丹参酮ⅡA对帕金森病大鼠黑质内磷酸化c-Jun氨基末端激酶表达的影响  

Effects of tanshinone ⅡA on the expression of phosphorylated JNK in the substantia nigra in rats with Parkinson’s disease

作　　者：徐玉英[1] 彭普基 游言文[1] 任秀花[3] 

机构地区：[1]河南中医学院人体解剖学与组织学胚胎学教研室,郑州450008 [2]郑州大学第一附属医院消化内科,郑州450052 [3]郑州大学人体解剖学教研室,郑州450001

出　　处：《解剖学杂志》2016年第4期448-451,共4页Chinese Journal of Anatomy

基　　金：河南中医学院博士科研基金(BSJJ2012-10)

摘　　要：摘要目的：研究丹参酮ⅡA对帕金森病（PD）模型大鼠中脑黑质内酪氨酸羟化酶（TH）、p-JNK和caspase-3表达的影响，探讨丹参酮ⅡA（TSA）对帕金森病模型大鼠的作用及机制。方法：SD雄性大鼠随机分为正常对照组、假手术组（sham组）和模型组。模型组又分为生理盐水组（NS组）和处理组（TSA组）。模型组大鼠采用颈背部皮下注射鱼藤酮制备PD模型；假手术组，在与模型组大鼠相同部位注射等量的不含鱼藤酮的葵花油乳化液；正常组不作处理。模型组在大鼠腹腔内注射生理盐水1m1和丹参酮ⅡA20mg／kg，连续注射14d。免疫组织化学检测正常对照组、NS组和TSA组大鼠中脑黑质内TH、p-JNK和caspase-3的表达。结果：与正常对照组及假手术组比较，模型组大鼠出现典型的PD样症状；与正常对照组比较，生理盐水组大鼠中脑黑质内TH的表达降低，矿JNK和caspase-3的表达增多；与生理盐水组比较，处理组大鼠中脑黑质内TH的表达增多，p-JNK和caspase-3的表达降低，差异均有统计学意义。结论：丹参酮ⅡA可在一定程度减轻PD模型大鼠多巴胺能神经元的损伤，其作用机制可能与JNK信号转导途径有关。Objective： To observe effects of tanshinone ⅡA on the expression of tyrosine hydroxylase （TH）, phosphorylated JNK and caspase-3 in the substantia nigra in rats with Parkinson＇s disease （PD）, and to explore the role of tanshinone ⅡA and its mechanism in PD rats. Methods： SD male rats were randomly divided into control group, sham group and PD model group. PD model group was randomly and evenly divided into two groups： saline group（NS group） and treatment group（TSA group）. The PD model group was established by subcutaneous injection of rotenone in the neck and back, while the injection of sunflower oil emulsion without rotenone at the same point and quantity as the PD model group was applied in the sham group;the control group was not given any intervention. Normal saline （1 ml） and tanshinone ⅡA （20 mg/kg） were given through intraperitoneal injection respectively for 14 days in PD model group. Expression of TH, phosphorylated JNK and caspase-3 was measured with immunohistochemical staining. Results： Compared with the control group and sham group, there was typical PD symtoms in PD model group; compared with the control group, the expression of TH decreased, while the expression of phosphorylated JNK and caspase-3 increased significantly in the substantia nigra in the saline group. Compared with the saline group, the expression of TH increased, while the expression of phosphorylated JNK and caspase-3 decreased significantly in the substantia nigra in TSA group. Conclusion ： Tanshinone ⅡA can mitigate the loss of dopaminergic neurons in the PD model rats induced by rotenone, which may be related with JNK signaling pathway.

关 键 词：帕金森病 丹参酮ⅡA 鱼藤酮 黑质 磷酸化c-Jun氨基末端激酶 大鼠 

分 类 号：R742.5[医药卫生—神经病学与精神病学]