(RT-PCR). Results The levels of activity in nonalcoholic steatosis rats induced by high fat diet at 2, 4, 8, and 12 weeks were (0.88?0.32), (0.76?0.37), (0.48?0.26), (0.39?0.21) nmol?mg~ -1 ?min~ -1 , respectively, significantly lower than (0.98?0.37) nmol?mg~ -1 ?min~ -1 in control group (P