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Progesterone receptor membrane component 1 as a potential prognostic biomarker for hepatocellular carcinoma

World Journal of Gastroenterology 2018年第10期24卷 1152-1166页

作者： Hung-Wen Tsai Chung-Liang Ho Shu-Wen Cheng Yih-Jyh Lin Chou-Cheng Chen Pin-nan Cheng Chia-Jui Yen Ting-Tsung Chang Po-Min Chiang Shih-Huang Chan Cheng-Hsun Ho Shu-Hui Chen Yi-Wen Wang nan-haw chow Jou-Chun Lin Institute of Clinical Medicine National Cheng Kung University Hospital College of Medicine National Cheng Kung University Department of Pathology National Cheng Kung University Hospital College of Medicine National Cheng Kung University Institute of Basic Medical Sciences College of Medicine National Cheng Kung University Center of Infectious Disease and Signaling Research College of Medicine National Cheng Kung University Department of Surgery National Cheng Kung University Hospital College of Medicine National Cheng Kung University Department of Internal Medicine National Cheng Kung University Hospital College of Medicine National Cheng Kung University Department of Statistics College of Management National Cheng Kung University Research Center of Clinical Medicine National Cheng Kung University Hospital College of Medicine National Cheng Kung University Department of Chemistry College of Sciences National Cheng Kung University

AIM To investigate the clinicopathological significance of progesterone receptor membrane component 1(PGRMC1) and PGRMC2 in hepatocellular carcinoma(HCC). METHODS We performed immunohistochemical staining to evaluate the estrogen receptor(ER), progesterone receptor(PR), PGRMC1, and PGRMC2 in a clinical cohort consisting of 89 paired HCC and non-tumor liver samples. We also analyzed HCC data(n = 373) from The Cancer Genome Atlas(TCGA). We correlated the expression status of PGRMC1 and PGRMC2 with clinicopathological indicators and the clinical outcomes of the HCC patients. We knocked down or overexpressed PGRMC1 in HCC cell lines to evaluate its biological significance in HCC cell proliferation, differentiation, migration, and invasion. RESULTS We found that few HCC cases expressed ER(5.6%) and PR(4.5%). In contrast, most HCC cases expressed PGRMC1(89.9%) and PGRMC2(100%). PGRMC1 and PGRMC2 exhibited significantly lower expression in tumor tissue than in non-tumor tissue(P < 0.001). Lower PGRMC1 expression in HCC was significantly associated with higher serum alpha-fetoprotein expression(P = 0.004), poorer tumor differentiation(P = 0.045) and liver capsule penetration(P = 0.038). Low PGRMC1 expression was an independent predictor for worse disease-free survival(P = 0.002, HR = 2.384,CI: 1.377-4.128) in our cases, as well as in the TCGA cohort(P < 0.001, HR = 2.857, CI: 1.781-4.584). The expression of PGRMC2 did not relate to patient outcome. PGRMC1 knockdown promoted a poorly differentiated phenotype and proliferation of HCC cells in vitro, while PGRMC1 overexpression caused the opposite effects.CONCLUSION PGRMC1 is a non-classical hormonal receptor that negatively regulates hepatocarcinogenesis. PGRMC1 down-regulation is associated with progression of HCC and is a poor prognostic indicator.

关键词： progesterone receptor membrane component 1 hormonal receptor proliferation hepatocellular carcinoma prognosis

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褪黑素通过改善胆汁酸代谢减轻胆汁淤积肝损伤

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陆军军医大学学报 2024年第11期46卷 1187-1193页

作者：张弘佳谭雅赵楠柴进陆军军医大学(第三军医大学)第一附属医院消化内科全军消化病研究所胆汁淤积肝病中心代谢相关脂肪性肝病中心重庆400038

目的初步探究褪黑素(melatonin,Mel)减轻胆酸(cholic acid,CA)诱导的胆汁淤积肝损伤的机制。方法将15只8周龄雄性C57BL/6J小鼠按随机数字表法分为3组(n=5):对照组、1%CA组和1%CA+Mel组,对照组喂养正常饮食,1%CA组和1%CA+Mel组喂养1%CA饮... 详细信息

目的初步探究褪黑素(melatonin,Mel)减轻胆酸(cholic acid,CA)诱导的胆汁淤积肝损伤的机制。方法将15只8周龄雄性C57BL/6J小鼠按随机数字表法分为3组(n=5):对照组、1%CA组和1%CA+Mel组,对照组喂养正常饮食,1%CA组和1%CA+Mel组喂养1%CA饮食14 d构建胆汁淤积小鼠模型,1%CA+Mel组同时腹腔注射褪黑素(100 mg/kg)。对1%CA组和1%CA+Mel组小鼠的肝组织进行α-SMA免疫组化染色,采用RT-qPCR检测小鼠肝纤维化相关指标的mRNA表达水平。采用液相色谱-串联质谱联用技术检测肝脏总胆汁酸,自动生化分析仪检测血清总胆汁酸。为了进一步了解胆汁酸代谢的机制,采用RT-qPCR检测小鼠胆汁酸合成和肝脏解毒酶相关指标的mRNA表达水平,Western blot检测胆汁酸合成和肝脏解毒酶相关指标的蛋白表达水平。结果与1%CA组相比,1%CA+Mel组的小鼠肝纤维化相关指标Tgfβ1、ColⅠa1、ColⅡa1和α-SMA的mRNA表达水平明显降低(P<0.05),小鼠肝组织α-SMA免疫组化染色结果显示肝星状细胞活化明显减少。与1%CA组相比,1%CA+Mel组小鼠血清与肝脏中胆汁酸含量显著减少,其中TCA含量显著降低,胆汁酸合成酶胆固醇7α-羟化酶(cholesterol 7α-hydroxylase,Cyp7a1)和Cyp8b1的mRNA水平均显著降低,肝脏解毒酶Cyp2b10和尿苷二磷酸葡萄糖醛基酶1A1(udp-glucuronosyltransferase,Ugt1a1)的mRNA水平明显升高,Cyp2b10和胆盐磺基转移酶(sulfotransferase family 2A member 1,Sult2a1/2)的蛋白水平明显升高(P<0.05)。结论褪黑素通过减少胆汁酸合成和增加肝脏解毒酶的方式改善胆汁淤积。

关键词：肝损伤胆汁淤积褪黑素胆汁酸代谢

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黄蒲通窍胶囊改善Wilson病铜负荷大鼠的认知损害:基于抑制内质网应激介导的凋亡途径

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南方医科大学学报 2024年第3期44卷 447-454页

作者：张笑颜王谢王杰邵楠蔡标谢道俊安徽中医药大学中西医结合学院安徽合肥230012 安徽中医药大学第一临床医学院安徽合肥230012 安徽中医药大学护理学院安徽合肥230012 安徽中医药大学第一附属医院脑病中心安徽合肥230031

目的探究黄蒲通窍胶囊(HPTQ)对Wilson病(WD)铜负荷大鼠模型的神经保护作用及其可能的作用机制。方法SD大鼠随机分为6组:对照组、模型组、黄蒲通窍胶囊低剂量组(HPTQ-L,0.47 g/kg)、黄蒲通窍胶囊中剂量组(HPTQ-M,1.41 g/kg)、黄蒲通窍胶... 详细信息

目的探究黄蒲通窍胶囊(HPTQ)对Wilson病(WD)铜负荷大鼠模型的神经保护作用及其可能的作用机制。方法SD大鼠随机分为6组:对照组、模型组、黄蒲通窍胶囊低剂量组(HPTQ-L,0.47 g/kg)、黄蒲通窍胶囊中剂量组(HPTQ-M,1.41 g/kg)、黄蒲通窍胶囊高剂量组(HPTQ-H,4.23 g/kg)、青霉胺组(PCA,0.09 g/kg),10只/组。通过含铜(1 g/kg)饲料、含铜(0.185%)水喂养12周构建WD铜负荷大鼠模型,铜离子(Cu)测定试剂盒检测肝铜、24 h尿铜水平;Morris水迷宫实验评估大鼠学习记忆能力;HE染色法观察海马组织CA1区神经元形态学改变;TUNEL染色观察海马组织CA1区神经元凋亡水平;免疫荧光法检测内质网应激(ERS)标志蛋白GRP78的表达情况;RT-qPCR和Western blot法检测GRP78、CHOP、caspase-12、cleaved caspase-9、cleaved caspase-3基因和蛋白表达水平。结果与对照组比较,模型组肝铜及24 h尿铜水平明显升高(P<0.01);学习记忆能力明显减弱(P<0.01);CA1区海马神经元出现损伤;TUNEL阳性神经元数量增多(P<0.01);GRP78、CHOP、caspase-12、cleaved caspase-9、cleaved caspase-3基因和蛋白表达水平升高(P<0.01)。与模型组比较,HPTQ各组及PCA组肝铜水平降低、24 h尿铜水平升高(P<0.01);学习记忆能力改善(P<0.01,P<0.05);海马神经元损伤减轻;TUNEL阳性神经元数量减少(P<0.01);GRP78、CHOP、caspase-12、cleaved caspase-9、cleaved caspase-3基因和蛋白表达水平降低(P<0.01,P<0.05)。结论HPTQ对WD铜负荷大鼠模型具有神经保护作用,其机制可能与抑制ERS介导的凋亡途径有关。

关键词： Wilson病黄蒲通窍胶囊认知损害内质网应激凋亡

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Green Tea Polyphenols Prevent Early Vascular Aging Induced by High-Fat Diet via Promoting Autophagy in Young Adult Rats

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Current Medical Science 2022年第5期42卷 981-990页

作者： Xiang-tian XIAO Shui-qing HE nan-nan WU Xue-chun LIN Jing ZHAO Chong TIAN Medical College of Wuhan University of Science and Technology Wuhan430081China Department of Nutrition and Food Hygiene Hubei Key Laboratory of Food Nutrition and SafetySchool of Public HealthTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China School of Public Health and Management Research Center for Medicine and Social DevelopmentInnovation Center for Social Risk Governance in HealthChongqing Medical UniversityChongqing400016China School of Nursing Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Epidemiology studies indicate that green tea polyphenols(GTP)perform a protective effect on cardiovascular diseases,but the underlying mechanisms are complex.The present study aimed to investigate the effect of GTP on high-fat diets(HFD)induced-early vascular aging.Methods Six-week young adult Wistar rats were fed with standard chow or HFD in the presence and absence of GTP(200 mg/kg body weight)for 18 weeks.In vitro experiment,human umbilical vascular endothelial cells(HUVECs)were treated with palmitic acid(PA)and GTP.Results The results showed that GTP alleviated the disorganized arterial wall and the increased intima-media thickness induced by HFD.In addition,the vascular oxidative injury was suppressed following GTP treatment.Furthermore,GTP elevated the ratio of LC3-II/LC3-I and suppressed expression of p62/SQSTM1,and restored SIRT3 expression in the aorta of HFD rats.Consistently,in cultured HUVECs,GTP inhibited cell senescence indicated by SA-β-gal and promoted endothelial autophagy compared with the PA treatment group.The activity of SIRT3 was specifically inhibited by 3-TYP,and the protective effect of GTP was consequently abolished.Conclusion The findings indicated that GTP protected against early vascular senescence in young HFD rats via ameliorating oxidative injury and promoting autophagy which was partially regulated by the SIRT3 pathway.

关键词： high-fat diets green tea polyphenols early vascular aging autophagy Sirtuin 3

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基于代谢组学的六神曲降血脂作用机制研究

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中国中药杂志 2024年第3期49卷 770-778页

作者：刘金辉田颖颖赵新月李依林吕英楠刘闯林兆洲王子健左泽平王志斌北京中医药大学中药学院北京100029 北京同仁堂股份有限公司科学研究所北京100079

研究六神曲对高脂血症模型大鼠的治疗作用,并借助非靶向代谢组学探究六神曲降血脂的作用机制。通过给予高脂饲料构建混合型高脂血症模型大鼠,造模成功后分为模型组、普伐他汀钠组(4.4 mg·kg^(-1))、血脂康组(0.1 g·kg^(-1))、六神曲... 详细信息

研究六神曲对高脂血症模型大鼠的治疗作用,并借助非靶向代谢组学探究六神曲降血脂的作用机制。通过给予高脂饲料构建混合型高脂血症模型大鼠,造模成功后分为模型组、普伐他汀钠组(4.4 mg·kg^(-1))、血脂康组(0.1 g·kg^(-1))、六神曲高剂量组(2.4 g·kg^(-1))、六神曲中剂量组(1.2 g·kg^(-1))、六神曲低剂量组(0.6 g·kg^(-1)),给药周期4周,每日1次,空白组和模型组给予等体积超纯水。以血清脂质水平、肝脏苏木精-伊红(hematoxylin-eosin,HE)染色作为考察指标,研究六神曲对混合型高脂血症的干预作用,并通过非靶向代谢组学技术分析六神曲对混合型高脂血症模型大鼠血浆内代谢物变化的影响,而后通过代谢物通路富集,分析六神曲发挥降血脂作用的机制。结果显示,与模型组相比,六神曲尤其是高剂量可显著降低总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-c)含量(P<0.05或P<0.01);肝脏HE染色发现高剂量组脂肪细胞数量有一定程度的减少。通过非靶向代谢组学技术筛选得到的潜在生物标志物有3-磷酸甘油、鞘氨醇、1-磷酸鞘氨醇、脱氧尿苷等,主要涉及鞘脂代谢过程、甘油磷脂代谢过程、甘油酯代谢途径、嘧啶代谢途径共4条可能与脂质代谢相关的代谢通路。该研究为深入探究六神曲降血脂机制提供借鉴,对进一步推广六神曲的临床应用及增加适应症具有重要意义。

关键词：代谢组学高脂血症六神曲脂质代谢 1-磷酸鞘氨醇

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Carbohydrate-associated epitope-based anti-cancer drugs and vaccines

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Advances in Bioscience and Biotechnology 2013年第9期4卷 18-23页

作者： Gregory Lee Cheng-Yuan Huang Song-nan chow Chin-Hsiang Chien Department of Obstetrics/Gynecology National Taiwan University Hospital Taipei Chinese Taipei Institute of Biochemistry and Molecular Biology National Yang Ming University Taipei Chinese Taipei UBC Center for Reproductive Health University of British Columbia Vancouver Canada Vancouver BioTech Ltd. Vancouver Canada

RP215 is one of the three thousand monoclonal antibodies (Mabs) which were generated against the OC-3-VGH ovarian cancer cell line. RP215 was shown to react with a carbohydrate-associated epitope located specifically on glycoproteins, known as CA215, from cancer cells. Further molecular analysis by matrix adsorption laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) revealed that CA215 consists mainly of immunoglobulin super-family (IgSF) proteins, including immunoglobulins, T-cell receptors, and cell adhesion molecules, as well as several other unrelated proteins. Peptide mappings and glycoanalysis were performed with CA215 and revealed high-mannose and complex bisecting structures with terminal sialic acid in N-glycans. As many as ten O-glycans, which are structurally similar to those of mucins, were also identified. In addition, two additional O-linked glycans were exclusively detected in cancerous immunoglobulins but not in normal B cell-derived immunoglobulins. Immunizations of mice with purified CA215 resulted in the predominant generation of RP215-related Mabs, indicating the immunodominance of this carbohydrate-associated epitope. Anti-idiotype (anti-id) Mabs of RP215, which were generated in the rat, were shown to contain the internal images of the carbohydrate-associated epitope. Following immunizations of these anti-id Mabs in mice, the resulting anti-anti-id (Ab3) responses in mice were found to be immunologically similar to that of RP215. Judging from these observations, anti-id Mabs, which carry the internal image of the RP215-specific epitope, may be suitable candidates for anticancer vaccine development in humans.

关键词： Anti-Cancer Drugs Anti-Cancer Vaccines Anti-Idiotype CA215 Carbohydrate-Associated Epitope Immunodominance RP215

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生物类似药证据链完备性的合成P值法评估(英文)

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药物分析杂志 2015年第5期35卷 832-836页

作者： Zhi-ying Pan nan Zhang Yao Yu Eric Chi Shein-chung chow Amgen Inc. Thousand Oaks California USA Duke University School of Medicine Durham North Carolina USA

最近几年,许多生物制药/生物技术公司对研发生物类似药物的兴趣越来越强。根据生物类似药物的研发需求,美国药监局(FDA)在2012年颁布了3个相关指导原则草案。FDA在这3个指导原则中表示,对于生物类似药物的注册申请的全部提交资料采用"... 详细信息

最近几年,许多生物制药/生物技术公司对研发生物类似药物的兴趣越来越强。根据生物类似药物的研发需求,美国药监局(FDA)在2012年颁布了3个相关指导原则草案。FDA在这3个指导原则中表示,对于生物类似药物的注册申请的全部提交资料采用"证据链完备性(totality-of-the-evidence)"的方法来审查,并鼓励研发企业使用"逐步递进法stepwise"来找出与原研产品相比,仿制生物制品在每一工艺步骤中的残余不确定度,进而在后续的研发步骤中设法解决这些残余不确定度。尽管要获得"具有较小不确定度的充足证据链完备性"这样的概念可以理解,但是,如何根据提交的所有注册申请信息客观地评价"证据链完备性",以及如何基于已有信息确定下一步研发步骤的程度和范围仍然是需解决的具体操作问题。本研究探索了费舍尔合成P值的概念(Fisher,1932)在等效性检验设置中的应用,更具体地说,在一个生物类似药物的临床研究中,根据"逐步递进法"和"临床证据完备性"的概念,用它来设计和分析2个生物类似药物的临床相似性。

关键词：生物相似性证据链完备性逐步法方式合成P值法 P值的权重总和法 Fisher法等效性检验

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Folic acid attenuates high-fat diet-induced steatohepatitis via deacetylase SIRT1-dependent restoration of PPARα

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World Journal of Gastroenterology 2020年第18期26卷 2203-2220页

作者： Feng-Zhi Xin Ze-Hua Zhao Rui-nan Zhang Qin Pan Zi-Zhen Gong Chao Sun Jian-Gao Fan Center for Fatty Liver Department of GastroenterologyXinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200092China Shanghai Key Lab of Pediatric Gastroenterology and Nutrition Shanghai 200092China Shanghai Institute for Pediatric Research Shanghai Jiao Tong University School of MedicineShanghai 200092China Department of Pediatric Surgery Xinhua HospitalShanghai Jiao Tong University School of MedicineShanghai 200092China

BACKGROUND Folic acid has been shown to improve non-alcoholic steatohepatitis(NASH),but its roles in hepatic lipid metabolism,hepatic one-carbon metabolism,and gut microbiota are still unknown.AIM To demonstrate the role of folic acid in lipid metabolism and gut microbiota in NASH.METHODS Twenty-four Sprague-Dawley rats were assigned into three groups:chow diet,high-fat diet(HFD),and HFD with folic acid administration.At the end of 16 wk,the liver histology,the expression of hepatic genes related to lipid metabolism,one-carbon metabolism,and gut microbiota structure analysis of fecal samples based on 16 S r RNA sequencing were measured to evaluate the effect of folic acid.Palmitic acid-exposed Huh7 cell line was used to evaluate the role of folic acid in hepatic lipid metabolism.RESULTS Folic acid treatment attenuated steatosis,lobular inflammation,and hepatocellular ballooning in rats with HFD-induced steatohepatitis.Genes related to lipid de novo lipogenesis,β-oxidation,and lipid uptake were improvedin HFD-fed folic acid-treated rats.Furthermore,peroxisome proliferator-activated receptor alpha(PPARα)and silence information regulation factor 1(SIRT1)were restored by folic acid in HFD-fed rats and palmitic acid-exposed Huh7 cell line.The restoration of PPARαby folic acid was blocked after transfection with SIRT1 si RNA in the Huh7 cell line.Additionally,folic acid administration ameliorated depleted hepatic one-carbon metabolism and restored the diversity of the gut microbiota in rats with HFD-induced steatohepatitis.CONCLUSION Folic acid improves hepatic lipid metabolism by upregulating PPARαlevels via a SIRT1-dependent mechanism and restores hepatic one-carbon metabolism and diversity of gut microbiota,thereby attenuating HFD-induced NASH in rats.

关键词： Nonalcoholic fatty liver disease Folic acid Gut microbiota PPARα SIRT1

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Edible Bird's Nest Attenuates Menopause-Related Bone Degeneration in Rats via Increasing Bone Estrogen-Receptor Expression

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Chinese Journal of Integrative Medicine 2021年第4期27卷 280-285页

作者： HOU Zhi-ping TANG Shi-ying Jl Hai-ru HE Pei-yuan LI Yu-hong DONG Xian-ling DU Meng-nan Ismail Maznah HE Wen-jing Department of Pathology Chengde Medical UniversityChengdeHebei Province(067000)China Department of Gastroenterology The Affiliated Hospital of Chengde Medical UniversityChengdeHebei Province(067000)China Department of Pathology The Affiliated Hospital of Hebei University BaodingHebei Province(0671000)China Laboratory of Molecular Biomedicine Institute of BioscienceUniversiti Putra MalaysiaSerdangSelangor(43400)Malaysia Department of Gastroscopy Kuancheng Manchu Autonomous County HospitalChengdeHebei Province(067000)China

Objective:To investigate the mechanistic basis for the attenuation of bone degeneration by edible bird's nest(EBN)in ovariectomized rats.Methods:Forty-two female Sprage-Dawley rats were randomized into 7 groups(6 in each group).The ovariectomized(OVX)and OVX+6%,3%,and 1.5%EBN and OVX+estrogen groups were given standard rat chow alone,standard rat chow+6%,3%,and 1.5%EBN,or standard rat chow+estrogen therapy(0.2mg/kg per day),respectively.The sham-operation group was surgically opened without removing the ovaries.The control group did not have any surgical intervention.After 12 weeks of intervention,blood samples were taken for serum estrogen,osteocalcin,and osteoprotegerin,as well as the measurement of magnesium,calcium abd zinc concentrations.While femurs were removed from the surrounding muscles to measure bone mass density using the X-ray edge detection technique,then collected for histology and estrogen receptor(ER)immunohistochemistry.Results:Ovariectomy altered serum estrogen levels resulting in increased food intake and weight gain,while estrogen and EBN supplementation attenuated these changes.Ovariectomy also reduced bone ER expression and density,and the production of osteopcalcin and osteorotegerin,which are important pro-osteoplastic hormones that promote bone mineraliztion and density.Conversely,estrogen and EBN increased serum estrogen levels leading to increased bone ER expression,pro-osteoplastic hormone production and bone density(all P<0.05).Conclusion:EBN could be used as a safe alternative to hormone replacement therapys for managing menopausal complications like bone degeneration.

关键词： edible bird's nest menopause ovariectomy rats bone osteoporosis

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Sodium butyrate attenuates high-fat diet-induced steatohepatitis in mice by improving gut microbiota and gastrointestinal barrier

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World Journal of Gastroenterology 2017年第1期23卷 60-75页

作者： Da Zhou Qin Pan Feng-Zhi Xin Rui-nan Zhang Chong-Xin He Guang-Yu Chen Chang Liu Yuan-Wen Chen Jian-Gao Fan Department of Gastroenterology Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Clinical Epidemiology Center Shanghai Jiaotong University School of Medicine Department of Medical Microbiology and Parasito-logy Institutes of Medical SciencesShanghai Jiao Tong University School of Medicine

AIM To investigate whether gut microbiota metabolite sodium butyrate(Na B)is an effective substance for attenuating non-alcoholic fatty liver disease(NAFLD)and the internal mechanisms.METHODS Male C57BL/6J mice were divided into three groups,normal control were fed standard chow and model group were fed a high-fat diet(HFD)for 16 wk,the intervention group were fed HFD for 16 wk and treated with Na B for 8 wk.Gut microbiota from each group were detected at baseline and at 16 wk,liver histology were evaluated and gastrointestinal barrier indicator such as zonula occluden-1(ZO-1)were detected by immunohistochemistry and realtime-PCR,further serum or liver endotoxin were determined by ELISA and inflammation-or metabolism-associated genes were quantified by real-time PCR.RESULTS Na B corrected the HFD-induced gut microbiota imbalance in mice,while it considerably elevated the abundances of the beneficial bacteria Christensenellaceae,Blautia and Lactobacil us.These bacteria can produce butyric acid in what seems like a virtuous circle.And butyrate restored HFD induced intestinal mucosa damage,increased the expression of ZO-1 in small intestine,further decreased the levels of gut endotoxin in serum and liver compared with HF group.Endotoxin-associated genes such as TLR4 and Myd88,pro-inflammation genes such as MCP-1,TNF-α,IL-1,IL-2,IL-6 and IFN-γin liver or epididymal fat were obviously downregulated after Na B intervention.Liver inflammation and fat accumulation were ameliorated,the levels of TG and cholesterol in liver were decreased after Na B intervention,NAS score was significantly decreased,metabolic indices such as FBG and HOMA-IR and liver function indicators ALT and AST were improved compared with HF group.CONCLUSION Na B may restore the dysbiosis of gut microbiota to attenuate steatohepatitis,which is suggested to be a potential gut microbiota modulator and therapeutic substance for NAFLD.

关键词：非酒精的脂肪肝疾病钠丁酸盐内脏 microbiota 胃肠的障碍内毒素

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