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双语推荐：SIRT3

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目的探讨沉默信息调节因子1(SIRT1)在胃癌发展中的可能分子机制和信号通路。方法人胃癌细胞株HGC-27分为转染shRNA-SIRT1组及对照组,应用实时定量PCR及免疫印迹法检测转录激活因子3(STAT3)在两组中的表达;免疫共沉淀法分析SIRT1同STAT3、磷酸化STAT3在胃癌中的相互作用关系;建立STAT3敲除转基因小鼠胃癌模型,免疫组织化学方法检测STAT3敲除转基因小鼠胃癌组织中SIRT1的表达情况。结果 STAT3mRNA在shRNA-SIRT1组和对照组中表达无明显区别,免疫印迹检测发现STAT3蛋白水平在胃癌细胞组和空转组中较shRNA组中表达增高,磷酸化P-STAT3与STAT3表达水平相同,而乙酰化A-STAT3的表达水平正好相反。免疫共沉淀发现SIRT1同STAT3和PSTAT3能形成复合物。应用STAT3敲除转基因小鼠胃癌模型,进行SIRT1表达的对比研究,发现SIRT1在STAT3敲除转基因小鼠胃癌组织中的表达较对照组降低。结论通过研究SIRT1同STAT3在胃癌中的相互作用关系,推测SIRT1可能通过对STA13的去乙酰化作用,间接增强活化的磷酸化STAT3,并形成SIRT1-STAT3复合物,促进胃癌的发展。SIRT1可能通过JAK1-STAT3途径或直接激活STAT3参与胃癌的进展过程。
Objective To explore the possible molecular mechanism and signal channel of SIRT1 in progress of gas-tric cancer. Method STAT3 expression in shRNA-SIRT1 infected gastric cancer cells and control group were detec-ted by real time PCR and immunoblotting. Co-immunoprecipitation was used for analyzing the relationship between SIRT1 and STAT3,PSTAT3 in gastric cancer;STAT3 knock out mice model was successfully built. SIRT1 expression in gastric cancer tissue were detected by the method of immunohistochemical staining in STAT3-KO mice. Result There was no obvious difference of STAT3 mRNA level between shRNA-SIRT1 group and control,but we found the protein level of STAT3 was higher on gastric cancer cell group and control by immunoblotting analysis. P-STAT3 was same with STAT3,but the A-STAT3 was opposite. The SIRT1 could form complexes with STAT3 and P-STAT3 by co-immunoprecipitation. After analyzing the SIRT1 expression in STAT3 knock out mice gastric cancer model, we found the SIRT1 was lo

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探讨全脑缺血再灌注大鼠大脑运动皮质内沉默信息调节因子3(SIRT3)的表达规律。方法:应用免疫组织化学染色方法测定全脑缺血再灌注后不同时间点(6h、24h、72h、5d及7d组)大鼠大脑运动皮质内SIRT3的表达情况。结果:6h组、24h组至72h组脑缺血再灌注大鼠大脑运动皮质内SIRT3的含量随再灌注时间延长而增加(P0.01);72h组、5d组至7d组大鼠大脑运动皮质内SIRT3含量随再灌注时间延长而减少(P0.01)。结论:全脑缺血再灌注后大鼠大脑运动皮质内SIRT3的表达随再灌注时间延长呈抛物线改变,提示SIRT3可能参与脑缺血再灌注损伤的病理生理过程。
Objective:To observe the changes in the expression of silent information regulator 3 (SIRT3 ) in the cerebral motor cortex of rats following global cerebral ischemic reperfusion .Methods:The cerebral tissues were collected from rats following global cerebral ischemic reperfusion at time point of 6h ,24h ,72h ,5d ,and 7d (7 in each group) ,and the expression of SIRT3 in the cerebral cortex was detected by immunohistochemistry .Results :Under optical microscope ,SIRT3-positive cells were found in every group .Within the time range of 6h ,24h and 72h following global cerebral ischemic reperfusion ,SIRT3-positive cells increased significantly (P<0 .01) ,but within the time range of 72h ,5d and 7d ,the number of SIRT3-positive cells reduced significantly (P<0 .01) .Conclusion :The parabola-like change of SIRT3 expression time-phase in the cerebral cortex indicate that SIRT 3 might be related to pathophysiological processes of cerebral ischemic reperfusion .

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目的探讨沉默调节蛋白1(Sirt1)对神经元轴突生长的影响。方法体外原代分离培养胚胎海马神经元,观察Sirt1在72 h神经元的分布表达;通过RNAi技术下调Sirt1基因,观察其对72 h神经元轴突长度的影响;通过质粒转染过表达Sirt1基因或药物白藜芦醇(RES)激活Sirt1蛋白,检测其对72 h神经元轴突长度的影响。结果免疫荧光染色结果显示Sirt1位于海马神经元的生长圆锥以及胞体和突起,尤其是轴突末端;与正常对照组(Sirt1正常表达组)相比,Sirt1表达下调可显著缩短72 h海马神经元轴突的长度[由(178.3±3.2)μm缩短到(110.2±18.30)μm,P0.01];与正常对照组(Sirt1正常表达组)相比,基因过表达Sirt1可显著增加72 h海马神经元轴突的长度[由(178.3±3.2)μm增长到(310.6±39.5)μm,P0.01]。与药物对照组(DMSO处理组)相比,药物RES激活Sirt1蛋白亦可显著增加72 h海马神经元轴突的长度[由(292.8±11.2)μm增长到(525.1±49.7)μm,P0.01]。结论Sirt1在神经元的轴突生长中起着重要的作用,可作为轴突再生一个潜在的治疗靶点。
Objective To investigate the effect of silence regulatory protein 1 (Sirt1) on axonal outgrowth. Methods The hippocampal neurons was first isolated in vitro from rat embryos. The distribution and expression of Sirt1 were then detected 72 h later. The down-regulation of Sirt1 was induced by RNAi technology and up-regulation of Sirt1 was in-duced by overexpression of Sirt1 and resveratrol (RES). Immunofluorescence staining was used to examine the axon length. Results Immunofluorescence staining showed that Sirt 1 was located in neuronal cell body and neurite, especially in the distal axons. Down-regulation of Sirt1 significantly decreased axonal length compared with siRNA control group [(178.3 ± 3.2) μm vs. (110.2 ± 18.30) μm, P< 0.01 ]; Overexpression of Sirt1 significantly increased axonal length com-pared with eGFP control group [(178.3±3.2)μm vs (310.6±39.5)μm, P<0.01 ];Activation of Sirt1 by RES treatment al-so significantly increased axonal length compared with ve

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目的 克隆沉默信息调节因子1(SIRTl)基因的全长cDNA,构建含有SIRT1基因及其突变体T200I、E420K的重组真核表达载体,为进一步研究SIRT1基因功能奠定基础.方法 采用RT-PCR方法扩增SIRT1基因的全长cDNA,扩增产物通过双酶切将全长cDNA克隆到真核表达载体pcDNA3.1(+),得到pcDNA3.1 (+)-SIRT1重组质粒;同时采用定点突变法构建其突变体pcDNA3.1 (+)-T200I和pcDNA3.1(+)-E420K表达载体.重组质粒经酶切鉴定和DNA序列测定,筛选出重组成功的真核表达载体.结果 成功克隆了SIRT1基因全长cDNA,并成功构建了pcDNA3.1 (+)-SIRT1及其突变体的真核表达载体;阳性重组质粒酶切后经测序比对鉴定,与预期序列完全相符,转染293T细胞后可以表达带有HIS标签的SIRT1蛋白.结论 此方法可成功构建重组质粒pcDNA3.1(+)-SIRT1及其突变体pcDNA3.1(+)-T200I、pcDNA3.1(+)-E420K真核表达载体,为SIRT1基因及其突变体T200I、E420K的生物学功能研究提供了基因材料.
Objective To clone silent information regulator 1 (SIRT1) gene full-length cDNA,construct recombinant eukaryotic expression vector containing SIRT1 gene and its mutant T200I,E420K,so as to lay the foundation for further research of SIRT1 gene function.Methods RT-PCR amplified SIRT1 gene full-length cDNA.PCR products were cloned into the eukaryotic expression vector pcDNA3.1 (+) through double digestion and pcDNA3.1(+)-SIRT1 recombinant plasmid was obtained.Meanwhile,site-directed mutagenesis was applied to build its mutant pcDNA3.1 (+)-T200I and pcDNA3.1 (+)-E420K expression vector.Recombinant plasmid was identified by enzyme digestion and DNA sequencing and the recombinant eukaryotic expression vector of success was screened out.Results SIRT1 gene full-length cDNA was successfully cloned,and pcDNA3.1 (+)-SIRT1 eukaryotic expression vector and its mutant were also successfully constructed.Positive recombinant plasmid sequencing was compared after enzyme digestion,and it was completely

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目的 观察293T细胞经不同剂量137Cs γ射线照射后,细胞中沉默信息调节因子3(sirt3)及相关抗氧化因子的变化,研究sirt3基因在辐射防护中的抗氧化活性机理.方法 采用137Cs对293T细胞分别进行2、4、8和16 Gy照射,采用Real-Time PCR的方法,检测照后6、12、24和48 h,细胞中sirt3和超氧化物歧化酶2(SOD2) mRNA的表达水平变化;采用免疫印迹法,检测细胞中sirt3和SOD2蛋白水平随时间的变化;采用siRNA干扰和抑制剂处理的方法,检测sirt3与SOD2的作用关系;采用SOD Assay Kit-WST试剂盒检测细胞中SOD2酶活力的变化;流式细胞术检测细胞中活性氧(ROS)随时间的变化.结果 各组细胞中sirt3和SOD2的mRNA水平和蛋白质水平均表现出不同程度的上升,与0 Gy组比较,分别在12 h(t =6.75、13.59、6.59、10.13,P＜0.05)和24 h(t=6.80、8.73、11.09,P＜0.05)达到最大值;sirt3 siRNA干扰和抑制剂处理结果显示sirt3是SOD2的上游调控因子;照射24 h后细胞中SOD2的活性显著增加,与0 Gy组比较,差异有统计学意义(t =46.04、23.19、26.28、14.70,P＜0.05),细胞中ROS水平也发生相应变化.结论 sirt3可能通过对细胞中SOD2的表达量及活性的调控加强抗氧化保护系统,为临床辐射防护和治疗提供实验依据.
Objective To study the effects of the silent information regulator 3 (sirt3) and its relative anti-oxidation factors on ionizing radiation (IR)-induced damage in 293T cells.Methods 293T cells irradiated with 2,4,8,16 Gy of γ-rays,after 6,12,24 and 48 h of exposure,the expressions of sirt3 mRNA and SOD2 protein were examined by Real-Time PCR and immunoblotting assay,respectively.sirt3 siRNA was applied to knock down sirt3 in the cells.SOD2 activities were measured by a WST kit and the cellular ROS level was detected by a flow cytometry.Results The mRNA levels of sirt3 and SOD2 in each group campared with the 0 Gy group were reached the maximum at 12 h (t =6.75,13.59,6.59,10.13,P ＜ 0.05) and 24 h(t =6.80,8.73,11.09,P ＜ 0.05),and protein levels also increased.It was found that sirt3 was a upstream regulatory factor of SOD2.The activity of SOD2 were much higher at 24 h (t=46.04,23.19,26.28,14.70,P ＜ 0.05) than that in the 0 Gy group as well as the level of ROS.Conclusion Sirt

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SIRT3是线粒体内一种重要的去乙酰化酶,对协调线粒体内复杂的代谢反应起关键作用。在抑制肿瘤发生方面,SIRT3通过抗肿瘤代谢再编程保护正常细胞而避免向肿瘤细胞转化和肿瘤发生。SIRT3调节细胞对葡萄糖的摄取,增加细胞抗氧化能力,提高电子传递链中复合体的活性,促进细胞内NADPH的生成,控制能量产生等,从多层次和多角度实现抗肿瘤代谢再编程。这对临床肿瘤诊断和治疗有一定的理论指导,并为肿瘤治疗提供新的策略和方法。
SIRT3 is an important deacetylase in the mitochondria, and plays a critical role in coordinating multiple mitochondrial metabolism. With respect to its inhibition of tumor formation, SIRT3 protects normal cells from developing into tumor cells and tumorigenesis through against the reprogramming of tumor metabolism. SIRT3 regulates cells to intake the glucose,improves the ability of defending oxidation and the activities of oxidative phosphorylation complexes, promotes NADPH production and controls the production of energy. So SIRT3 indeed resists the reprogramming of tumor metabolism by multiple mitochondrial processes. This theory that SIRT3 can inhibit the reprogramming of tumor metabolism plays a guiding role in the early detection and treatment of clinical cancer, which will provide new strategies and methods for the treatment of cancer.

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组蛋白赖氨酸去甲基化酶1(lysine specific demethylase 1,LSD1)是重要的染色质修饰蛋白之一,可以通过调节染色质的结构调节基因的转录调控,进而影响肿瘤的发生、发展、侵袭、转移以及代谢异常等恶性潜能,是判断肿瘤预后的生物标志物。Sirtuins家族去乙酰化酶3(sirtuin3,SIRT3)基因是位于线粒体内的抑癌基因,通过调控肿瘤代谢异常以及氧化损伤行使抑癌基因的功能。本研究通过基因转录调控的手段,研究胰腺癌细胞PANC-1中LSD1与SIRT3的关系。方法:通过RNA干扰(RAN interference,RNAi)、免疫共沉淀(co-immunoprecipitation,CoIP)、染色质免疫共沉淀(chromatin immunoprecipitation assay,ChIP)及启动子活性分析等分子生物学实验手段,探讨LSD1与SIRT3在PANC-1细胞中的关系。结果:通过RNAi的手段干扰LSD1的表达,发现SIRT3基因转录水平和蛋白水平明显上升;通过蛋白相互作用的手段,发现LSD1可以与SIRT3转录调控的重要转录因子过氧化物酶增殖体激活受体辅激动子-1α(peroxisome proliferator-activated receptor gamma,coactivator 1 alpha,PGC-1α)相互作用;通过ChIP方法,发现LSD1与PGC-1α共同募集到SIRT3基因的启动子区域染色质上;通过启动子活性分析,发现LSD1基因可以显著抑制PGC-1α对SIRT3基因的转录调控。结论:LSD1可以表观遗传调控抑癌基因SIRT3的转录,为深入研究LSD1与肿瘤代谢异常以及氧化应激提供了理论依据。
Background and purpose: Lysine specific demethylase 1(LSD1) is an important chromatin modifier. It epigenetically regulates gene expression pattern through chromatin modification and participates in maintenance of tumor malignant properties, such as oncogenesis, development, invasion, migration and metabolic transformation. SIRT3 (sirtuin 3) is a mitochondria localized tumor suppressor and regulates tumor metabolic transformation and oxidative stress. The correlation between LSD1 and SIRT3 has never been reported before. This study aimed to elucidate the correlation between LSD1 and SIRT3 with gene transcriptional regulation methods. Methods: RNA interference technique, co-immunoprecipitation assay(CoIP), chromatin immune-precipitation assay(ChIP) and ifrelfy luciferase activity assay were employed to elucidate the correlation between LSD1 and SIRT3 in pancreatic cancer. Results:mRNA and protein levels of SIRT3 were signiifcantly elevated in LSD1 knock-down PANC-1 cells. LSD1 interacts

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沉默交配型信息调节因子2同源蛋白3（SIRT3）是Sirtuins脱乙酰基酶家族中的一员，是酵母沉默信息调节因子2的同源物，是一种依赖于烟酰胺腺嘌呤二核苷酸的Ⅲ类去乙酰化酶，它调节许多线粒体的蛋白质，这些蛋白质的功能关系到代谢、氧化应激及细胞存活。 SIRT3是线粒体适应性反应的调节因子，调节线粒体对应激等的适应性反应，包括代谢程序重排、加强抗氧化剂的防御机制等。另外，调控SIRT3可能是治疗线粒体功能障碍疾病的一个有希望的靶点。
Silent mating type information regulation 2 homolog 3(SIRT3) is a member of Sirtuins family and is also homologue of silence information regulator 2.SIRT3 is a kind of NAD +-dependent deacetylase that regulates the function of numerous mitochondrial proteins with roles in metabolism , oxidative stress,and cell survival.It is emerging as an instrumental regulator of the mitochondrial adaptive responses to stress ,in-cluding metabolic reprogramming and enhancing antioxidant defense mechanisms .Mitochondrial dysfunction is a key contributing factor in many diseases .The manipulation of SIRT3 could be a promising target for some diseases therapies.

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观察8周中等强度低负荷量训练对老龄雌性大鼠腓肠肌Bax和Bcl-2蛋白水平及去乙酰化酶1(SIRT1)/去乙酰化酶3(SIRT3)轴基因信使核糖核酸(mRNA)表达的影响。16只18月龄雌性SD大鼠随机分为对照组和运动组(各8只)。运动组在跑台上以15 km/h(60%~75%VO2max)进行有氧运动,15 min/d,5 d/周,持续运动8周;对照组自由生活。第8周末运动后24 h宰杀并测定腓肠肌指数、蛋白免疫印迹法测定腓肠肌Bax和Bcl-2蛋白水平;逆转录聚合酶链式反应(RT-PCR)测定SIRT3、SIRT1、锰超氧化物歧化酶(MnSOD)、半胱氨酸蛋白酶-3(Caspase-3)、过氧化物酶体增殖活化受体γ辅助活化因子-1α(PGC-1α)、线粒体转录因子A(TFAM)和核呼吸因子1(NRF1)mRNA水平。结果显示,运动组腓肠肌质量(P0.05)和腓肠肌指数均显著增加(P0.01)、Bax蛋白水平显著降低(P0.05),Bcl-2蛋白水平和Bcl-2/Bax值显著增加(P0.05);运动组SIRT3、SIRT1、PGC-1α、NRF1、TFAM、MnSOD mRNA水平显著增加(P0.05),Caspase-3 mRNA水平显著降低(P0.05)。结果表明:中等强度低负荷训练可延缓老龄雌性大鼠肌细胞凋亡信号的改变;SIRT1/SIRT3轴介导的内稳态机制在中等强度低负荷训练提升老龄大鼠骨骼肌线粒体更新速率及抗氧化酶水平起重要作用。
In order to observe the effects of 8-week medium intensity low load training on the levels of proteins Bax and Bcl-2 and the gene messenger RNA (mRNA) expression of axis sirtuin 1 (SIRT1)/sirtuin 3 (SIRT3) of gastrocne-mius of aged rats, the authors divided 16 18-month old female SD rats randomly into a control group and an exercise group, each of which contained 8 rats, let the rats in the exercise group do an aerobic exercise on a treadmill for con-secutive 8 weeks, at a speed of 15 km/h (with 60%~75%VO2max), 15 minutes a day, 5 days a week, let the rats in the control group live freely, in 24 hours after rat exercising at the end of week 8, killed the rats, measured gastrocnemius index, measured the levels of proteins Bax and Bcl-2 of gastrocnemius by means of Western blot analysis, measured the mRNA levels of SIRT3, SIRT1, manganese superoxide dismutase (MnSOD), Caspase 3, peroxisome prolifera-tor-activated receptor-γcoactivator-1 (PGC-1α), mitochondrial transcription f

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蛋白去乙酰化酶在细胞生理过程中发挥着极为重要的作用。人蛋白去乙酰化酶包括HDACⅠ、HDACⅡ、HDACⅢ和HDACⅣ4个家族。其中第Ⅲ类即Sir2(Silent information regulator 2)家族包括7个成员——SIRT1~SIRT7，每个成员都具有不同的细胞定位，并且发挥不同的生物学功能。作为主要定位于线粒体的组蛋白去乙酰化酶，SIRT3不仅调节细胞的能量代谢，并在细胞凋亡、肿瘤生长和一些疾病中发挥作用。文章综述了SIRT3在细胞代谢中的生物学功能以及其在心血管疾病中的研究进展。
Protein deacetylases play an extremely crucial role in cellular biological processes and have been cate-gorized into four families (HDACⅠ, HDACⅡ, HDACⅢ and HDACⅣ) in human. Of them, HDACⅢ, also known as the Sir2 (Silent information regulator 2) family, contains seven members, SIRT1?7, each exhibiting different cellular localiza-tion and biological function. As a major mitochondrial deacetylase, SIRT3 not only modulates cellular metabol-ism, but also plays important roles in apoptosis, tumor growth, aging and a number of other diseases. In this review, we summarize recent findings related to SIRT3 with an emphasis on its biological functions in regulating cell meta-bolism and its possible roles in cardiovascular diseases.

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