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白藜芦醇通过Sirt3-SOD2-ROS途径诱导人卵巢癌SKOV3细胞凋亡 被引量:6
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作者 李松岩 于洋 +3 位作者 刘师兵 徐路 孙奇 徐冶 《中国病理生理杂志》 CAS CSCD 北大核心 2020年第2期229-233,共5页
目的:观察白藜芦醇是否通过Sirt3-SOD2-ROS途径诱导人卵巢癌SKOV3细胞凋亡。方法:体外培养SKOV3细胞,分别加入2.5、5、10、20、40和80 mg/L白藜芦醇,作用24 h后,MTT法检测白藜芦醇对SKOV3细胞活力的影响。将SKOV3细胞随机分为空白对照... 目的:观察白藜芦醇是否通过Sirt3-SOD2-ROS途径诱导人卵巢癌SKOV3细胞凋亡。方法:体外培养SKOV3细胞,分别加入2.5、5、10、20、40和80 mg/L白藜芦醇,作用24 h后,MTT法检测白藜芦醇对SKOV3细胞活力的影响。将SKOV3细胞随机分为空白对照组、白藜芦醇(10 mg/L)组、白藜芦醇(20 mg/L)组和白藜芦醇(40 mg/L)组,分别处理24 h后,用Hoechst 33342染色,应用激光共聚焦显微镜观察细胞核变化;用荧光探针标记细胞内活性氧(ROS),应用激光共聚焦显微镜观察细胞内ROS变化;采用Western blot检测沉默交配型信息调节因子2同源蛋白3(Sirt3)、超氧化物歧化酶2(SOD2)、Bcl-2、Bax和cleaved caspase-3蛋白表达。结果:MTT结果显示,白藜芦醇(2.5、5、10、20、40和80 mg/L)作用SKOV3细胞24 h,SKOV3细胞活力显著降低,IC 50为(47.6±0.1)mg/L。应用激光共聚焦显微镜观察,与空白对照组相比,白藜芦醇各浓度组SKOV3细胞核内出现明显固缩,且着色增强现象。ROS荧光标记显示,与空白对照组相比,白藜芦醇各浓度组中ROS红色荧光数量显著减少。Western blot检测结果表明,与空白对照组相比,白藜芦醇各浓度组Sirt3、SOD2、Bax和cleaved caspase-3蛋白表达显著上升(P<0.05),而Bcl-2蛋白表达显著降低(P<0.05)。结论:白藜芦醇可以通过调控Sirt3-SOD2-ROS途径诱导SKOV3细胞凋亡。 展开更多
关键词 白藜芦醇 卵巢癌 sirt3-sod2-ros信号通路 细胞凋亡
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Novel nervous and multi-system regenerative therapeutic strategies for diabetes mellitus with mTOR 被引量:13
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作者 Kenneth Maiese 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第3期372-385,共14页
Throughout the globe,diabetes mellitus(DM) is increasing in incidence with limited therapies presently available to prevent or resolve the significant complications of this disorder.DM impacts multiple organs and af... Throughout the globe,diabetes mellitus(DM) is increasing in incidence with limited therapies presently available to prevent or resolve the significant complications of this disorder.DM impacts multiple organs and affects all components of the central and peripheral nervous systems that can range from dementia to diabetic neuropathy.The mechanistic target of rapamycin(m TOR) is a promising agent for the development of novel regenerative strategies for the treatment of DM.m TOR and its related signaling pathways impact multiple metabolic parameters that include cellular metabolic homeostasis,insulin resistance,insulin secretion,stem cell proliferation and differentiation,pancreatic β-cell function,and programmed cell death with apoptosis and autophagy.m TOR is central element for the protein complexes m TOR Complex 1(m TORC1) and m TOR Complex 2(m TORC2) and is a critical component for a number of signaling pathways that involve phosphoinositide 3-kinase(PI 3-K),protein kinase B(Akt),AMP activated protein kinase(AMPK),silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae)(SIRT1),Wnt1 inducible signaling pathway protein 1(WISP1),and growth factors.As a result,m TOR represents an exciting target to offer new clinical avenues for the treatment of DM and the complications of this disease.Future studies directed to elucidate the delicate balance m TOR holds over cellular metabolism and the impact of its broad signaling pathways should foster the translation of these targets into effective clinical regimens for DM. 展开更多
关键词 Akt AMP activated protein kinase(AMPK) apoptosis Alzheimer’s disease autophagy β-cell cancer cardiovascular disease caspase CCN family diabetes mellitus epidermal growth factor erythropoietin fibroblast growth factor forkhead transcription factors Fox O FRAP1 hamartin(tuberous sclerosis 1)/tuberin(tuberous sclerosis 2)(TSC1/TSC2) insulin mechanistic target of rapamycin(mTOR) m TOR Complex 1(m T ORC1) m TOR Complex 2(m TORC2) nicotinamide nicotinamide adenine dinucleotide(NAD+) non-communicable diseases oxidative stress phosphoinositide 3-kinase(PI 3-K) programmed cell death silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae)(sirt1) sirtuin stem cells wingless Wnt Wnt1 inducible signaling pathway protein 1(WISP1)
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