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干扰SIRT7抑制甲状腺癌细胞的增殖、迁移和侵袭能力 预览
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作者 陈晓曦 陈旭旭 +2 位作者 林佳浩 陈吉彩 黄国裕 《温州医科大学学报》 CAS 2019年第1期11-14,23共5页
目的:研究干扰SIRT7对甲状腺癌细胞BCPAP的体外增殖、迁移和侵袭能力的影响。方法:通过慢病毒构建干扰SIRT7的甲状腺癌BCPAP的稳定株,并在mRNA和蛋白水平验证干扰效果,然后通过CCK-8、细胞划痕、细胞迁移和细胞侵袭实验来研究SIRT7对甲... 目的:研究干扰SIRT7对甲状腺癌细胞BCPAP的体外增殖、迁移和侵袭能力的影响。方法:通过慢病毒构建干扰SIRT7的甲状腺癌BCPAP的稳定株,并在mRNA和蛋白水平验证干扰效果,然后通过CCK-8、细胞划痕、细胞迁移和细胞侵袭实验来研究SIRT7对甲状腺癌细胞BCPAP体外增殖、迁移和侵袭能力的影响。结果:成功构建干扰SIRT7的甲状腺癌细胞BCPAP的稳定株;干扰SIRT7之后,甲状腺癌细胞BCPAP的体外增殖活力显著降低,划痕愈合能力、细胞迁移和侵袭能力也明显减弱,差异均有统计学意义(P<0.05)。结论:SIRT7可能在甲状腺癌中扮演了癌基因的角色,并且SIRT7可能是甲状腺癌一个潜在的治疗靶点。 展开更多
关键词 甲状腺肿瘤 癌基因 SIRTUIN SIRT7
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SIRT7通过抑制内质网应激蛋白GRP78减轻脂多糖或D-氨基半乳糖/脂多糖诱导的肝细胞凋亡 预览
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作者 阮昕 张颖婷 +7 位作者 韩可琪 林龙帅 陈晨 岳铭 王楚翘 孙英刚 赵庆华 贺明 《上海交通大学学报:医学版》 CAS CSCD 北大核心 2019年第8期812-819,共8页
目的·探究SIRT7(sirtuin 7)对脂多糖(lipopolysaccharide,LPS)或D-氨基半乳糖(D-galactosamine,D-GalN)/LPS诱导的急性肝损伤的作用及机制。方法·将13周龄的C57BL/6J小鼠随机分为生理盐水组(n=5)、LPS组(n=7)和D-GalN/LPS组(n... 目的·探究SIRT7(sirtuin 7)对脂多糖(lipopolysaccharide,LPS)或D-氨基半乳糖(D-galactosamine,D-GalN)/LPS诱导的急性肝损伤的作用及机制。方法·将13周龄的C57BL/6J小鼠随机分为生理盐水组(n=5)、LPS组(n=7)和D-GalN/LPS组(n=8),分别腹腔注射生理盐水、LPS和D-GalN/LPS。24 h后收集生理盐水组和LPS组的小鼠血清和肝脏,D-GalN/LPS组于注射后8 h收集血清和肝脏。利用苏木精-伊红(H-E)染色比较3组小鼠肝脏病理学改变,同时观察血清学生化指标的变化;利用TUNEL染色和F4/80染色明确小鼠肝脏内细胞凋亡和炎症细胞浸润程度;利用realtime-PCR检测各组小鼠肝组织中SIRT7、白介素-1β(interleukin 1β,IL-1β)、IL-6、肿瘤坏死因子α(tumor necrosis factorα,TNF-α)等的mRNA水平;利用Western blotting检测各组小鼠肝组织中SIRT7、激活型胱天蛋白酶3(cleaved-caspase3)和伴侣葡萄糖调节蛋白(the 78 kDa glucose regulated protein,GRP78)等的蛋白水平。体外实验中,在正常小鼠肝细胞AML-12细胞中过表达SIRT7,并给予LPS刺激,利用Western blotting明确SIRT7对LPS引起的内质网应激信号通路分子的调控。结果·注射LPS或D-GalN/LPS后,小鼠肝脏出现明显的炎症细胞浸润、充血及肝细胞凋亡,血清中谷丙转氨酶(glutamic-pyruvic transaminase,GPT)和谷草转氨酶(glutamic-oxalacetic transaminase,GOT)水平明显升高,肝组织中SIRT7的mRNA和蛋白水平均明显降低,内质网应激蛋白GRP78表达明显上调。在AML-12细胞系中,SIRT7过表达可明显抑制LPS引起的GRP78蛋白上调。结论·SIRT7通过抑制内质网应激中的GRP78减轻LPS或D-GalN/LPS诱导的肝细胞凋亡。 展开更多
关键词 去乙酰化酶(sirtuin) 脓毒症 SIRT7 急性肝损伤 内质网应激 细胞凋亡
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在癫痫猝死模型中昼夜节律改变和时钟基因及Sirtuin 1的振荡
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作者 Eli Wallace Samantha Wright +4 位作者 Barry Schoenike 高慧(译) 童馨(审) 慕洁(审) Rama K. Maganti 《癫痫杂志》 2019年第3期209-219,共11页
许多神经系统疾病都会影响昼夜节律。尽管已知癫痫常伴睡眠障碍,但与癫痫昼夜节律紊乱相关的数据却很少。文章检验了Kcna1缺失小鼠的昼夜休息活动以及睡眠-觉醒模式。该小鼠模型表现出反复自发癫痫发作,也是研究癫痫猝死的模型。此外,... 许多神经系统疾病都会影响昼夜节律。尽管已知癫痫常伴睡眠障碍,但与癫痫昼夜节律紊乱相关的数据却很少。文章检验了Kcna1缺失小鼠的昼夜休息活动以及睡眠-觉醒模式。该小鼠模型表现出反复自发癫痫发作,也是研究癫痫猝死的模型。此外,研究试图确定癫痫发作以及核心时钟基因和调节因子Sirtuin 1(Sirt1)的异常变化是否与昼夜节律紊乱有关。研究使用被动红外活动记录仪评估休息活动模式,使用脑电图(EEG)进行癫痫发作和睡眠分析,并且使用逆转录聚合酶链反应和蛋白质印迹法评估时钟基因和Sirt1在Kcna1缺失和野生型小鼠中的表达情况。癫痫Kcna1缺失动物模型存在昼夜休息活动模式紊乱,趋于表现出延长的昼夜节律。EEG分析证实了睡眠结构的破坏,清醒时间更多并且睡眠不足。尽管所有癫痫小鼠都表现出昼夜休息活动模式的紊乱,但该研究发现实际癫痫发作负担与睡眠紊乱程度之间没有相关性。发现前下丘脑中几个时钟基因(即Clock,Bmal1,Per1和Per2)和昼间Sirt1 mRNA的衰减振荡。几个核心时钟基因的振荡衰减与Kcna1缺失小鼠中观察到的异常昼夜休息活动以及睡眠-觉醒模式改变相关,可能是其基础原因,并可能导致癫痫晚期并发症,例如癫痫猝死。Sirt1可能是恢复生物钟基因节律和癫痫睡眠模式的潜在治疗靶点之一。 展开更多
关键词 昼夜节律 时钟基因 癫痫 Kcna1缺失 SIRTUIN
LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway 预览
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作者 Xue-Yang Chen Chang-Zhou Cai +5 位作者 Meng-Li Yu Ze-Min Feng Yu-Wei Zhang Pei-Hao Liu Hang Zeng Chao-Hui Yu 《世界胃肠病学杂志:英文版》 SCIE CAS 2019年第45期6607-6618,共12页
BACKGROUND It is well known that nonalcoholic fatty liver disease(NAFLD)is associated with insulin resistance(IR).LB100,a serine/threonine protein phosphatase 2A(PP2A)inhibitor,is closely related to IR.However,there i... BACKGROUND It is well known that nonalcoholic fatty liver disease(NAFLD)is associated with insulin resistance(IR).LB100,a serine/threonine protein phosphatase 2A(PP2A)inhibitor,is closely related to IR.However,there is little data regarding its direct influence on NAFLD.AIM To elucidate the effect and underlying mechanism of LB100 in NAFLD.METHODS After 10 wk of high fat diet(HFD)feeding,male C57BL/6 mice were injected intraperitoneally with vehicle or LB100 for an additional 6 wk(three times a week).The L02 cell line was treated with LB100 and free fatty acids(FFAs)for 24 h.Hematoxylin and eosin and oil red O staining were performed for histological examination.Western blot analysis was used to detect the protein expression of Sirtuin 1(Sirt1),total and phosphorylated AMP-activated protein kinaseα(AMPKα),and the proteins involved in lipogenesis and fatty acid oxidation.The mRNA levels were determined by qPCR.Pharmacological inhibition of AMPK was performed to further examine the exact mechanism of LB100 in NAFLD.RESULTS LB100 significantly ameliorated HFD-induced obesity,hepatic lipid accumulation and hepatic injury in mice.In addition,LB100 significantly downregulated the protein levels of acetyl-CoA carboxylase,sterol regulatory element-binding protein 1 and its lipogenesis target genes,including stearoyl-CoA desaturase-1 and fatty acid synthase,and upregulated the levels of proteins involved in fatty acidβ-oxidation,such as peroxisome proliferator-activated receptorα(PPARα),peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α),carnitine palmitoyltransferase 1α,acyl-CoA oxidase 1 and uncoupling protein 2,as well as the upstream mediators Sirt1 and AMPKαin the livers of HFD-fed mice.In vitro,LB100 alleviated FFA-induced lipid accumulation in L02 cells through the AMPK/Sirt1 signaling pathway.Further studies showed that the curative effect of LB100 on lipid accumulation was abolished by inhibiting AMPKαin L02 cells.CONCLUSION PP2A inhibition by LB100 significantly ameliorates hepatic 展开更多
关键词 LB100 Nonalcoholic fatty liver disease Serine/threonine-protein phosphatase 2A Lipid metabolism AMP-activated protein kinaseα Sirtuin 1
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Network-centric medicine for peripheral nerve injury:treating the whole to boost endogenous mechanisms of neuroprotection and regeneration 预览
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作者 David Romeo-Guitart Caty Casas 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第7期1122-1128,共7页
Peripheral nerve injuries caused by accidents may lead to paralysis,sensory disturbances,anaesthesia,and lack of autonomic functions.Functional recovery after disconnection of the motoneuronal soma from target tissue ... Peripheral nerve injuries caused by accidents may lead to paralysis,sensory disturbances,anaesthesia,and lack of autonomic functions.Functional recovery after disconnection of the motoneuronal soma from target tissue with proximal rupture of axons is determined by several factors:motoneuronal soma viability,proper axonal sprouting across inhibitory zones and elongation toward specific muscle,effective synapse contact rebuilding,and prevention of muscle atrophy.Therapies,such as adjuvant drugs with pleiotropic effects,that promote functional recovery after peripheral nerve injury are needed.Toward this aim,we designed a drug discovery workflow based on a network-centric molecular vision using unbiased proteomic data and neural artificial computational tools.Our focus is on boosting intrinsic capabilities of neurons for neuroprotection;this is in contrast to the common approach based on suppression of a pathobiological pathway known to be associated with disease condition.Using our workflow,we discovered neuroheal,a combination of two repurposed drugs that promotes motoneuronal soma neuroprotection,is anti-inflammatory,enhances axonal regeneration after axotomy,and reduces muscle atrophy.This drug discovery workflow has thus yielded a therapy that is close to its clinical application. 展开更多
关键词 MOTONEURON NEURODEGENERATION AXONAL REGENERATION muscle ATROPHY systems biology neuroheal PI3K/AKT SIRTUIN 1 motor function recovery
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Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis 预览
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作者 Meng-Ting Ren Meng-Li Gu +4 位作者 Xin-Xin Zhou Mo-Sang Yu Hang-Hai Pan Feng Ji Chen-Yan Ding 《世界胃肠病学杂志:英文版》 SCIE CAS 2019年第38期5800-5813,共14页
BACKGROUND Sirtuin 1(SIRT1)is a nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase that is involved in various diseases,including cancers,metabolic diseases,and inflammation-associated diseases.Howe... BACKGROUND Sirtuin 1(SIRT1)is a nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase that is involved in various diseases,including cancers,metabolic diseases,and inflammation-associated diseases.However,the role of SIRT1 in ulcerative colitis(UC)is still confusing.AIM To investigate the role of SIRT1 in intestinal epithelial cells(IECs)in UC and further explore the underlying mechanisms.METHODS We developed a coculture model using macrophages and Caco-2 cells.After treatment with the SIRT1 activator SRT1720 or inhibitor nicotinamide(NAM),the expression of occludin and zona occludens 1(ZO-1)was assessed by Western blot analysis.Annexin V-APC/7-AAD assays were performed to evaluate Caco-2 apoptosis.Dextran sodium sulfate(DSS)-induced colitis mice were exposed to SRT1720 or NAM for 7 d.Transferase-mediated dUTP nick-end labeling(TUNEL)assays were conducted to assess apoptosis in colon tissues.The expression levels of glucose-regulated protein 78(GRP78),CCAAT/enhancerbinding protein homologous protein(CHOP),caspase-12,caspase-9,and caspase-3 in Caco-2 cells and the colon tissues of treated mice were examined by quantitative real-time PCR and Western blot.RESULTS SRT1720 treatment increased the protein levels of occludin and ZO-1 and inhibited Caco-2 apoptosis,whereas NAM administration caused the opposite effects.DSS-induced colitis mice treated with SRT1720 had a lower disease activity index(P<0.01),histological score(P<0.001),inflammatory cytokine levels(P<0.01),and apoptotic cell rate(P<0.01),while exposure to NAM caused the opposite effects.Moreover,SIRT1 activation reduced the expression levels of GRP78,CHOP,cleaved caspase-12,cleaved caspase-9,and cleaved caspase-3 in Caco-2 cells and the colon tissues of treated mice.CONCLUSION SIRT1 activation reduces apoptosis of IECs via the suppression of endoplasmic reticulum stress-mediated apoptosis-associated molecules CHOP and caspase-12.SIRT1 activation may be a potential therapeutic strategy for UC. 展开更多
关键词 SIRTUIN 1 Endoplasmic reticulum stress Apoptosis ULCERATIVE COLITIS INTESTINAL BARRIER
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SIRT3在心血管疾病中的作用 预览
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作者 薛晓帆 齐丹 +1 位作者 周立春 曲爱娟 《生理科学进展》 CAS 北大核心 2019年第4期256-258,共3页
沉默信息调节因子2相关酶类3(silent mating type information regulation2 homolog-3,SIRT3)是一种依赖于烟酰胺腺嘌呤二核苷酸(nicotinamide-adenine dinucleotide,NAD)的III类去乙酰化酶。SIRT3主要定位于线粒体,广泛分布于肾脏、脑... 沉默信息调节因子2相关酶类3(silent mating type information regulation2 homolog-3,SIRT3)是一种依赖于烟酰胺腺嘌呤二核苷酸(nicotinamide-adenine dinucleotide,NAD)的III类去乙酰化酶。SIRT3主要定位于线粒体,广泛分布于肾脏、脑、心脏及肝脏等富含线粒体的组织器官中,其可对组蛋白和非组蛋白去乙酰化在调控细胞代谢、细胞周期、细胞凋亡及细胞寿命方面起着重要的作用。SIRT3通过去乙酰化相关靶蛋白调节其生物活性,在抵抗氧化应激反应,改善血管内皮细胞功能等多种心血管疾病中,都起到了保护性作用。该文旨在对SIRT3在常见的心血管疾病中的作用的研究进展进行综述。 展开更多
关键词 SIRTUIN 3 线粒体 去乙酰化 心血管疾病
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利拉鲁肽调节Sirtuin表达对高糖诱导的人内皮集落形成细胞生物学行为的影响 预览
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作者 张路 唐康 周波 《解放军医学杂志》 CAS CSCD 北大核心 2019年第5期361-368,共8页
目的探索利拉鲁肽是否通过调节Sirtuin影响高糖诱导的人内皮集落形成细胞(ECFC)的生物学行为。方法采用密度梯度离心法从外周血中分离获取单个核细胞,用EBM-2诱导培养出ECFC,随机分为正糖组(5.5 mmol/L D-葡萄糖)、渗透压组(5.5mmol/LD... 目的探索利拉鲁肽是否通过调节Sirtuin影响高糖诱导的人内皮集落形成细胞(ECFC)的生物学行为。方法采用密度梯度离心法从外周血中分离获取单个核细胞,用EBM-2诱导培养出ECFC,随机分为正糖组(5.5 mmol/L D-葡萄糖)、渗透压组(5.5mmol/LD-葡萄糖+24.5 mmol/L甘露醇)、高糖组(30 mmol/LD-葡萄糖),均处理6d。随后采用EdU实验、Transwell实验、成管实验、β-半乳糖苷酶实验分别测定ECFC的增殖、迁移、成管及衰老情况,采用免疫印迹法测定Sirtuins(Sirtuin1–7)、血管内皮生长因子(VEGF)、血管生成素的表达水平。研究利拉鲁肽对ECFC的影响时,将细胞分为4组,除上述正糖组与高糖组外,还设有正糖利拉鲁肽干预组(5.5 mmol/L D-葡萄糖+100 nmol/L利拉鲁肽)、高糖利拉鲁肽干预组(30 mmol/L D-葡萄糖+100 nmol/L利拉鲁肽),均处理6d,观察4组细胞的生物学行为变化并测定VEGF和血管生成素的表达水平。结果 EdU实验显示高糖组的细胞增殖率明显低于正糖组[(30.16±12.36)%vs.(88.00±13.77)%],Transwell实验显示高糖组的细胞迁移能力明显低于正糖组(25.11±6.05vs.64.89±10.73),成管实验显示高糖组细胞成管能力明显低于正糖组(27.50±3.90 vs. 69.61±5.48),β-半乳糖苷酶染色实验显示高糖组细胞衰老率明显高于正糖组[(87.63±9.63)%vs.(71.35±7.58)%],差异均有统计学意义(P<0.05)。高糖情况下,Sirtuins家族表达普遍降低,VEGF和血管生成素表达均显著下降(P<0.05),Sirtuin1的表达随利拉鲁肽浓度的升高而升高。予以适宜浓度的利拉鲁肽干预后,VEGF和血管生成素的表达均明显增加(P<0.05)。EdU实验显示高糖利拉鲁肽干预组的细胞增殖率明显高于正糖组[(54.09±27.29)%vs.(29.01±7.56)%],Transwell实验显示高糖利拉鲁肽干预组的细胞迁移能力明显高于高糖组(32.25±4.99 vs. 21.75±3.10),成管实验显示高糖利拉鲁肽干预组的细胞成管能力明显高于高糖组(69.61±8.11vs.39. 展开更多
关键词 内皮集落形成细胞 利拉鲁肽 沉默信息调节因子 血管内皮生长因子 血管生成素
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Melatonin modifies SOX2~+ cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation 预览
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作者 Alan Hinojosa-Godínez Luis F. Jave-Suarez +5 位作者 Mario Flores-Soto Alma Y. Gálvez-Contreras Sonia Luquín Edith Oregon-Romero Oscar González-Pérez Rocio E. González-Castaneda 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1787-1795,共9页
Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep depri... Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep deprivation.The precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this process.In this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword clusterization.Our results showed that the administration of melatonin under sleep-deprived conditions increased the MECP2 expression and reduced the SIRT1 expression in the dentate gyrus.We observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep deprivation.In addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated group.These findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived conditions.All procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval No.CI-16610)on January 2,2016. 展开更多
关键词 sleep-deprivation MELATONIN microRNA NEUROGENESIS SIRTUIN 1 SIRT1 methyl-CpG-binding protein 2 MECP2 epigenetic text-mining mir-9 let-7b
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Expression of SIRT1 signaling pathway in intestinal tissues of neonatal necrotizing enterocolitis
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作者 Lan Zhang Bo-Liang Wang +4 位作者 Li Wang Qiong Gao Zhao-Xia Xi Yan-Hong Gui Hui-Ping Wang 《海南医科大学学报(英文版)》 2019年第8期18-23,共6页
Objective:To analyze the expression of sirtuin type 1 (SIRT1) signal pathway in intestinal tissues of neonatal necrotizing enterocolitis (NEC), and to preliminarily explore the role of SIRT1 in the occurrence of NEC.M... Objective:To analyze the expression of sirtuin type 1 (SIRT1) signal pathway in intestinal tissues of neonatal necrotizing enterocolitis (NEC), and to preliminarily explore the role of SIRT1 in the occurrence of NEC.Methods: From January 2017 to June 2017, the ileal tissues of 35 neonates with NEC underwent one-stage fistula treatment were selected as NEC group, and the ileal tissues of these 35 neonates underwent two-stage fistula treatment were selected as control group. The expression levels of SIRT1, transcription factor-nuclear factor (NF-κB), and SUMO specific protease 1 (SENP1) were detected by qRT-PCR;the expressions of SIRT1, NF-κB, and SENP1 were detected by immunohistochemistry and Western blotting (WB). Results: SIRT1 mRNA, protein positive expression rate, average optical density, and relative protein expression in intestinal tissues of children in NEC group were significantly lower than those in control group (P<0.05), however, the expression of NF-κB, the SENP1 mRNA and protein positive expression rates, the average optical density, and relative protein expression were significantly increased (P<0.05).Conclusion: SIRT1 is low expressed in intestinal tissues of children with NEC, the possible reason is that SIRT1 signaling pathway is suppressed and then NEC occurs. 展开更多
关键词 SIRTUIN type 1 NEONATAL NECROTIZING ENTEROCOLITIS Transcription factor-nuclear factor SUMO-specific PROTEASE 1
Berberine Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Rats via Activation of SIRT3/AMPK/ACC Pathway 预览
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作者 Yu-pei ZHANG Yuan-jun DENG +8 位作者 Kai-rui TANG Run-sen CHEN Shu LIANG Yin-ji LIANG Li HAN Ling JIN Zi-en LIANG Yan-ning CHEN Qin-he YANG 《当代医学科学(英文)》 SCIE CAS 2019年第1期37-43,共7页
This study aimed to verify the effects of berberine(BBR)on the fat metabolism proteins involved in the sirtuin 3(SIRT3)/adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pat... This study aimed to verify the effects of berberine(BBR)on the fat metabolism proteins involved in the sirtuin 3(SIRT3)/adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pathway in the liver tissues of rats with high-fat diet(HFD)-induced non-alcoholic fatty liver disease(NAFLD).Forty-eight rats were randomly divided into the normal control(NC)group,HFD group or BBR group,with 16 rats in each group.After 8 and 16 weeks of treatment,serum and liver samples were collected.Subsequently,body parameters,biochemical parameters and liver pathology were examined.The expression levels of proteins involved in the SIRT3/AMPK/ACC pathway in the liver were detected by Western blotting.After 8 and 16 weeks of a HFD,the successful establishment of rat models with different degrees of NAFLD was confirmed by hematoxylin and eosin(H&E)and Oil Red O staining.NAFLD rat models exhibited obesity and hyperlipidemia,and the protein expression levels of SIRT3,p-AMPK.p-ACC,and CPT-1A in the liver were significantly decreased compared to those in the NC group.The concurrent administration of BBR with the HFD effectively improved serum and liver lipid profiles and ameliorated liver injury.Furthermore,the protein expression levels of SIRT3,p-AMPK,p-ACC,and CPT-1 A in the liver were significantly increased in the BBR group as compared with those in the HFD group.In conclusion,our data suggest that the mechanism by which BBR ameliorates HFD-induced hepatic steatosis may be related to the activation of the SIRT3/AMPK/ACC pathway in the liver. 展开更多
关键词 BERBERINE non-alcoholic FATTY liver disease SIRTUIN 3 LIPID METABOLISM
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SIRT2在肝癌发生发展中的作用 预览 被引量:2
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作者 韩可琪 阮昕 贺明 《上海交通大学学报:医学版》 CSCD 北大核心 2018年第10期1247-1251,共5页
沉默信息调节因子(silence information regulator,sirtuin)是一类高度保守的烟酰胺腺嘌呤二核苷酸(NAD+)依赖的组蛋白去乙酰化酶,在衰老、代谢、细胞凋亡、基因转录、炎症发生等过程中发挥重要作用。哺乳动物有7种sirtuin,即SIRT1~SIRT... 沉默信息调节因子(silence information regulator,sirtuin)是一类高度保守的烟酰胺腺嘌呤二核苷酸(NAD+)依赖的组蛋白去乙酰化酶,在衰老、代谢、细胞凋亡、基因转录、炎症发生等过程中发挥重要作用。哺乳动物有7种sirtuin,即SIRT1~SIRT7。其中SIRT2的异常表达与包括肝癌在内的多种癌症相关:SIRT2既可以发挥癌基因的作用,也可以发挥抑癌基因的作用。而SIRT2如何通过对不同底物去乙酰化发挥不同的作用仍然存在争议。该文主要对SIRT2在肝癌发生发展中的作用进行综述。 展开更多
关键词 沉默信息调节因子 SIRT2 有丝分裂 Β连环蛋白 肝癌 线粒体代谢
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SIRT1-dependent modulation of methylation and acetylation of histone H3 on lysine 9(H3K9)in the zygotic pronuclei improves porcine embryo development 预览
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作者 Katerina Adamkova Young-Joo Yi +8 位作者 Jaroslav Petr Tereza Zalmanova Kristyna Hoskova Pavla Jelinkova Jiri Moravec Milena Kralickova Miriam Sutovsky Peter Sutovsky Jan Nevoral 《畜牧与生物技术杂志:英文版》 SCIE CAS CSCD 2018年第2期339-350,共12页
Background:The histone code is an established epigenetic regulator of early embryonic development in mammals.The lysine residue K9 of histone H3(H3K9)is a prime target of SIRT1,a member of NAD+-dependent histone deace... Background:The histone code is an established epigenetic regulator of early embryonic development in mammals.The lysine residue K9 of histone H3(H3K9)is a prime target of SIRT1,a member of NAD+-dependent histone deacetylase family of enzymes targeting both histone and non-histone substrates.At present,little is known about SIRT1-modulation of H3K9 in zygotic pronuclei and its association with the success of preimplantation embryo development.Therefore,we evaluated the effect of SIRT1 activity on H3K9 methylation and acetylation in porcine zygotes and the significance of H3K9 modifications for early embryonic development.Results:Our results show that SIRT1 activators resveratrol and BML-278 increased H3K9 methylation and suppressed H3K9 acetylation in both the paternal and maternal pronucleus.Inversely,SIRT1 inhibitors nicotinamide and sirtinol suppressed methylation and increased acetylation of pronuclear H3K9.Evaluation of early embryonic development confirmed positive effect of selective SIRT1 activation on blastocyst formation rate(5.2±2.9%versus 32.9±8.1%in vehicle control and BML-278 group,respectively;P≤0.05).Stimulation of SIRT1 activity coincided with fluorometric signal intensity of ooplasmic ubiquitin ligase MDM2,a known substrate of SIRT1 and known limiting factor of epigenome remodeling.Conclusions:We conclude that SIRT1 modulates zygotic histone code,obviously through direct deacetylation and via non-histone targets resulting in increased H3K9me3.These changes in zygotes lead to more successful pre-implantation embryonic development and,indeed,the specific SIRT1 activation due to BML-278 is beneficial for in vitro embryo production and blastocyst achievement. 展开更多
关键词 Embryonic DEVELOPMENT EPIGENETICS H3K9 METHYLATION SIRT1 SIRTUIN
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Sirtuin在低氧诱导人脐带间充质干细胞增殖中的作用 被引量:2
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作者 王凯民 谭娟娟 +1 位作者 严志强 李志强 《山东大学学报:医学版》 北大核心 2017年第7期23-30,共8页
目的 探讨低氧对人脐带间充质干细胞(h UC-MSCs)中Sirtuin(SIRT)蛋白表达影响及与细胞增殖的关系。方法 组织块贴壁法分离和培养h UC-MSCs;流式细胞仪鉴定细胞表面标志物;CCK-8法测定低氧与常氧下不同时间点h UC-MSCs的增殖能力;流... 目的 探讨低氧对人脐带间充质干细胞(h UC-MSCs)中Sirtuin(SIRT)蛋白表达影响及与细胞增殖的关系。方法 组织块贴壁法分离和培养h UC-MSCs;流式细胞仪鉴定细胞表面标志物;CCK-8法测定低氧与常氧下不同时间点h UC-MSCs的增殖能力;流式细胞仪检测低氧与常氧下细胞周期的变化;免疫荧光与Western blotting测定低氧与常氧下细胞SIRT蛋白定位与表达。结果 成功分离h UC-MSCs;细胞CD90、CD105、CD29、CD44高表达,CD14、CD19、CD34、CD45、HLA-DR无表达;CCK-8测定低氧培养24、48、72 h细胞的增殖能力均高于常氧培养(P均〈0.05);在低氧下培养24、48 h后S期细胞比率高于常氧培养(P均〈0.05);免疫荧光检测SIRT1、6位于细胞核内,SIRT2定位于胞浆,SIRT3、4、5定位于线粒体。Western blotting测定SIRT1在低氧培养24、48 h蛋白表达量均高于常氧条件(P均〈0.05),常氧培养72 h的SIRT1表达量高于24 h及48 h(P均〈0.05);SIRT2表达量在低氧培养24 h高于常氧培养(P〈0.05),48 h后低于常氧培养,72 h后高于常氧培养(P〈0.05);低氧培养24、48、72 h后SIRT5的表达量均高于常氧处理(P均〈0.05),常氧与低氧培养细胞48 h和72 h后均高于24 h时SIRT5的表达(P均〈0.05)。结论 低氧处理24、48、72 h均可以促进h UC-MSCs的增殖。低氧诱导SIRT1、2与5表达改变提示SIRT1、2、5可能参与了低氧对h UC-MSCs增殖的调控。 展开更多
关键词 人脐带间充质干细胞 低氧 增殖 SIRTUIN
羟基酪醇对LPS引起的小鼠急性肺损伤的保护作用 预览
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作者 魏静元 《食品与机械》 CSCD 北大核心 2017年第6期7-12,共6页
探索了羟基酪醇通过调控自噬在小鼠ALI模型中发挥其抗炎作用的潜在分子机制。通过Western印迹和染色方法检测LPS诱导的ALI小鼠细胞因子活性、炎症因子水平、sirtuin(SIRT1/3/6)表达、丝裂原活化蛋白激酶(MAPK)激活和自噬标志物表达,... 探索了羟基酪醇通过调控自噬在小鼠ALI模型中发挥其抗炎作用的潜在分子机制。通过Western印迹和染色方法检测LPS诱导的ALI小鼠细胞因子活性、炎症因子水平、sirtuin(SIRT1/3/6)表达、丝裂原活化蛋白激酶(MAPK)激活和自噬标志物表达,用Sybyl/Surflex模块研究了HT与SIRT和MAPK之间的分子对接。结果显示,LPS刺激的SIRT抑制、MAPK磷酸化和自噬抑制均被HT给药显著消除。伴随着BAL液中肺W/D比值、蛋白质浓度和炎症细胞水平的降低,HT治疗显著减弱肺水肿和炎症细胞浸润到肺组织中。包括TNF-α、IL-1β、IL-6、IL-10和MCP-1等炎症介质的LPS驱动释放,被HT强烈调控。 展开更多
关键词 羟基酪醇 脂多糖 自噬 急性肺损伤 sirtuin蛋白
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Histone Deacetylase AtSRT1 Links Metabolic Flux and Stress Response in Arabidopsis
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作者 Xiaoyun Liu Wei Wei +5 位作者 Wenjun Zhu Lufang Su Zeyang Xiong Man Zhou Yu Zheng and Dao-Xiu Zhou 《分子植物:英文版》 SCIE CAS CSCD 2017年第12期1510-1522,共13页
怎么种新陈代谢的流动,改变基因表示优化植物生长,对应力的反应仍然保持大部分不清楚。这里,我们报导 Arabidopsis thaliana NAD <sup>+</sup>-dependent histone deacetylase AtSRT1 否定地调整植物公差到应力和 glycol... 怎么种新陈代谢的流动,改变基因表示优化植物生长,对应力的反应仍然保持大部分不清楚。这里,我们报导 Arabidopsis thaliana NAD <sup>+</sup>-dependent histone deacetylase AtSRT1 否定地调整植物公差到应力和 glycolysis,但是刺激 mitochondrial 呼吸。我们发现 AtSRT1 与 Arabidopsis cMyc 有约束力的蛋白质 1 交往(AtMBP-1 ) ,一个 transcriptional 抑压者由 cytosolic glycolytic enolase 基因 LOS2/ENO2 的其他的翻译生产了。我们证明 AtSRT1 能与 AtMBP-1 目标 LOS2/ENO2 和 STZ/ZAT10 的染色质联系,哪个编码关键压力管理者,并且在这些基因减少 H3K9ac 层次镇压他们的抄写。AtSRT1 和 AtMBP-1 的 Overexpression 在 glycolytic 基因的表示上有 synergistic 效果, glycolytic 酶的活动,和 mitochondrial 呼吸。而且,我们发现 AtMBP-1 是 lysine-acetylated 并且对 proteasomal 蛋白质降级脆弱,当 AtSRT1 能移开它的离氨酸 acetylation 并且显著地提高它的稳定性在时 ? vivo。一起拿,这些结果显示 AtSRT1 在 Arabidopsis 由 epigenetic 规定和 AtMBP-1 transcriptional 活动的调整调整主要新陈代谢和压力反应。 展开更多
关键词 chromartin histone 修正 HDAC SIRTUIN 离氨酸 acetylation 新陈代谢
Sirtuin 1对免疫细胞调节效应及机制研究进展 预览 被引量:2
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作者 岳浩迪 朱小飞 《新乡医学院学报》 CAS 2017年第6期455-459,共5页
免疫细胞(巨噬细胞、树突状细胞、淋巴细胞等)是免疫应答的重要参与者,是机体免疫系统免疫防御、免疫监视及免疫自稳体现的重要实施者。当机体对免疫细胞功能的正常调节出现失常,往往易导致各种疾病(自身免疫性疾病、感染性疾病、肿... 免疫细胞(巨噬细胞、树突状细胞、淋巴细胞等)是免疫应答的重要参与者,是机体免疫系统免疫防御、免疫监视及免疫自稳体现的重要实施者。当机体对免疫细胞功能的正常调节出现失常,往往易导致各种疾病(自身免疫性疾病、感染性疾病、肿瘤及心血管疾病等)的发生和发展。Sirtuin 1是具有烟酰胺腺嘌呤二核苷酸依赖性的第3类组蛋白去乙酰化酶家族成员,是细胞寿命与代谢等生理活动中重要的转录调控因子,广泛参与癌症、神经退行性病变和代谢性疾病等老年性疾病的病理发展过程。近年来,Sirtuin 1在免疫细胞功能调控方面的研究逐渐获得关注,本文就此方面研究进展进行述评。 展开更多
关键词 SIRTUIN 1 去乙酰化 巨噬细胞 树突状细胞 T细胞 免疫调节
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Sirtuin家族与DNA损伤修复 被引量:1
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作者 黄海姣 徐舜 陈维春 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2016年第4期365-372,共8页
DNA损伤的发生与积累是造成细胞功能紊乱的根本原因,也是引起衰老与肿瘤等疾病发生的关键事件。为维持机体自身遗传物质的完整性与稳定性,生物体内拥有多种针对不同类型DNA损伤的修复方式。Sirtuin蛋白是一组NAD+依赖的、高度保守的组... DNA损伤的发生与积累是造成细胞功能紊乱的根本原因,也是引起衰老与肿瘤等疾病发生的关键事件。为维持机体自身遗传物质的完整性与稳定性,生物体内拥有多种针对不同类型DNA损伤的修复方式。Sirtuin蛋白是一组NAD+依赖的、高度保守的组蛋白去乙酰化酶,可通过去乙酰化作用调节众多底物蛋白质的表达、活性与稳定性。近来的研究显示,DNA损伤修复途径的多个关键蛋白质是Sirtuin的下游底物。Sirtuin蛋白通过调节同源重组修复、非同源末端修复、核苷酸切除修复等途径中的核心蛋白质参与修复包括双链断裂(double stranded breakes,DSBs)在内的多种DNA损伤类型,从而在维持基因组稳定性、寿命以及细胞能量代谢调节等一系列生物学作用中发挥至关重要的作用。本综述将介绍近年来Sirtuin与DNA损伤修复的研究进展。 展开更多
关键词 DNA损伤修复 去乙酰化酶 SIRTUIN
Sirtuin家族及其生物学特性 预览 被引量:6
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作者 戚欣欣 孙莉 《华夏医学》 CAS 2016年第1期169-174,共6页
沉默蛋白(sir2-related enzymes,sirtuin)或沉默信息调节因子2(silence information negulator2,Sir2)是一类从古细菌到人类都高度保守的烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD)依赖的组蛋白去乙酰化酶(hi... 沉默蛋白(sir2-related enzymes,sirtuin)或沉默信息调节因子2(silence information negulator2,Sir2)是一类从古细菌到人类都高度保守的烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD)依赖的组蛋白去乙酰化酶(histone deacetylase,HDAC),哺乳动物有7种sirtuin同源基因SIRT1-SIRT7,具有不同的亚细胞定位和功能。这些蛋白在细胞周期控制、维持线粒体的动态平衡、自噬和细胞生长调节等过程中发挥重要作用。笔者将对sirtuin家族的蛋白结构、酶学功能、家族成员及其生物学功能做一综述。 展开更多
关键词 SIRTUIN 沉默信息调节因子2 去乙酰化酶
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去乙酰化酶Sirtuins在干细胞功能调节中的作用及前景 预览
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作者 毛中伏 李怡芳 +1 位作者 栗原博 何蓉蓉 《中国组织工程研究》 CAS 北大核心 2016年第36期5450-5457,共8页
背景:氧化应激严重制约着干细胞治疗效能,而去乙酰化酶Sirtuin(SIRT)家族作为细胞内重要的抗氧化酶在调节干细胞结构和功能完整性中发挥重要作用,能有效降低干细胞损伤和增强干细胞生存能力。目的:综述SIRT家族在干细胞中的调控作... 背景:氧化应激严重制约着干细胞治疗效能,而去乙酰化酶Sirtuin(SIRT)家族作为细胞内重要的抗氧化酶在调节干细胞结构和功能完整性中发挥重要作用,能有效降低干细胞损伤和增强干细胞生存能力。目的:综述SIRT家族在干细胞中的调控作用及其机制,为SIRT家族在干细胞相关病理及生理学研究提供有益的参考。方法:由第一作者检索1990至2015年Web of Science平台,PubM ed数据库,CNKI中国知网数据库收录的与SIRT和干细胞氧化应激有关的文献。中文检索词为"去乙酰化酶,干细胞,细胞代谢";英文检索词为"SIRT,stem cells,oxidative stress,molecular mechanisms"。共纳入55篇文章进行综述。结果与结论:NAD+依赖的SIRT家族是机体组蛋白和其他蛋白去乙酰化的重要酶体,在调节机体新陈代谢、基因组稳定性、DNA损伤修复、染色质重塑和应激反应中起到了关键的调节作用。随着干细胞和SIRT家族研究的逐步深入,将为改善干细胞治疗能效从而为临床进行干细胞移植治疗提供更多的依据。 展开更多
关键词 干细胞 抗衰老酶 抗氧化剂 组织工程 移植 去乙酰化酶 SIRTUIN SIRT 去乙酰化 抗氧化 国家自然科学基金
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