首页> 中文期刊> 《针刺研究 》 >'嗅三针'对阿尔茨海默病鼠海马Bcl-2和Bax表达的干预效应

'嗅三针'对阿尔茨海默病鼠海马Bcl-2和Bax表达的干预效应

         

摘要

Objective To observe the effect of electroacupuncture (EA) of “Xiusanzhen”[3 acupoints, i.e., bilateral “Yingxiang” (LI 20) and “Yintang” (EX-HN 3)] on expression of B-cell lymphoma/leukemia-2 (Bcl-2, an antiapoptosis protein) and Bax (a protein for promoting apoptosis) in the hippocampus in Alzheimer disease(AD)rats, so as to explore its clinical mechanisms underlying relieving AD. Methods A total of 40 Sprague Dawley rats were randomly divided into normal control,AD model, EA and olfactory nerve transaction(ONT) + EA groups, with 10 rats in each. AD model was established by injection of β-amyloid (Aβ)1-40 (2 μL containing 10 μg) into the hippocampus (Bregma: 3.5 mm, L; 2.0 mm, H: - 2.8 mm below dura), and the ON was sectioned by using a fine needle. EA (80-100 Hz, 1-3 mA) was applied to bilateral LI 20 and EX-HN 3 for 10 m in, once daily (except Saturdays and Sundays) for 6 weeks. The expression of Bcl-2 and Bax of hippocampus was measured by immunohistochemistory. Results Compared with the normal control group, the expression of Bcl-2 of hippocampus was significantly lower in the AD model group(P<0.05), and that of Bax in AD model group was much higher( P<0.01 ). In comparison with the model group, the expression of hippocampal Bcl-2 was up-regulated significantly( P<0.01 ), and that of hippocampal Bax protein downregulated considerably in the EA group( P<0.01 ). No significant differences were found between AD model and ONT+ EA groups in the expression of hippocampal Bcl-2 and Bax proteins ( P>0.05), suggesting a necessary premise condition for EA in regulating hippocampal Bcl-2 and Bax expression. Conclusion “Xiusanzhen” can regulate the expression of hippocampal Bcl-2 and Bax proteins in AD rats, which may contribute to its clinical effect in relieving AD, and the therapeutic effect depends on the integrity of the olfactory nerve pathway.%目的:探讨"嗅三针"通过嗅觉通路对阿尔茨海默病(AD)模型大鼠海马神经元细胞凋亡的影响,以阐明其治疗AD的作用机制.方法:成年SD雄性大鼠40只,随机分为正常对照组、AD模型组、嗅神经切断嗅三针组、嗅三针组,每组10只.β-淀粉样蛋白(Aβ1-40肤段注射法制作AD大鼠模型,嗅神经切断术造大鼠嗅觉通路阻断模型."印堂"穴及两侧"迎香"穴交替电针刺激行"嗅三针"治疗,每次10min,每周治疗5次,共治疗6周.免疫组化法检测海马Bcl-2和Bax表达.结果:AD模型组较正常对照组Bcl-2阳性细胞减少(P<0.05),Bax阳性细胞表达增多(P<0.01);嗅三针组较AD模型组Bcl-2阳性细胞明显增多(P<0.01),Bax阳性细胞显著减少(P<0.01);嗅神经切断嗅三针组与AD模型组比较Bcl-2,Ba x阳性细胞变化不明显(P>0.05).结论:"嗅三针"能够调节海马Bcl-2和Bax的表达,其治疗效应的发挥依赖于嗅觉传导通路的完整性.

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