摘要
目的通过STZ诱导糖尿病胃动力障碍大鼠模型制备,观察胃窦平滑肌线粒体锰超氧化物歧化酶(MnSOD)表达,探讨MnSOD在糖尿病胃动力障碍发生过程中的作用。方法 Wistar大鼠随机分为模型(A)组和正常对照(B)组,4周后离体肌条实验确定糖尿病胃动力障碍模型建立,利用RT-PCR和Western blotting法检测胃窦平滑肌线粒体MnSOD的表达。结果 (1)胃窦平滑肌自发性收缩活动频率A组(2.23±0.13)次/min,且收缩节律紊乱,B组(3.10±0.14)次/min;两组胃窦平滑肌收缩振幅比较差异有统计学意义(P<0.01);两组收缩振幅差异无统计学意义(P>0.05)。(2)MnSOD mRNA表达(与β-actin的比值)B组(1.05±0.12)高于A组(0.43±0.13)(P<0.01)。(3)MnSOD蛋白表达(与β-actin的比值)B组(0.54±0.06)高于A组(0.20±0.24)(P<0.01)。结论 STZ诱导4周后大鼠出现胃动力障碍;线粒体MnSOD在糖尿病胃动力障碍发生中起重要作用,可能与呼吸量缺陷至ATP供应不足有关。
Objective To observe the changes in the mitochondrial MnSOD expression of gastric smooth muscles of rats with STZ induced diabetic gastroparesis to study the role of MnSOD in diabetic gastroparesis.Methods The rat model of diabetic gastroparesis was made with STZ.They were randomized into the model group （group A） and normal control group （group B）.After 4 weeks,the gastric smooth muscle in vitro experiment was carried out to confirm the successful modeling of diabetic gastroparesis.The expression of mitochondrial MnSOD was determined with RT-PCR and Western blotting.Results （1）In group A,the rhythm of spontaneous gastric smooth muscle contraction was disordered,and the frequency of spontaneous contraction was （2.23±0.13） times/min.In group B,the frequency of spontaneous contraction was （3.10 ± 0.14） times/min.There was a significant difference between the two groups （P＜0.01）.While there was no significant difference between the two groups in contraction amplitude （P＞0.05）.（2）The MnSOD mRNA expression in group B was （1.05±0.12）,higher than in group A（0.43±0.13） （P＜0.01）.（3）The expression of MnSOD protein in group B was （0.54±0.06）,higher than in group A（0.20 ± 0.24） （P＜0.01）.Conclusion STZ induces diabetic gastroparesis after 4 weeks.Mitochondrial MnSOD plays an important role in the development of diabetic gastroparesis.It may be related to the respiration defect causing the inadequate supply of ATP.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2013年第11期1029-1031,共3页
Chinese Journal of Diabetes
基金
国家自然科学基金项目(81060036)
延边大学校级科研项目(601010049)
