电针对胰岛素抵抗模型大鼠血管内皮NF-κB通路的影响

Effect of eletroacupuncture on expression of NF-κB in vascular endothelium with insulin resistance rats

目的观察电针对高脂诱导的胰岛素抵抗(IR)模型大鼠血管内皮炎症反应的分子生物学机制。方法将24只雄性SD大鼠随机分配至空白组,模型组及电针组,每组8只。空白组SD大鼠喂以12 w的普通饲料,模型组、电针组SD大鼠喂以12 w的D12492高脂饲料。电针组针刺双侧内关、三阴交、足三里及肾俞,1次/d,20 min/次,持续4 w。模型组及空白组不给予电针处理。治疗结束后,禁食12 h,检测葡萄糖输注率(GIR),眼眶静脉窦采血检测各组大鼠空腹血糖(FPG)、空腹胰岛素(FINS)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6等指标含量,使用Western印迹分析血管内皮中核因子(NF)-κB p65表达水平,并于电镜下观察血管内皮超微结构变化。结果治疗后,与空白组比较,模型组大鼠血清FPG、FINS、TNF-α、IL-6水平显著升高(P<0.01),GIR水平明显降低(P<0.01);与模型组比较,电针组大鼠血清FPG、FINS、TNF-α、IL-6水平显著降低,GIR水平明显升高(P<0.01)。与空白组比较,模型组大鼠血管内皮的NF-κB p65磷酸化水平及蛋白表达显著升高(P<0.01);电针组大鼠血管内皮NF-κB p65磷酸化水平及蛋白表达较模型组显著降低(P<0.01)。电针组中大鼠的内皮细胞与壁间隙稍增宽,部分线粒体形态改变,嵴部局部消失。结论电针可通过改善炎症反应而发挥防治IR的作用,其机制可能与调节NF-κB信号转导通路有关。

Objective To explore the molecular biology mechanism of acupuncture on regulating inflammatory reaction to improve insulin resistance.Methods Twenty-four male Sprague Dawley rats were separated into three groups(n=8):blank control group,HFD group and HFD+EA group,respectively.The HFD and HFD+EA groups were fed with D12492 diet to induce the insulin resistance models.Acupuncture was applied to PC6,ST36,SP6,and BL23,for 20 min/day,lasted for four weeks.After the intervention,glucose infusion rate(GIR)was detected in each group.The fasting blood glucose(FPG),serum insulin(FINS),TNF-αand IL-6 were determined.The protein expression of NF-κB/P65 in vascular endothelium was detected by Western blot.The vascular endothelial ultrastructure was observed under electron microscopy.Results After four weeks treatment,the levels of FPG,FINS,TNF-αand IL-6 in HFD+EA group were significantly decreased but the level of GIR increased compared with HFD group(P<0.01).Compared with HFD group,the protein expressions of p-NF-κB/P65 and NF-κB/P65 in vascular endothelium in HFD+EA group were significantly reduced(P<0.01).It was showed that the gap between endothelium and arterial wall was slightly widened in HFD+EA group,and some changes of mitochondrial morphology appeared such as cristae of mitochondria disappearing.Conclusions EA might mitigate insulin resistance and endothelial dysfunction through modulating inflammatory reaction which is likely to be related with regulating NF-κB signal pathway.