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CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury

Genes & Diseases 2024年第1期11卷 449-463页

作者： Yixin Ma Lili Huang Zheng Zhang Pengfei Yang Qingsong Chen Xujia Zeng Fangyan Tan Chunxia Wang xiongzhong ruan Xiaohui Liao Department of Nephrology The Second Affiliated HospitalChongqing Medical UniversityChongqing 400010China Department of Cell Biology and Genetics Chongqing Medical UniversityChongqing 400016China Centre for Nephrology Royal Free and University College Medical SchoolUniversity College LondonRoyal Free CampusRowland Hill StreetLondon NW32PFUnited Kingdom Centre for Lipid Research Key Laboratory of Molecular Biology on Infectious DiseasesMinistry of EducationChongqing Medical UniversityChongqing 400016China Kuanren Laboratory of Translational Lipidology Centre for Lipid ResearchSecond Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China

Reactive oxidative species(ROos)production-driven ferroptosis plays a role in acute kidney injury(Akl).However,its exact molecular mechanism is poorly *** receptor CD36 has important roles in oxidizing lipids,lipid accumulation,metabolic syndrome,and insulin resistance in chronic kidney disease,but its roles remain unexplored in *** present study investigated the role and mechanism of CD36 in regulating proximal tubular cell ferroptosis and *** expression of CD36 was found to be significantly up-regulated in AKI renal tissues and correlated with renal function,which might serve as an independent biomarker for AKl ***,in adult mice subjected to AKl,deletion of CD36(CD36-/-)induced tubular cell Ros accumulation,ferroptosis activation,and renal ***,combining LC-MS/MS,co-IP,and ubiquitination analyses revealed that CD36 could specifically bind to ferroptosis suppressor protein 1(FSP1)and regulate its ubiquitination at sites K16 and K24,leading to FSP1 degradation and progression of ferroptosis in *** present results emphasize a novel mechanism of CD36 in cisplatin-induced *** discovery of the special CD36 roles in promoting ferroptosis and AKI development by regulating the ubiquitination of FSP1 in proximal tubular cells may be potential therapeutic targets for ***,CD36 may play a key role in the progression of ***,targeting CD36 may provide a promising treatment option for AKI.

关键词： Acute kidney injury CD36 Ferroptosis FSP1 Ubiquitin-dependent degradation

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A genomic association study revealing subphenotypes of childhood steroid-sensitive nephrotic syndrome in a larger genomic sequencing cohort

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Genes & Diseases 2024年第4期11卷 400-410页

作者： Han Chan Fenfen Ni Bo Zhao Huimin Jiang Juanjuan Ding Li Wang Xiaowen Wang Jingjing Cui Shipin Feng Xiaojie Gao Xueying Yang Huan Chi Hao Lee Xuelan Chen Xiaoqin Li Jia Jiao Daoqi Wu Gaofu Zhang Mo Wang Yupeng Cun xiongzhong ruan Haiping Yang Qiu Li Department of Nephrology Children's Hospital of Chongqing Medical UniversityNational Clinical Research Center for Child Health and DisordersMinistry of Education Key Laboratory of Child Development and DisordersChongqing Key Laboratory of PediatricsChongqing 400014China Department of Nephrology Shenzhen Children's HospitalShenzhenGuangdong 518034China Department of Nephrology Kunming Children's HospitalKunming Medical UniversityKunmingYunnan 650228China Department of Nephrology Wuhan Children's HospitalTongji Medical College of Huazhong University of Science and TechnologyWuhanHubei 430015China Department of Nephrology Chengdu Women and Children Central HospitalChengduSichuan 610073China Pediatric Research Institute Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory DisordersChildren's Hospital of Chongqing Medical UniversityChongqing 400014China Department of Nephrology John Moorhead Research LaboratoryUniversity College London Medical SchoolRoyal Free CampusUniversity College LondonLondon NW32PFUnited Kingdom

Dissecting the genetic components that contribute to the two main subphenotypes of steroid-sensitive nephrotic syndrome(SSNS)using genome-wide association studies(GWAS)strategy is important for understanding the *** conducted a multicenter cohort study(360 patients and 1835 controls)combined with a GWAS strategy to identify susceptibility var-iants associated with the following two subphenotypes of ssNS:steroid-sensitive nephrotic syn-drome without relapse(SSNswR,181 patients)and steroid-dependent/frequent relapse nephrotic syndrome(SDNS/FRNS,179 patients).The distribution of two single-nucleotide poly-morphisms(SNPs)in ANKRD36 and ALPG was significant between SSNSWR and healthy controls,and that of two SNPs in GAD1 and HLA-DQA1 was significant between SDNS/FRNS and healthy ***,rs1047989 in HLA-DQA1 was a candidate locus for SDNS/FRNS but not for *** significant SNPs were observed between SSNSWR and SDNS/***,chromosome 2:171713702 in GAD1 was associated with a greater steroid dose(>0.75 mg/kg/d)upon relapse to first remission in patients with SDNS/FRNS(odds ratio=3.14;95%confidence interval,0.97-9.87;P=0.034).rs117014418 in APOL4 was significantly associated with a decrease in eGFR of greater than 20%compared with the baseline in SDNS/FRNS patients(P=0.0001).Protein-protein intersection network construction suggested that HLA-DQA1 and HLA-DQB1 function together through ***,SSNSWR belongs to non-HLA region-dependent nephropathy,and the HLA-DQA/DQB region is likely strongly associated with dis-ease relapse,especially in SDNS/*** study provides a novel approach for the GWAS strategy of SsNS and contributes to our understanding of the pathological mechanisms of SSNSWRandSDNS/FRNS.

关键词： Frequentrelapse Genome-wide association study Human leukocyte antigen region Steroid-sensitive nephrotic syndrome

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Targeting both sides of the GDF15-GFRALRET receptor complex:A new approach to achieve body weight homeostasis

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Genes & Diseases 2017年第4期4卷 183-184页

作者： Fei Li xiongzhong ruan Le Min The Editorial Office of Genes&Diseases Chongqing Medical UniversityChongqingChina John Moorhead Research Laboratory Centre for NephrologyUniversity College LondonLondonUK Division of Endocrinology Diabetesand HypertensionBrigham and Women’s HospitalBostonMAUnited States

Obesity is a chronic,complex disease,which is associated with several comorbidities,including diabetes mellitus,hypertension,and cardiovascular *** is estimated that the prevalence of obesity among both adults and children nearly tripled between 1975 and 2016,highlighting a huge unmet treatment ***,the currently available antiobesity drugs have serious side effects,which limit their long-term *** finding that the newly-identified brain GDF15-GFRAL-RET receptor signaling complex is involved in stress/disease-induced anorexia will certainly impact our knowledge of body weight homeostasis under healthy and disease *** on this breakthrough,a new class of GFRAL/RETbased drugs is highly anticipated for the treatment of obesity,as well as cancer-induced cachexia.

关键词： Anorexia Brain GDF15 GFRAL MIC-1 Obesity RET

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Whole-exome sequencing of a multicenter cohort identifies genetic changes associated with clinical phenotypes in pediatric nephrotic syndrome

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Genes & Diseases 2022年第6期9卷 1662-1673页

作者： Jia Jiao Li Wang Fenfen Ni Mo Wang Shipin Feng Xiaojie Gao Han Chan Xueying Yang Hao Lee Huan Chi Xuelan Chen Daoqi Wu Gaofu Zhang Baohui Yang Anshuo Wang Qin Yang Junli Wan Sijie Yu Xiaoqin Li Mei Wang Xiaofeng Chen Xianying Mai xiongzhong ruan Haiping Yang Qiu Li Department of Nephrology Children’s Hospital of Chongqing Medical UniversityNational Clinical Research Center for Child Health and DisordersMinistry of Education Key Laboratory of Child Development and DisordersChongqing Key Laboratory of PediatricsChongqing 400015PR China Department of Nephrology Chengdu Women and Children Central HospitalChengduSichuan 610091PR China Department of Nephrology Sheen Children’s HospitalShenzhenGuangdong 518034PR China Centre for Lipid Research&Key Laboratory of Molecular Biology for Infectious Diseases(Ministry of Education) Institute for Viral HepatitisDepartment of Infectious DiseasesThe Second Affiliated Hospital Chongqing Medical UniversityChongqing 400016PR ChinaJohn Moorhead Research LaboratoryCentre for NephrologyUniversity College London Medical SchoolRoyal Free CampusUniversity College LondonLondon WC1E 6BTUnited Kingdom

Understanding the association between the genetic and clinical phenotypes in children with nephrotic syndrome(NS)of different etiologies is critical for early clinical *** employed whole-exome sequencing(WES)to detect monogenic causes of NS in a multicenter cohort of 637 *** this study,a genetic cause was identified in 30.0%of the idiopathic steroid-resistant nephrotic syndrome(SRNS)*** than congenital nephrotic syndrome(CNS),there were no significant differences in the incidence of monogenic diseases based on the age at *** mutations were detected in 39.5%of patients with focal segmental glomerulosclerosis(FSGS)and 9.2%of those with minimal change disease(MCD).In terms of the patterns in patients with different types of steroid resistance,a single gene mutation was identified in 34.8%of patients with primary resistance,2.9%with secondary resistance,and 71.4%of children with multidrug *** the various intensified immunosuppressive therapies,tacrolimus(TAC)showed the highest response rate,with 49.7%of idiopathic SRNS patients achieving complete *** SRNS patients with monogenic disease showed a similar multidrug resistance pattern,and only 31.4%of patients with monogenic disease achieved a partial remission on *** an average 4.1-year follow-up,21.4%of idiopathic SRNS patients with monogenic disease progressed to end-stage renal disease(ESRD).Collectively,this study provides evidence that genetic testing is necessary for presumed steroid-resistant and idiopathic SRNS patients,especially those with primary and/or multidrug resistance.

关键词： Clinical phenotypes Genetic phenotypes Multicenter cohort Nephrotic syndrome Pediatric Whole-exome sequencing

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“脂质肾毒性学说”的最新研究进展

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中国科学：生命科学 2018年第1期48卷 47-55页

作者：阮雄中深圳大学医学部阿什利康-深圳大学联合肾脏病研究所(Hon.)深圳518060 John Moorhead Laboratory Centre for NephrologyUniversity College LondonRowland Hill StreetLondon NW32PFUK

1982年,Moorhead教授综合了高血脂症和肾脏病领域的很多不同实验结果提出"脂质肾毒性假说",指出当最初的肾小球损伤因素消失后,持续的伴随性高血脂症和蛋白尿会引起肾脏损伤,这个过程与动脉粥样硬化类似,并提出"肾小球-动脉硬化"的概念.... 详细信息

1982年,Moorhead教授综合了高血脂症和肾脏病领域的很多不同实验结果提出"脂质肾毒性假说",指出当最初的肾小球损伤因素消失后,持续的伴随性高血脂症和蛋白尿会引起肾脏损伤,这个过程与动脉粥样硬化类似,并提出"肾小球-动脉硬化"的概念.自1982年以来,越来越多的证据支持该假说,即脂质异常会引起动脉粥样硬化和肾小球硬化症.本综述将讨论脂质肾毒性假说的最新研究进展.例如,伴随慢性肾脏病的炎症应激通过上调脂蛋白受体增加胆固醇吸收、减少细胞胆固醇外流,以及增加细胞的胆固醇合成来影响细胞内脂质稳态,最终引起胆固醇重新分布并聚集在肾脏、血管、肝脏以及其他组织中;同时细胞内胆固醇的大量聚集会引起组织损伤以及血浆胆固醇水平的相对下降("胆固醇重新分布学说"),出现了血LDL胆固醇不高,但心肾损害却加重的临床现象.另外,研究还发现炎症应激会引起一定程度的他汀抵抗,提示慢性肾脏病人群在血脂代谢稳态,血脂的风险评估和治疗上都有其特殊性.这些现象改变了对脂质介导的肾脏以及血管损伤的发病机理的传统认识,挑战了传统的对肾脏和心血管疾病发病风险的临床评估方法,并促使研究者们思考针对CKD降脂治疗的新思路.

关键词：脂质炎症肾脏病他汀类药物

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代谢性炎症与脂质异常分布在NAFLD发病中的作用

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重庆医科大学学报 2017年第7期42卷 768-770页

作者：阮雄中重庆医科大学脂糖代谢性疾病重庆市重点实验室

代谢性炎症主要指营养物和代谢过剩所触发的,由内脏组织(主要是脂肪组织)介导的,多种细胞(包括巨噬细胞)与细胞因子共同参与的慢性低丰度性炎症反应。CD36(fatty acid translocase,cluster of differentiation 36,FAT/CD36)又名脂肪酸... 详细信息

代谢性炎症主要指营养物和代谢过剩所触发的,由内脏组织(主要是脂肪组织)介导的,多种细胞(包括巨噬细胞)与细胞因子共同参与的慢性低丰度性炎症反应。CD36(fatty acid translocase,cluster of differentiation 36,FAT/CD36)又名脂肪酸转运酶,被认为是将机体的天然免疫和代谢有机联合在一起的重要靶点。脂肪酸能诱导肝细胞CD36的表达,并与Toll样受体(toll-like receptors,TLR)TLR4和TLR6结合成异三聚体,促使炎症反应的发生。在代谢性炎症作用下,肝脏摄取合成脂质增加,导致非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)脂肪肝发生和发展。CD36可能成为治疗NAFLD的潜在靶点。

关键词：代谢性炎症 CD36 非酒精性脂肪肝

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代谢性炎症与非酒精性脂肪性肝病的发生与发展

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中华消化杂志 2020年第9期40卷 581-584页

作者：阮雄中陈压西重庆医科大学感染性疾病分子生物学教育部重点实验室重庆医科大学脂质研究中心重庆医科大学脂糖代谢性疾病重庆市重点实验室400016

代谢性炎症在非酒精性脂肪性肝病(NAFLD)的发生与发展过程中扮演了极其重要的角色。现重点论述肝脏炎症的产生,以及炎症应激下肝细胞内脂质稳态失衡、脂质发生"二次异常转运",过多的脂质又通过内质网应激、氧化应激等发挥脂毒性作用,加... 详细信息

代谢性炎症在非酒精性脂肪性肝病(NAFLD)的发生与发展过程中扮演了极其重要的角色。现重点论述肝脏炎症的产生,以及炎症应激下肝细胞内脂质稳态失衡、脂质发生"二次异常转运",过多的脂质又通过内质网应激、氧化应激等发挥脂毒性作用,加重和放大肝脏的炎症效应,从而导致NAFLD由单纯性肝脂肪变性向脂肪性肝炎演变的病理生理过程,旨在为临床深入了解NAFLD的发病机制和发现新的治疗靶点提供理论依据。

关键词：脂肪肝代谢性炎症脂质重分布脂质稳态

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血管平滑肌SCAP过表达抑制自噬促进脂质积聚的机制研究

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陆军军医大学学报 2022年第9期44卷 891-897页

作者：饶雨涵李丹阳侯晓俐姚盈程苏玉陈压西阮雄中重庆医科大学脂糖代谢性疾病重庆市重点实验室脂质研究中心重庆400016

目的探讨固醇调节元件结合蛋白裂解活化蛋白(sterol regulatory element binding proteins cleavage activating protein,SCAP)对血管平滑肌细胞(vascular smooth muscle cells,VSMCs)泡沫化的影响及其分子机制。方法构建LV-SCAP与LV-Control血管平滑肌细胞系,免疫印迹法检测SCAP及其下游相关蛋白nSREBP2表达水平;油红O染色观察负荷LDL胆固醇后脂滴积聚,酶标仪检测细胞总胆固醇(total cholesterol,TC)、甘油三酯(triglycerides,TG)水平;单丹磺酰尸胺(monodansyl cadaverine,MDC)染色检测自噬小泡聚集;Western blot检测自噬相关蛋白LC3b、P62与AMPK-mTOR通路表达;mTOR抑制剂雷帕霉素处理LV-SCAP过表达细胞株,Western blot与油红O染色验证处理后效果。结果与LV-Control组相比,LV-SCAP组nSREBP2表达明显上调(P<0.05),经LDL胆固醇负荷后产生的脂滴增多,TC、TG水平明显增高(P<0.05);LV-SCAP组细胞内自噬小泡聚集减少,自噬相关蛋白LC3b下调,P62上调,p-AMPK/AMPK水平降低,p-mTOR/mTOR水平升高(P<0.05)。Rapa处理结果显示LC3b表达增加,P62水平降低(P<0.05),油红O染色脂滴沉积减少(P<0.05)。结论SCAP可能通过影响AMPK-mTOR信号通路抑制血管平滑肌细胞的自噬过程,促进其泡沫化,进而参与血管动脉粥样硬化的发生发展。

关键词： SCAP 血管平滑肌细胞自噬 AMPK-mTOR信号通路

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CD36基因缺失通过上调PTP1B基因表达降低小鼠肌肉胰岛素敏感性

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南方医科大学学报 2022年第3期42卷 392-398页

作者：陈琳曾晗秦虹阮雄中杨萍重庆医科大学脂糖代谢性疾病重庆市重点实验室重庆400016

目的探讨在正常饮食状态下,CD36基因缺失对小鼠肌肉胰岛素信号通路的影响及作用机制。方法野生型小鼠(WT)和CD36基因敲除小鼠(CD36^(-/-))给予正常饮食喂养14周(n=12)。小鼠禁食4 h,腹腔注射胰岛素(1 U/kg)进行胰岛素耐量实验。Real-tim... 详细信息

目的探讨在正常饮食状态下,CD36基因缺失对小鼠肌肉胰岛素信号通路的影响及作用机制。方法野生型小鼠(WT)和CD36基因敲除小鼠(CD36^(-/-))给予正常饮食喂养14周(n=12)。小鼠禁食4 h,腹腔注射胰岛素(1 U/kg)进行胰岛素耐量实验。Real-timePCR检测小鼠肌肉胰岛素受体(IR)、胰岛素受体底物1/2(IRS1/2)、蛋白酪氨酸磷酸酶1B(PTP1B)基因表达。Western blot检测小鼠肌肉蛋白激酶B(AKT)、IR、IRS1/2和PTP1B的蛋白表达。免疫共沉淀(Co-IP)检测肌肉IR和IRS1的酪氨酸磷酸化程度。染色质免疫共沉淀(ChIP)技术检测肌肉PTP1B启动子组蛋白乙酰化水平。结果在正常饮食状态下,与WT小鼠相比,CD36^(-/-)小鼠的胰岛素耐量显著增强(P0.05)。Co-IP实验显示IR和IRS1的酪氨酸磷酸化水平在CD36^(-/-)小鼠中显著降低(P<0.05)。CD36^(-/-)小鼠肌肉中PTP1B mRNA和蛋白表达均高于WT小鼠(P<0.05),ChIP实验显示PTP1B基因启动子的组蛋白乙酰化水平显著升高(P<0.01)。腹腔注射PTP1B的抑制剂可改善CD36^(-/-)小鼠的胰岛素敏感性。结论在正常饮食条件下,CD36基因对于维持生理肌肉胰岛素敏感性十分重要,小鼠CD36基因缺失通过上调PTP1B基因表达,诱导IR、IRS1去酪氨酸磷酸化而使肌肉胰岛素信号传导受损。

关键词： CD36 胰岛素敏感性肌肉 PTP1B

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CD36在棕榈酸诱导的HepG2细胞炎症反应中的作用

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重庆医科大学学报 2017年第7期42卷 864-869页

作者：韦莉杨萍陈压西阮雄中赵蕾重庆医科大学脂糖代谢性疾病重庆市重点实验室脂质研究中心重庆400016

目的:探讨白细胞分化抗原36(cluster of differentiation 36,CD36)是否参与了棕榈酸诱导的HepG2细胞炎症反应。方法:给予HepG2细胞不同浓度的棕榈酸(0.00、0.08、0.16、0.32、0.64 mmol/L)处理24 h,使用实时荧光定量PCR方法检测CD36和... 详细信息

目的:探讨白细胞分化抗原36(cluster of differentiation 36,CD36)是否参与了棕榈酸诱导的HepG2细胞炎症反应。方法:给予HepG2细胞不同浓度的棕榈酸(0.00、0.08、0.16、0.32、0.64 mmol/L)处理24 h,使用实时荧光定量PCR方法检测CD36和炎症因子的mRNA表达水平,Western blot检测CD36蛋白表达水平。然后利用小RNA干扰技术,构建低表达CD36的HepG2细胞(CD36RNAi HepG2)和对照细胞(NCi HepG2)模型。通过实时荧光定量PCR检测棕榈酸负荷的NCi HepG2和CD36RNAi HepG2中炎症因子的表达情况,荧光探针DCFH DA法检测细胞内活性氧含量,Western blot检测细胞核内的核转录因子-κB的蛋白表达水平。结果:棕榈酸能够上调HepG2细胞中CD36及炎症因子——肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白介素-6(interleukin-6,IL-6)的表达。棕榈酸浓度分别为0.00、0.08、0.16、0.32及0.64 mmol/L时,CD36的mRNA表达相对值分别为(1.001±0.078)、(1.510±0.341)(q=4.763,P=0.007)、(1.780±0.070)(q=7.301,P=0.000)、(2.510±0.141)(q=14.16,P=0.000)及(2.103±0.150)(q=10.34,P=0.000)。TNF-α的mRNA表达相对值分别为(1.000±0.098)、(1.571±0.177)(q=1.598,P=0.141)、(1.725±0.274)(q=2.016,P=0.071)、(2.113±0.341)(q=3.102,P=0.011)及(5.282±0.855)(q=11.940,P=0.000)。IL-6的mRNA表达相对值分别为(0.999±0.047)、(1.791±0.596)(q=1.486,P=0.168)、(2.119±0.294)(q=2.107,P=0.061)、(2.808±0.147)(q=3.398,P=0.007)及(6.916±1.284)(q=11.130,P=0.000)。抑制HepG2细胞中CD36表达,可以显著降低棕榈酸所诱导的细胞内活性氧(reactive oxygen species,ROS)增加和核转录因子-κB在核内分布的增强,降低HepG2细胞内炎症因子表达水平。NCi HepG2、NCi HepG2+棕榈酸组及CD36 RNAi HepG2+棕榈酸组的ROS相对含量分别为(1.000±0.113)、(1.968±0.293)(与NCi组相比,t=6.888,P=0.000)、(0.519±0.129)(与NCi+棕榈酸组相比,t=10.106,P=0.000)。NCi HepG2、NCi HepG2+棕榈酸组及CD36 RNAi HepG2+棕榈酸组的核转录因子-κB的蛋白相对值分别为(0.997±0.093)、(2.443±0.085)(与NC相比,t=19.892,P=0.000)、(1.607±0.107)(与NCi+棕榈酸组相比,t=10.607,P=0.000)。抑制HepG2细胞中CD36表达后,棕榈酸浓度分别为0.08、0.16、0.32及0.64 mmol/L时,NCi HepG2及CD36 RNAi HepG2组的TNF-α的表达水平分别为(1.004±0.113)和(0.185±0.071)(t=10.716,P=0.000);(1.009±0.160)和(0.221±0.028)(t=8.389,P=0.001);(1.008±0.163)和(0.173±0.011)(t=8.780,P=0.001);(1.009±0.163)和(0.147±0.013)(t=9.013,P=0.000)。抑制HepG2细胞中CD36表达后,棕榈酸浓度分别为0.08、0.16、0.32及0.64 mmol/L时,NCi HepG2及CD36 RNAi HepG2组的IL-6的表达水平分别为(1.044±0.347)和(0.207±0.033)(t=4.121,P=0.015);(1.006±0.139)和(0.198±0.007)(t=10.110,P=0.001);(1.001±0.052)和(0.125±0.006)(t=28.443,P=0.000);(1.012±0.188)和(0.114±0.015)(t=8.367,P=0.001)。结论:棕榈酸能够上调HepG2细胞CD36表达,促进HepG2炎症反应;抑制CD36可能通过减少氧化应激、抑制核转录

关键词： CD36 棕榈酸 HepG2 炎症

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