荞麦花叶黄酮对2型糖尿病大鼠肝损伤及IRS-2、PI3K、NF-κB表达的影响

Effects of flavones of buckwheat flower and leaf on IRS-2,PI3K,NF-κB expressions and its protection on liver injury in T2DM rats

目的观察荞麦花叶黄酮(FBFL)对2型糖尿病大鼠肝损伤和IRS-2、PI3K及NF-κB表达的影响,并探讨其可能机制。方法用高脂饲料和链脲佐菌素建立大鼠2型糖尿病模型,以FBFL为干预因素,动态观察随机血糖(PBG)、空腹血糖(FBG)、空腹血胰岛素(FINS)、血ALT、AST,光镜和电镜观察肝脏病理改变,免疫组化和Western blot检测肝IRS-2和PI3K蛋白表达。ELISA法检测肝组织NF-κB含量。结果与正常组比较,模型组大鼠血中PBG、FBG、FINS、HOMA-IR(胰岛素抵抗指数)、ALT、AST均明显升高(P<0.05,P<0.01),肝病理损伤明显,同时IRS-2、PI3K蛋白表达减少,NF-κB含量增加;FBFL治疗组能明显改善上述指标的变化,增加胰岛素敏感性,使肝组织损伤减轻和上调IRS-2、PI3K蛋白表达及减少NF-κB含量,且FBFL高剂量作用更明显。结论 FBFL对糖尿病肝损伤有抑制作用,其机制可能是通过降低血糖、改善胰岛素抵抗,上调IRS-2、PI3K蛋白表达及下调NF-κB蛋白表达等多途径实现的。

Aim To study the effects of flavones of buckwheat flower and leaf （FBFL）on IRS-2/PI3K, NF-κB expression and liver injury in T2DM rats, and to explore its mechanism. Methods The T2DM rats model was induced by feeding high-fat diet and intraperitoneal injection with streptozotocin. In this experiment, FBFI, was as intervention factor. The postprandial （PBG） and fasting blood glucose （FBG）, the fast serum insulin （FINS）, serum ALT and serum AST were observed. The changes of the liver tissue were observed by optical microscope and electron microscope. Immunohistochemistry and Western blot techniques were used to measure IRS-2 and PI3K expression. ELISA assay was applied to measure NF-κB. Results Compared with normal control group, the levels of PBG, FBG, FINS, ALT, AST and HOMA-IR （ insulin resistance index） in model group were significantly increased （ P 〈 0. 05, P 〈 0. 01 ）. While liver pathological damage was obvious, IRS-2 and PI3K expression decreased. NF-κB expression increased. FBFL could significantly improve the above-mentioned changes, increase insulin sensitivity, protect the damage of liver tissue,upregulate IRS-2, PI3K expression, and down- regulate NF-κB protein expression. And the effect of FBFL high-dose was more obvious. Conclusions FB- FL can inhibit the liver injury in type 2 diabetic rats. The mechanism is related to reducing PBG, improving insulin resistance,upregulating IRS-2 and PI3K expression and downregulating protein NF-κB.