摘要
目的:探究龟羚帕安丸对帕金森病大鼠模型氧化应激反应的影响。方法:用6-羟基多巴胺(6-OHDA)建立帕金森病(PD)大鼠模型,随机分为模型组,美多巴组,龟羚帕安丸大剂量组、中剂量组、小剂量组。分别每日管饲同体积的生理盐水,美多巴10 mg·(kg·d)-1,龟羚帕安丸4.0 g·(kg·d)-1、2.0 g·(kg·d)-1、1.0 g·(kg·d)-1。另设假手术组,常规饲养,每日管饲同体积的生理盐水。每日1次,共30 d。观察血浆中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)实验后的变化。结果:与假手术组比较,模型组SOD的活性、GSH含量明显减少,MDA含量明显增多,差异具有统计学意义(P<0.05);与模型组比较,药物组SOD的活性、GSH含量明显增多,MDA含量明显减少,两组之间的差异具有统计学意义(P<0.05);龟羚帕安丸大剂量组SOD值显著高于美多巴组(P<0.05),龟羚帕安丸大剂量组GSH、MDA与美多巴组比较,差异无统计学意义(P>0.05)。结论:龟羚帕安丸可增加帕金森大鼠模型血浆中增加SOD的活性和GSH的含量,减少MDA的含量,减轻氧化应激对神经细胞的损伤,可能是其治疗帕金森病的作用机制之一。
Objective : To explore the effect of Gui Ling Pa An Wan on oxidation stress response of Parkinson disease rats. Methods : PD model rats were produced by injection of 6-OHDA. Parkinson disease rats were randomly divided into five groups : Madopar group, high- dose Gui Ling Pa An Wan group, middle-dose Gui Ling Pa An Wan group,low-dose Gui Ling Pa An Wan group. Each group was respectively intragastric administration of normal saline of the same volume, Madopar 10 mg·(kg·d)-1 , Gui Ling Pa An Wan 4.0 g·(kg·d)-1 ,GuiLing Pa An Wan 2.0 gg·(kg·d)-1 ,Gui Ling Pa An Wan 1.0 g·(kg·d)-1 for 30 days. Then observed the levels of superoxidase dismutase ( SOD), malonaldehyde ( MDA), glutathione (GSH) in plasma of the rats after experiment. Results: Compared with Sham operation group,SOD activity and GSH contents in the model group were obviously reduced and MDA contents were obviously increased in the model group, the differences were statistically significant ( P 〈 0.05 ). Compared with model group, SOD activity and GSH contents in the drug group were obviously increased and MDA contents were obviously reduced in the drug group, and the differences had statistical significance (P 〈 0.05 ). SOD activity in high-dose Chinese medicine were obviously higher than that of Madopar ( P 〈 0.05 ), and GSH and MDA contents didn't change significantly ( P 〉 0.05 ). Conclusion : SOD activity and GSH contents were increased and MDA contents were reduced in plasma of the PD rats with treated by Gui Ling Pa An Wan. Gui Ling Pa An Wan could reduce the injury of nerve cell by oxidation stress response, and it maybe one of the mechanisms of anti-Parkinson disease.
出处
《中医学报》
CAS
2014年第2期230-232,共3页
Acta Chinese Medicine
基金
河南省教育厅自然科学研究项目(编号:2010A360017)