摘要
为了观察糖尿病胃动力障碍大鼠胃窦平滑肌组织中PDE2和PDE3的蛋白含量变化,由腹腔注射STZ制备糖尿病动物模型,利用多道生理信号记录系统记录糖尿病大鼠胃窦平滑肌收缩活动,将发生胃窦平滑肌收缩活动紊乱的大鼠列入糖尿病胃动力障碍模型,再采用免疫组织化学方法观察糖尿病胃动力障碍组大鼠胃窦平滑肌中PDE2和PDE3的分布。结果发现,糖尿病发病胃动力障碍大鼠与正常对照组相比,胃窦平滑肌组织PDE2表达无明显差异,但PDE3表达明显减少(P<0.05)。因此,糖尿病大鼠发生胃动力障碍可能与胃窦平滑肌中PDE3下调有关,糖尿病大鼠胃c GMP-PDE3的改变可能参与胃动力障碍的发生。
In order to observe the changes of PDE2 and PDE3 in gastric smooth muscle of diabetic gastropare- sis rats, rat model of diabetes mellitus was induced by injected streptozotocin (STZ). To record gastric smooth muscle contraction of diabetes rat with multichannel physiology signal recording system. Diabetes rats with gastric smooth muscle contraction indiscriminate were identified as diabetic gastroparesis model. Then to observe content of PDE2 and PDE3 in diabetic gastroparesis rats gastric smooth muscle by immunohistochemistry. Compared with con- trol group rats, PDE2 content in gastroparesis rat gastric smooth content increased significantly -regulation in gastric smooth ( P 〈 0.05 ). Thus, Gastroparesis muscle was not significantly different, but PDE3 of diabetes rats may be correlated with PDE3 down muscle, and cGMP- PDE3 signal system may be involved in the pathogenesis and development of diabetic gastropathy of gastroparesis.
出处
《辽东学院学报(自然科学版)》
CAS
2016年第4期272-275,共4页
Journal of Eastern Liaoning University:Natural Science Edition
基金
国家自然科学基金项目(81360070)