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作 者:李志亮 周敏 唐中生 蒙潇 王佑乾 韦杰尹 LI Zhi-liang;ZHOU Min;TANG Zhong-sheng;MENG Xiao;WANG You-qian;WEI Jie-yin(Guizhou University of Traditional Chinese Medicine,Guiyang 550025,China)
出 处:《云南中医中药杂志》2024年第9期71-74,共4页Yunnan Journal of Traditional Chinese Medicine and Materia Medica
基 金:2020年贵州省校级大学生创新创业训练计划项目(2020-120397)。
摘 要:目的通过观察抗衰延年方对衰老大鼠细胞凋亡相关因子Bcl-2、Bax表达的影响,探讨抗衰延年方延缓衰老的可能机制。方法健康SD雄性大鼠40只,将其随机分为正常组、衰老模型组、中药组和吡拉西坦组;正常组不做任何处理,衰老模型组、中药组和吡拉西坦组每日颈背部皮下注射D-半乳糖500 mg/kg,连续注射30 d;经过30 d治疗后以Morris水迷宫进行大鼠行为学测试后取材应用原位杂交法检测其Bcl-2 mRNA、Bax mRNA表达。结果与正常组比较,模型组大鼠行动迟缓,逃避潜伏期增多(P<0.05),Bcl-2 mRNA的表达降低(P<0.05),Bax mRNA的表达增高(P<0.05);与模型组相比,中药组大鼠活力增强,逃避潜伏期时间减少(P<0.05),Bcl-2 mRNA的表达增强(P<0.05),Bax mRNA的表达降低(P<0.05)。结论抗衰延年方可改善衰老大鼠空间学习记忆能力,其机制可能与其上调抑制细胞凋亡因子Bcl2表达,下调促凋亡关键因子Bax表达有关。Objective:To study the effect of Anti-aging and Life-prolonging Prescription on the expression of apoptosis-related factors Bcl-2 and Bax in aging rats,and to explore the possible mechanism of the prescription.Methods:40 healthy SD male rats were randomly divided into normal group,aging model group,TCM group and piracetam group.The normal group was not treated,and the aging model group,TCM group and piracetam group were injected with 500 mg/kg D-galactose subcutaneously daily on the neck and back for 30 days.After 30 days of treatment,Morris water maze was used to conduct behavioral tests on the rats,and Bcl-2 mRNA and Bax mRNA expression were detected by in situ hybridization.Results:Compared with the rats in the normal group,the rats in the model group acted slowly,the escape latency increased(P<0.05),the expression of Bcl-2 mRNA decreased(P<0.05),and the expression of Bax mRNA increased(P<0.05).Compared with that of the model group,the activity of rats in the TCM group increased,the escape latency time decreased(P<0.05),the expression of Bcl-2 mRNA increased(P<0.05),and the expression of Bax mRNA decreased(P<0.05).Conclusion:Anti-aging and Life-prolonging Prescription can improve the spatial learning and memory ability of aging rats,and its mechanism may be related to the up-regulation of the expression of anti-apoptotic factor Bcl2 and the down-regulation of key pro-apoptotic factor Bax.
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