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目的:研究NF-κB在脂多糖(LPS)诱导的帕金森病(PD)模型大鼠中的作用。方法:52只SD大鼠按体重随机分为3组,实验组(LPS组)、预防组(PDTC+LPS组)和对照组,每组14只:(1)实验组SD大鼠按体重50mg/kg经腹腔注射生理盐水后经脑立体定位单侧黑质注射LPS4μl/只(4μg/只)后7d制成帕金森病模型;(2)预防组SD大鼠按体重50mg/kg经腹腔注射PDTC1h后再经脑立体定位单侧黑质注射LPS4μl/只(4μg/只);(3)对照组SD大鼠按体重50mg/kg经腹腔注射生理盐水后经脑立体定位单侧黑质注射生理盐水4μl/只。7d后观察三组大鼠皮下注射阿扑吗啡后的行为学变化,采用免疫荧光法检测注射7d后黑质部NF-κBp65的表达,并用western blotting检测其蛋白表达。结果:7d后,实验组大鼠有明显的行为学变化,预防组和对照组则无异常行为学表现。免疫荧光结果显示,与注射对侧相比,实验组大鼠经脑立体定位注射内毒素LPS后,注射侧黑质部TH表达显著减少,而NF-κBp65阳性表达则显著增加,western blotting得到同样结果(P<0.05);预防组和对照组大鼠黑质部TH和NF-κBp65阳性表达无显著性变化,western blotting得到同样结果(P>0.05)。结论:NF-κB参与了LPS PD大鼠发病过程,黑质中NF-κBp65过度激活是LPS对大鼠造成损害作用的机制之一。预先使用PDTC对LPS PD鼠起到一定神经保护作用。
Objective: To investigate the role of NF-κB in lipopolysaccharide (LPS) -induced Parkinson’s disease (PD) model in rats. Methods: Fifty-two SD rats were randomly divided into three groups according to body weight: experimental group (LPS group), prophylaxis group (PDTC + LPS group) and control group, with 14 rats in each group. (1) / kg after intraperitoneal injection of normal saline, stereotactic unilateral substantia nigra injection of LPS 4μl / only (4μg / only) made 7d after Parkinson’s disease model; (2) prevention group SD rats by body weight 50mg / kg by intraperitoneal injection PDTC1h and then stereotactic stereotactic unilateral substantia nigra injection of LPS4μl / only (4μg / only); (3) control group SD rats by body weight 50mg / kg by intraperitoneal injection of normal saline stereotactic unilateral substantia nigra injection of physiology Saline 4μl / only. Seven days later, the behavioral changes of three groups of rats were observed after subcutaneous injection of apomorphine. The expression of NF-κBp65 in substantia nigra was detected by immunofluorescence method 7 d after injection, and the protein expression was detected by western blotting. Results: After 7 days, the experimental rats had obvious behavioral changes, while the preventive and control groups showed no abnormal behavior. Immunofluorescence results showed that, compared with contralateral contralateral injection, the expression of TH in substantia nigra at injection side was significantly decreased and the positive expression of NF-κBp65 was significantly increased in experimental group after endotoxin LPS injection (P <0.05). There was no significant change in the expression of TH and NF-κBp65 in the substantia nigra in the prevention group and the control group, and the same result was obtained by western blotting (P> 0.05). CONCLUSION: NF-κB is involved in the pathogenesis of LPS PD. Overexpression of NF-κBp65 in substantia nigra is one of the mechanisms of LPS injury in rats. Pre-use PDTC on LPS PD rats play a neuroprotective effect.