枸杞多糖对P38MAPK介导2型糖尿病大鼠背根神经节细胞凋亡的保护作用

目的探讨枸杞多糖对氧化应激激活P38MAPK信号转导通路诱导2型糖尿病大鼠背根神经元细胞凋亡的保护作用及其机制。方法取SD大鼠高脂高糖喂养8周后,腹腔小剂量注射STZ(35 mg/kg)诱导2型糖尿病大鼠模型后,分为模型组、枸杞多糖小剂量组、大剂量组及α-硫辛酸对照组,治疗10周后通过免疫组化方法检测大鼠背根神经节中pP38MAPK及其诱导的凋亡指标Bcl-2、Bax和Caspase-3蛋白的表达。结果经图像分析处理,枸杞多糖大剂量组对糖尿病大鼠背根神经节中Bcl-2蛋白的表达有上调作用,对pP38MAPK、Bax和Caspase-3蛋白的表达有抑制作用,其平均光密度值与模型对照组比较差异有统计学意义(P<0.05)。结论枸杞多糖可调节机体内的氧化应激状态,通过抑制P38MAPK途径,上调背根神经元细胞中Bcl-2表达,抑制Bax及Caspase-3的表达,从而保护神经细胞免受氧化应激损伤导致的凋亡,这可能是其保护DPN的作用机制之一。

Protective effects of lycium barbarum polysaccharides on P38MAPK induced apoptosis of dorsal root ganglion in type 2 diabetic rats

Objective To explore the protective effects of Lycium Barbarum Polysaccharides on oxidative stress activated P38MAPK to induce apoptosis of dorsal root ganglion(DRG) in type 2 diabetic rats and its mechanism.Methods SD rats fed with high-sucrose-high-fat diet for 8 weeks,and peritoneally injected with a low dose of STZ(35mg/kg) to induce hyperglycemia.The diabetic rats were randomly divided into the model group,low and high doses of LBP groups and α-Lipoic acid group.The course of treatment lasted for 10 weeks,the expression of pP38MAPK,Bcl-2,Bax and Caspase-3 protein were detected in DRG by immunohistochemisty.Results By image analysis,the expression level of Bcl-2 protein was higher and pP38MAPK,Bax and Caspase-3 protein was lower in high doses of LBP group.Its average level of light density was significantly different compared with model group(P<0.05).Conclusion LBP may up-regulate the expression of Bcl-2,inhibiting expression of Bax,pP38MAPK and Caspase-3 by controlling P38MAPK,and decreases apoptosis may be through adjusting the oxidative stress state of organism.This may be one of the function mechanisms of protective effects of LBP on diabetic peripheral neuropathy.