摘要
目的探讨PPARγ配体罗格列酮对STZ诱导的1型糖尿病大鼠胰腺β细胞的保护作用及其机制。方法实验用STZ诱导1型糖尿病大鼠动物模型,以罗格列酮5mg.kg-1.d-1连续给药30d。记录体质量和禁食血糖的变化。治疗第31天(停药后第1天)及治疗第61天取材观察胰腺形态学变化,应用免疫组织化学染色显示胰岛β细胞和nNOS的表达情况。结果与未治疗糖尿病动物相比,罗格列酮治疗组大鼠的糖尿病体征显著减轻,胰腺未见明显的病理改变,胰岛内胰岛素阳性细胞数量增多、接近正常水平,与此同时,胰腺内一氧化氮合酶(inducible nitric oxide synthase,iNOS)活性降低,而nNOS表达增强。结论罗格列酮对STZ诱导的1型糖尿病大鼠胰岛有一定的保护作用,其机制可能是通过抑制巨噬细胞内iNOS的活性,减轻胰岛的炎症反应,避免β细胞损害,促进胰岛功能的恢复。
Objective To investigate the protective effects and mechanism of rosiglitazone on streptozotocin （STZ） -induced diabetic rats. Methods The healthy Wistar rats were fasted for 12 h, then injected peritoneally 60 mg/kg STZ solution to establish type 1 diabetic models and randomly assigned to receive 5 mg/kg rosiglitazone for treatment or not once a day for 30 d （ n = 10 in each group）. Another five normal Wistar rats were injected with citrate buffer solution as normal controls. Plasma glucose concentration and weight of the rats were measured and recorded every three days. Rats were sacrificed on day 31 and 61 after the treatment began respectively. HE immunohistochemical staining were performed to observe the beta cells of pancreatic islet and the expression of nNOS. Results As compared with the untreated group, the diabetic symptoms of the treated rats relieved significantly, and no obvious pathologic changes were observed in pancreatic islets. The amount of beta ceils of pancreatic islet increased obviously, and the expression of nNOS was much stronger on day 61. Conclusion Rosiglitazone might play a protective role on the islets of STZ-induced diabetic rats and be helpful for the recovery of pancreatic function by inhibiting the activity of iNOS in macrophages at early phase, promoting the expression of nNOS at the late phase, reducing the inflammation of the pancreatic islets and preventing the pancreatic beta cell from being impaired.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2005年第21期2131-2134,共4页
Journal of Third Military Medical University
基金
第三军医大学科研基金资助项目(2003)~~
