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目的 探讨Bc1 2、Bc1 x1和Bax蛋白在人参皂甙Rgl抗帕金森病 (PD)小鼠模型黑质神经元凋亡过程中的可能作用。 方法 PD模型组单纯以 1 甲基 4 苯基 1,2 ,3,6 四氢吡啶 (MPTP)腹腔注射C5 7BL小鼠 ;预防组预先 3d腹腔注射Rg1(2 5、5 0、10 0mg kg) ,再注射MPTP ,以Niss1染色、TH组织化学染色、TUNEL染色观察黑质神经元的变化 ;免疫组织化学染色检测Bc1 2、Bc1 x1和Bax蛋白表达。 结果 5 0和 10 0mg kgRg1预处理PD模型鼠能使黑质致密带 (SNc)部位的Niss1和TH染色阳性神经元增多 ,TUNEL染色阳性率降低 ,以及Bc1 2和Bc1 x1表达增加 ,Bax表达减少。 结论 Rg1预处理对PD模型鼠黑质神经元凋元有明显的保护作用 ;Bc1 2和Bc1 x1表达水平升高和Bax表达水平降低可能是Rg1抗凋亡的重要机制
Objective To investigate the possible role of Bc1 2, BclX1 and Bax proteins in the apoptosis of substantia nigra neurons in mouse model of Parkinson’s disease (PD) induced by ginsenoside Rgl. Methods PD mice were injected intraperitoneally with 1 methyl-4-phenyl-1,2,6,6-tetrahydropyridine (MPTP) in C5 7BL mice. Preadjusted groups were given intraperitoneal injection of Rg1 (25,500, 10,0 mg kg) , And then injected MPTP. Nissl staining, TH histochemical staining and TUNEL staining were used to observe the changes of substantia nigra neurons. The expressions of Bc1 2, Bc1 x1 and Bax protein were detected by immunohistochemical staining. Results Pretreatment with 50 and 100 mg kgRg1 of PD rats increased Nissl and TH-stained neurons in the substantia nigra at SNc, decreased the positive rate of TUNEL staining, increased expression of Bc1 2 and Bc1 x1, and decreased expression of Bax . Conclusion Rg1 preconditioning can significantly protect the neurons of substantia nigra in PD model mice. The increased expression of Bc1 2, Bc1 x1 and the decrease of Bax expression may be important mechanisms of anti-apoptosis of Rg1