摘要
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。
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 ct - 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 immunohis- tochemisty. Results By image analysis, the expression level of Bcl -2 protein was higher and pP38MAPK, Bax and Caspase -3 pro- tein 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.
出处
《宁夏医学杂志》
CAS
2012年第9期857-859,I0001,共4页
Ningxia Medical Journal
基金
宁夏自然科学基金资助项目(NZ09141)
