摘要
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(cytc)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,平均体重明显低下对照组(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。
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:(Din 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).(2) Compared 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.
引文
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