CAJ | 학술논문

目的：探讨糖尿病胃病的相关机制及大黄素干预。方法：SD大鼠随机分为对照组（正常组）、实验组（糖尿病组）与大黄素组，实验组应用腹腔一次性注射链脲佐菌素（streptozotocin，STZ)建立糖尿病大鼠模型，造模成功10周后免疫组织化学检测胃黏膜腺细胞细胞色素C（cyt c）的表达情况。结果：①实验组和大黄素组大鼠于造模后均出现多尿、多饮、多食症状，体重减轻，平均体重明显低于对照组（P＜0.05)；平均血糖浓度显著高于对照组（P＜0.05)等糖尿病症状。但应用大黄素干预组大鼠的血糖浓度显著低于实验组。②实验组cyt c蛋白阳性表达的胃黏膜细胞数明显高于对照组（P＜0.05）；大黄素组cyt c蛋白阳性表达的胃黏膜细胞数明显少于实验组（P＜0.05）。结论：糖尿病引起大鼠胃黏膜细胞高表达cyt c蛋白，导致细胞死亡增加，参与糖尿病胃病的发生，而大黄素可降低胃黏膜细胞cyt c蛋白表达，从而缓解糖尿病胃病。
목적：탐토당뇨병위병적상관궤제급대황소간예。방법：SD대서수궤분위대조조（정상조）、실험조（당뇨병조）여대황소조，실험조응용복강일차성주사련뇨좌균소（streptozotocin，STZ)건립당뇨병대서모형，조모성공10주후면역조직화학검측위점막선세포세포색소C（cyt c）적표체정황。결과：①실험조화대황소조대서우조모후균출현다뇨、다음、다식증상，체중감경，평균체중명현저우대조조（P＜0.05)；평균혈당농도현저고우대조조（P＜0.05)등당뇨병증상。단응용대황소간예조대서적혈당농도현저저우실험조。②실험조cyt c단백양성표체적위점막세포수명현고우대조조（P＜0.05）；대황소조cyt c단백양성표체적위점막세포수명현소우실험조（P＜0.05）。결론：당뇨병인기대서위점막세포고표체cyt c단백，도치세포사망증가，삼여당뇨병위병적발생，이대황소가강저위점막세포cyt c단백표체，종이완해당뇨병위병。
Objective:To investigate the pathegenetic mechanism and effect of emodin on gastric disturbance of diabetic rats. Methods:SD rats were randomly divided into control group, diabetic group and emodin group. Ten weeks later, expression of cytochrome C in gastric mucosa was detected by immunohistochemistry. Results: ①In diabetic group and emodin group, typical symptoms of diabetes appeared, the average weight was significantly lower (P<0.05), and the blood glucose was significantly higher than those in control group (P<0.05).②Compared with rats in control group, the cytochrome C in diabetic group was significantly higher (P<0.05). Compared with diabetic group, the cytochrome C in emodin group was significantly lower (P<0.05). Conclusion:Diabetes causes high expression of cytochrome C in gastric mucosal cells, which induces cell death and gastric disturbance of diabetic rats. Emodin may decrease cytochrome C in gastric mucosa and therefore,alleviate the gastric disturbance of betic rats.