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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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Remodeling of the ryanodine receptor isoform 1 channel regulates the sweet and umami taste perception of Rattus norvegicus 被引量:1
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作者 Wenli Wang Dingqiang Lu +3 位作者 Qiuda Xu yulian jin Guangchang Pang Yuan Liu 《Fundamental Research》 CAS CSCD 2023年第3期459-468,共10页
Sweet and umami tastes are elicited by sweet and umami receptors on the tongue and palate epithelium,respectively.However,the molecular machinery allowing the taste reaction remains incompletely understood.Through a p... Sweet and umami tastes are elicited by sweet and umami receptors on the tongue and palate epithelium,respectively.However,the molecular machinery allowing the taste reaction remains incompletely understood.Through a phosphoproteomic approach,we identified the key proteins that trigger taste mechanisms based on phosphorylation cascades.Ryanodine receptor isoform 1(RYR1)was further verified by sensory and behavioral assays.We propose a model of RYR1-mediated sweet/umami signaling in which the RYR1 channel,which mediates Ca^(2+)release from the endoplasmic reticulum,is closed by dephosphorylation in bud tissue after sweet/umami treatment.The alteration in Ca^(2+)content in the cytosol induces transient membrane depolarization and generates a cell current for taste signal transduction.We demonstrate that RYR1 is a new channel involved in the regulation of sweet/umami signal transduction and propose a“metabolic clock”notion based on sweet/umami sensing.Our study provides a valuable foundation for a system-level understanding of the taste perception mechanism. 展开更多
关键词 UMAMI SWEET Phosphoproteomic Ryanodine receptor isoform 1 Metabolic clock
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