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目的:探讨中性调宁蛋白(calponin h2,CN2)在糖尿病肾损害过程中的作用。方法:分别给予中性调宁蛋白转基因(CN2-Tg)小鼠与野生性(WT)C57BL/6J小鼠腹腔注射链脲佐菌素(STZ)制备糖尿病模型,观察两组糖尿病小鼠在注射STZ前及后第8、30天的体重、血糖、血压、尿白蛋白、尿肌酐(Cr)、尿8羟基脱氧鸟苷(8-OHdG)变化及肾组织α-SMA、Ki-67、F4/80免疫组化染色评价肾间质炎症改善情况。结果:CN2-Tg组尿8-OHdG/Cr(ng/mg)明显低于WT组(P<0.05);在第8天CN2-Tg组肾间质细胞纤维化(Ki-67染色)受到明显抑制(P<0.05),第30天不明显(P>0.05);CN2-Tg组肾间质巨噬细胞浸润表现(F4/80染色)在第8(P<0.05)、30天(P<0.01)均受到明显抑制;两组间肾组织α-SMA表达和血压变化无区别。结论:CN2过表达能抑制糖尿病早期肾间质细胞增殖和巨噬细胞浸润,表明CN2可能在糖尿病肾病间质损害的过程中扮演着重要的角色,推断其可能成为治疗糖尿病肾病的新靶点。
Objective: To investigate the role of calponin h2 (CN2) in the process of diabetic nephropathy. Methods: Diabetic mice were induced by intraperitoneal injection of streptozotocin (STZ) in neutralizing protein transgenic (CN2-Tg) and wild (WT) C57BL / 6J mice, respectively. The changes of body weight, blood glucose, blood pressure, urinary albumin, urinary creatinine (8-OHdG) and urinary 8-OHdG in the 8th and 30th day before and after STZ and the changes of α-SMA, Ki- / 80 immunohistochemical evaluation of interstitial inflammation to improve the situation. Results: Urinary 8-OHdG / Cr (ng / mg) in CN2-Tg group was significantly lower than that in WT group (P <0.05). On day 8, renal interstitial fibrosis (Ki-67 staining) (P <0.05), but not obvious on the 30th day (P> 0.05). The infiltration of interstitial macrophages (F4 / 80) 0.01) were significantly inhibited; between the two groups α-SMA expression and blood pressure changes without distinction. CONCLUSION: Overexpression of CN2 can inhibit early renal interstitial cell proliferation and macrophage infiltration in diabetic patients, indicating that CN2 may play an important role in the process of interstitial damage of diabetic nephropathy, suggesting that CN2 may be a new target for the treatment of diabetic nephropathy.