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目的本研究旨在探讨诱生性一氧化氮合酶(iNOS)抑制剂氨基胍(Aminoguanidine,AG)对I型糖尿病(IDDM)大鼠胰岛β细胞损伤修复的作用。方法以链脲佐菌素腹腔注射大鼠建立IDDM模型,并用AG进行干预,采用免疫组织化学方法,分别检测正常组、糖尿病组和AG治疗组大鼠胰岛中iNOS含量和胰岛b细胞面密度。结果AG组胰岛β细胞面密度为70.58±3.26,与IDDM组(21.65±1.45)比较,具有显著差异(P<0.05),且IDDM组大鼠胰岛中β细胞面密度随iNOS增多而减少,两者呈负相关(r=-0.8175,P<0.01),iNOS阳性反应产物呈弥漫性分布,其色深于正常对照组;AG组胰岛中的iNOS反应物较IDDM组明显减弱(P<0.05),但与正常组比较无显著差异(P>0.05)。结论iNOS增多可能是造成IDDM胰岛β细胞损伤的因素之一,AG对IDDM胰岛β细胞的损伤具有修复作用。
Objective This study was designed to investigate the effect of iminositride (iNOS) inhibitor aminoguanidine (Aminoguanidine) on the repair of islet β cell injury in type 1 diabetic rats. Methods IDDM model was established by intraperitoneal injection of streptozotocin (STZ) and intervention with AG. Immunohistochemistry was used to detect iNOS content and islet b cell surface density of islets in normal group, diabetic group and AG-treated group. Results The density of islet β cells in AG group was 70.58 ± 3.26, which was significantly lower than that in IDDM group (21.65 ± 1.45) (P <0.05). The islet density of islet cells in IDDM group decreased with the increase of iNOS. (R = -0.8175, P <0.01). The positive reaction product of iNOS was diffusely distributed, and its color was darker than that of the normal control group. The iNOS response in islet of AG group was significantly weaker than that of IDDM group (P <0.05) , But no significant difference compared with the normal group (P> 0.05). Conclusions Increased iNOS may be one of the factors contributing to the injury of IDDM islet β cells. AG may repair the damage of IDDM islet β cells.