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作 者:乔锋 成云翠 刘湘萍 陈辉 毛少伟 邓叶华 QIAO Feng;CHENG Yun -cui;LIU Xiang -ping;CHEN Hui;MAO Shao -wei;DENG Ye -hua(Hengyang Central Hospital,Hengyang 421001,Hunan,China)
出 处:《湖南中医杂志》2018年第11期135-137,共3页Hunan Journal of Traditional Chinese Medicine
摘 要:目的:观察银杏提取物EGb761对大鼠视神经损伤后视网膜神经节细胞自噬活性及自噬流的影响,并探讨其作用机制。方法:将48只SD大鼠随机分为EGb761组和对照组,分别给予EGb761(150mg/kg·d)和0. 9%氯化钠注射液灌胃,均每天1次,直到处死。分别于损伤后第7天、第14天取材,采用免疫组化检测2组视网膜神经节细胞自噬相关蛋白LC3B、自噬标记蛋白p62及自噬基因Beclin-1及m TOR通路蛋白p-m TOR、p-S6表达水平,腺病毒GFP-m RFP-LC3荧光瞬时转染技术检测自噬流表达。结果:与对照组相比,EGb761组LC3B表达水平升高,p62、p-m TOR和p-S6蛋白表达水平均下降(均P <0. 05); 2组Beclin-1差异无统计学意义(P> 0. 05); 2组GFP和m RFP荧光点数比较,EGb761组的红点多于对照组,黄点少于对照组(均P <0. 05)。结论:EGb761能够促进大鼠视神经损伤后视网膜神经节细胞自噬流,其机制可能与促进m TOR信号通路中的相关蛋白表达有关。Objective:To investigate the effect of EGb761,a gingko extract,on the autophagy activity and autophagy flux of retinal ganglion cells after optic nerve damage in rats and its mechanism of action.Methods :A total of 48Sprague -Dawley rats were randomly divided into EGb761group and control group and were treated with EGb761(150mg/kg/day)or 0.9%sodium chloride injection by gavage once a day until being sacrificed.Samples were collected at 7and 14days after damage;immunohistochemistry was used to measure the expression of autophagy-related protein microtubule -associated protein light chain 3B (LC3B),autophagy marker protein p62,autophagic gene Beclin -1,and mTOR pathway proteins p -mTOR and p -S6,and adenovirus GFP -mRFP -LC3 transient transfection was used to measure the expression of autophagy flux. group ,the EGb761group had a significant increase in the expression of LC3B Results:Compared with the control and significant reductions in the expression of p62,p -roTOR,and p -$6(all P <0.05).There was no significant difference in Beclin -1 between the two groups (P >0.05).As for the comparison of fluorescence spots of GFP and mRFP,the EGb761group had more red spots and fewer yellow spots than the control group (both P <0.05).Conclusion :EGb761can promote autophagy flux of retinal ganglion cells after optic nerve damage in rats,possibly by promoting the expression of proteins involved in the mTOR signaling pathway.
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