摘要
目的观察神经节苷脂GM1对帕金森模型小鼠黑质细胞凋亡及Bcl-2和Bax表达的影响,探讨其预防帕金森病的机制。方法成年C57-BL雄性小鼠分为正常对照组、模型组和神经节苷脂GMI治疗组。应用TUNEL法和免疫荧光组织化学染色技术观察各组小鼠黑质神经元凋亡及Bcl-2和Bax表达情况。结果TUNEL、Bcl-2和Bax阳性神经元主要位于黑质致密部。模型组黑质神经元凋亡数明显多于正常对照组,神经节苷脂GM1组黑质神经元凋亡数明显少于模型组。在模型组Bcl-2阳性神经元和Bax阳性神经元的数量均较正常对照组明显增多;在神经节苷脂GM1组Bcl-2阳性神经元的数量较模型组明显增多,但Bax阳性神经元的数量较模型组明显减少。结论神经节苷脂GM1可能通过增强黑质神经元内Bcl-2基因表达及抑制Bax基因表达的途径抑制黑质神经元的凋亡。
Objective To investigate the effects of ganglioside GM1 on the apoptosis and the Bcl-2 and Bax expressions of substantia nigra （SN） neurons in mice with Parkinson＇s disease （PD）. Methods Adult C57-BL male mice were randomly dividedly into 3 groups： the control group （ConG）, PD model group （PDG） and ganglioside GM1 group （GMIG） . By using TUN-EL and immunofluorenscence staining the apoptosis and the Bcl-2 and Bax expressions of SN neurons were examined in all groups. Results Morphological examination showed that TUNEL, Bcl-2 and Bax immunopositive neurons were mainly in the compact part of SN. The number of nigral apoptosis in PDG was remarkably more than that of ConG, while the number of nigral apoptosis in GM1G was remarkably less than that of PDG. In PDG, the numbers of Bcl-2 and Bax immunopositive neurons were more than those of ConG. In GM1G, the number of Bcl-2 neurons was more than that of PDG, but the number of Bax immunopositive neurons was less than that of PDG. Conclusion Ganglioside GM1 might prevent the apoptosis of SN neurons by increasing Bcl-2 and inhibiting Bax expressions of SN neurons.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2007年第4期474-477,共4页
Chinese Journal of Histochemistry and Cytochemistry
作者简介
吴乐,男（1977年）,汉族,医学硕士.通讯作者（To whom correspondence should be addressed）
