糖尿病大鼠膀胱平滑肌的表型转化

目的检测链脲佐菌素造模后9周的糖尿病SD大鼠膀胱平滑肌收缩型标志物和关键调控基因myocardin的表达水平，了解糖尿病大鼠膀胱平滑肌是否发生表型转化。方法32只体质量200~220 g的8周龄雄性SD大鼠随机平均分为糖尿病（DM）组和非糖尿病（NDM）组，9周后取膀胱组织行HE和Masson三色染色观察膀胱组织病理变化，qRT-PCR、Western blotting分别检测膀胱组织平滑肌肌动蛋白（α-SMA）、平滑肌肌球蛋白重链收缩型平滑肌标志物及myocardin 基因的mRNA和蛋白表达水平。结果DM组大鼠较NDM组明显消瘦（286.25±71.20 g vs 412.71±102.74 g，P=0.001），多饮、多尿，膀胱中胶原纤维组织增多（P<0.001），myocardin、α-SMA、平滑肌肌球蛋白重链的mRNA和蛋白水平均显著下降（P均<0.05）。结论糖尿病大鼠膀胱平滑肌在造模9周时发生表型转化，引起膀胱平滑肌舒缩障碍，可能在糖尿病膀胱病理变化过程中起重要作用。

Phenotypic modulation of bladder smooth muscle in diabetic rats

Objective To investigate whether phenotypic modulation of bladder smooth muscle occurs in diabetic rats. Methods Thirty-two male SD rats were randomly assigned into diabetic group and control group. Diabetic rat models were established by a single intraperitoneal injection of streptozotocin (60 mg/kg). Nine weeks later, the bladder tissues of the rats were examined for structural changes using HE and Masson's trichrome staining , and the expressions of myocardin,α-SMA, and SMMHC in bladder smooth muscles were detected with RT-PCR and Western blotting. Results Compared with the control group, the diabetic rats showed obvious polydipsia and polyuria with significantly increased collagenous fibers and lowered expressions of myocardin,α-SMA, and SMMHC in the bladder tissue (P<0.05). Conclusions In rats at 9 weeks after diabetic model establishment, phenotypic transition of the bladder smooth muscles occurs to cause bladder contractile dysfunction, which may play an important role in the pathology of diabetic bladder dysfunction.