论文部分内容阅读
目的探讨格列喹酮干预治疗对糖尿病肾脏病变中肾小球病理改变的影响以及对核因子-κB(NF-κB)、环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)表达的影响。方法将8月龄雄性Wistar大鼠24只分为正常对照(NC)组、糖尿病(DM)组和格列喹酮干预(GI)组,每组8只。NC组予普通饮食喂养,糖尿病大鼠采用高糖高脂饮食及腹腔注射STZ制备。GI组在成模后予格列喹酮喂养干预。喂养2月后处死,留取各组肾脏标本,观察肾脏病理改变。采用分子生物学方法检测肾脏组织NF-κB、COX-2和iNOS表达情况。结果与NC组相比,DM、GI组肾脏均有不同程度受损表现,其中,DM组病理改变最明显。与NC组相比,DM、GI组肾脏组织NF-κB、COX-2和iNOS表达均增加,GI组表达低于DM组(P<0.05)。结论 NF-κB激活及其启动的下游炎症因子在DN发生发展过程中可能起重要作用,格列喹酮干预治疗可抑制NF-κB激活及相应炎症因子表达,间接起到肾脏保护作用。
Objective To investigate the effects of gliquidone on the pathological changes of glomeruli in diabetic nephropathy and the effects on the expression of nuclear factor-κB, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (INOS) expression. Methods Twenty-four male Wistar rats aged 8 months were divided into normal control (NC) group, diabetes mellitus group (DM) and gliquidone intervention group (GI). NC group fed normal diet, diabetic rats using high-sugar and high-fat diet and intraperitoneal injection of STZ preparation. The GI group was given gliquidone intervention after the model was established. Feeding after sacrifice in February, each group of kidney specimens were taken to observe the pathological changes of the kidney. The molecular biology method was used to detect the expression of NF-κB, COX-2 and iNOS in kidney. Results Compared with NC group, the kidneys in DM group and GI group were impaired to varying degrees. Among them, the pathological changes in DM group were the most obvious. Compared with NC group, the expression of NF-κB, COX-2 and iNOS were increased in DM and GI groups, while the expression of COX-2 and iNOS in GI group was lower than that in DM group (P <0.05). Conclusion NF-κB activation and downstream inflammatory cytokines may play an important role in the development and progression of DN. Gliquidone intervention may inhibit the activation of NF-κB and the expression of inflammatory cytokines and indirectly play a protective role in the kidney.