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Protective effect and mechanism of ginsenoside Rg1 on H2O2 induced hippocampal neurons aging due to down-regulate NOX2 mediated NLRP1 inflammasome activation in vitro 被引量:1
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作者 Tan-zhen XU Ya-li CHEN +4 位作者 Xiao-yan SHEN Ling-Ling SUN Bi-qiong ZHANG Da-ke HUANG Wei-zu LI 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第4期321-321,共1页
OBJECTIVE To explore the protective effects and mechanisms of Ginsenoside Rg1(Rg1) on H_2O_2-induced hippocampal neurons aging in vitro.METHODS The primary culture hippo.campal neurons(7 d) were randomly placed into s... OBJECTIVE To explore the protective effects and mechanisms of Ginsenoside Rg1(Rg1) on H_2O_2-induced hippocampal neurons aging in vitro.METHODS The primary culture hippo.campal neurons(7 d) were randomly placed into six groups:normal control group,H_2O_2(200 μM) treat.ment group,and H_2O_2+Rg1(1,5 and 10μM) groups.The neurons were with Rg1(1,5 and 10 μmol·L^(-1))for 6 h.H_2O_2(200 μmol · L-1) was added to the medium and incubate for 18 h.The Dihydroethidium(DHE) staining was performed for ROS production assessment.The LDH release and Hoechst 33258 were performed to examine the neuronal damage and apoptosis.The immunoblot was used to deter.mine the expression of β-Gal,NOX2,p22 phox,p47 phox,NLRP-1,ASC and Caspase-1 in hippocampal neurons.The ELISA was performed to detect the levels of IL-1β and IL-18 released in the supernatant in hippocampal neurons.RESULTS Rg1(5 and 10 μmol·L^(-1)) significantly reduced the ROS production,attenuated H_2O_2-induced neuronal damage and apoptosis(P<0.05,P<0.01).The immunoblot results showed that Rg1(5 and 10 μmol·L^(-1)) treatment significantly decreased the expression of β-Gal,NOX2,p22 phox,p47 phox,NLRP-1,ASC and Caspase-1 in hippocampal neurons(P<0.05,P<0.01).Additionally,Rg1(5 and 10 μmol·L^(-1)) treatment significantly decreased IL-1β and IL-18 release in the supernatant.CONCLUSION The protective effect of Rg1 in H_2O_2-induced hippocampal neurons aging may be due to inhibit NOX2-NLRP1 activation. 展开更多
关键词 人参皂甙 海马神经体 治疗方法 临床分析
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Buyang Huanwu Decoction fraction protects against cerebral ischemia/reperfusion injury by attenuating the inflammatory response and cellular apoptosis 被引量:11
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作者 Yulian Jin Liuyi Dong +5 位作者 Changqing Wu Jiang Qin Sheng Li Chunyan Wang Xu Shao Dake Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第3期197-207,共11页
Buyang Huanwu Decoction fraction extracted from Buyang Huanwu Decoction contains saponins of Astragalus, total paeony glycoside and safflower flavones. The aim of this study was to demonstrate the neuroprotective effe... Buyang Huanwu Decoction fraction extracted from Buyang Huanwu Decoction contains saponins of Astragalus, total paeony glycoside and safflower flavones. The aim of this study was to demonstrate the neuroprotective effect and mechanism of Buyang Huanwu Decoction fraction on ischemic injury both in vivo and in vitro. In vivo experiments showed that 50-200 mg/kg Buyang Huanwu Decoction fraction reduced infarct volume and pathological injury in ischemia/reperfusion rats, markedly inhibited expression of nuclear factor-κB and tumor necrosis factor-α and promoted nestin protein expression in brain tissue. Buyang Huanwu Decoction fraction (200 mg/kg) exhibited significant effects, which were similar to those of 100 mg/kg Ginkgo biloba extract. In vitro experimental results demonstrated that 10-100 mg/L Buyang Huanwu Decoction fraction significantly improved cell viability, decreased the release of lactate dehydrogenase and malondialdehyde levels, and inhibited the rate of apoptosis in HT22 cells following oxygen-glucose deprivation. Buyang Huanwu Decoction fraction (100 mg/L) exhibited significant effects, which were similar to those of 100 mg/L Ginkgo biloba extract. These findings suggest that Buyang Huanwu Decoction fraction may represent a novel, protective strategy against cerebral ischemia/reperfusion injury in rats and oxygen-glucose deprivation-induced damage in HT22 cells in vitro by attenuating the inflammatory response and cellular apoptosis. 展开更多
关键词 缺血 再灌注损伤 补阳还五汤 神经保护作用 细胞凋亡 炎症反应 脑组织 银杏叶提取物 缺血再灌注损伤
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