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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 investigate the effect of MnSOD on the development of gastric motility disorders in diabetic rats by observing the expression of manganese superoxide dismutase (MnSOD) in gastric smooth muscle of rats with STZ-induced gastric motility disorders. Methods Wistar rats were randomly divided into model group (A) and normal control group (B). After 4 weeks, the model of gastric motility disorders was established in vitro. RT-PCR and Western blotting were used to detect the mitochondrial MnSOD expression. Results (1) The frequency of spontaneous contractions of gastric smooth muscle in group A was (2.23 ± 0.13) times / min, and the systolic rhythm disorder was in group B (3.10 ± 0.14) / min. (P <0.01). There was no significant difference in contractile amplitude between the two groups (P> 0.05). (2) The MnSOD mRNA expression (ratio to β-actin) in group B (1.05 ± 0.12) was higher than that in group A (0.43 ± 0.13) (P <0.01). (3) The MnSOD protein expression (ratio of β-actin) in group B (0.54 ± 0.06) was higher than that in group A (0.20 ± 0.24) (P <0.01). Conclusion STZ induced gastric motility disorder in rats after 4 weeks of induction. Mitochondrial MnSOD plays an important role in the pathogenesis of diabetic gastric motility disorders, which may be related to the shortage of respiration to ATP supply.