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Prediction of hepatic inflammation in chronic hepatitis B patients with a random forest-backward feature elimination algorithm

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World Journal of Gastroenterology 2021年第21期27卷 2910-2920页

作者： Ji-Yuan Zhou Liu-Wei Song Rong Yuan Xiao-Ping Lu Gui-Qiang Wang Department of Gastroenterology The Second Affiliated Hospital of Guangzhou Medical UniversityGuangzhou 510260Guangdong ProvinceChina School of Public Health Xiamen UniversityXiamen 361005Fujian ProvinceChina Intervention and Cell Therapy Center Peking University Shenzhen HospitalShenzhen 518036Guangdong ProvinceChina Department of Infectious Disease Peking University First HospitalBeijing 100034China

BACKGROUND Persistent liver inflammatory damage is the main risk factor for developing liver fibrosis,cirrhosis,and even hepatocellular carcinoma in chronic hepatitis B(CHB)patients.Thus,accurate prediction of the degree of liver inflammation is a high priority and a growing medical need.AIM To build an effective and robust non-invasive model for predicting hepatitis Brelated hepatic inflammation.METHODS A total of 650 treatment-naïve CHB(402 HBeAg-positive and 248 HBeAgnegative)patients who underwent liver biopsy were enrolled in this study.Histological inflammation grading was assessed by the Ishak scoring system.Serum quantitative hepatitis B core antibody(qAnti-HBc)levels and 21 immunerelated inflammatory factors were measured quantitatively using a chemiluminescent microparticle immunoassay.A backward feature elimination(BFE)algorithm utilizing random forest(RF)was used to select optional features and construct a combined model.The diagnostic abilities of the model or variables were evaluated based on the estimated area under the receiver operating characteristics curve(AUROC)and compared using the DeLong test.RESULTS Four features were selected to predict moderate-to-severe inflammation in CHB patients using the RF-BFE method.These predictive features included qAnti-HBc,ALT,AST,and CXCL11.Spearman’s correlation analysis indicated that serum qAnti-HBc,ALT,AST,and CXCL11 levels were positively correlated with the histology activity index(HAI)score.These selected features were incorporated into the model to establish a novel model named I-3A index.The AUROC[0.822;95%confidence interval(CI):0.790-0.851]of the I-3A index was significantly increased compared with qAnti-HBc alone(0.760,95%CI:0.724-0.792,Pinflammation in HBeAg-positive and HBeAgnegative

关键词： hepatic inflammation Machine learning Quantitative hepatitis B core antibody CXCL11 Diagnostic efficiency

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Transcription factor ETV4 promotes the development of hepatocellular carcinoma by driving hepatic TNF-αsignaling

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Cancer Communications 2023年第12期43卷 1354-1372页

作者： Dandan Qi Min Lu Pengfei Xu Xinli Yao Yongchen Chen Lipeng Gan Yong Li Yahua Cui Xiaomei Tong Shuhong Liu Jingmin Zhao Ningning Liu Xin Ye Key Laboratory of Pathogenic Microbiology and Immunology Institute of Microbiology Chinese Academy of Sciences Beijing P. R. China Savaid Medical School University of Chinese Academy of Sciences Beijing P. R. China The Fifth Medical Center of Chinese People's Liberation Army General Hospital Beijing P. R. China School of Life Sciences University of Science and Technology of China Hefei Anhui P. R. China

Background hepatic inflammation is the major risk factor of hepatocellular carcinoma(HCC).However,the underlying mechanism by which hepatic inflammation progresses to HCC is poorly understood.This study was designed to investigate the role of ETS translocation variant 4(ETV4)in linking hepatic inflammation to HCC.Methods Quantitative real-time PCR and immunoblotting were used to detect the expression of ETV4 in HCC tissues and cell lines.RNA sequencing and luciferase reporter assays were performed to identify the target genes of ETV4.Hepatocyte-specific ETV4-knockout(ETV4fl/fl,alb-cre)and transgenic(ETV4Hep-TG)mice and diethylnitrosamine-carbon tetrachloride(DEN-CCL4)treatment experiments were applied to investigate the function of ETV4 in vivo.The Cancer Genome Atlas(TCGA)database mining and pathological analysis were carried out to determine the correlation of ETV4 with tumor necrosis factor-alpha(TNF-α)and mitogen-activated protein kinase 11(MAPK11).Results We revealed that ETV4 was highly expressed in HCC.High levels of ETV4 predicted a poor survival rate of HCC patients.Then we identified ETV4 as a transcription activator of TNF-αand MAPK11.ETV4 was positively correlated with TNF-αand MAPK11 in HCC patients.As expected,an increase in hepatic TNF-αsecretion and macrophage accumulation were observed in the livers of ETV4Hep-TG mice.The protein levels of TNF-α,MAPK11,and CD68 were significantly higher in the livers of ETV4Hep-TG mice compared with wild type mice but lower in ETV4fl/fl,alb-cre mice compared with ETV4fl/fl mice as treated with DEN-CCL4,indicating that ETV4 functioned as a driver of TNF-α/MAPK11 expression and macrophage accumulation during hepatic inflammation.Hepatocyte-specific knockout of ETV4 significantly prevented development of DEN-CCL4-induced HCC,while transgenic expression of ETV4 promoted growth of HCC.Conclusions ETV4 promoted hepatic inflammation and HCC by activating transcription of TNF-αand MAPK11.Both the ETV4/TNF-αand ETV4/MAPK11 axes represented two potential therapeutic target

关键词： ETV4 TNF-α MAPK11 macrophage hepatocellular carcinoma hepatic inflammation

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Persea americana attenuates inflammatory response associated with hyperlipidemia in ovariectomized and irradiated rats by regulating MMP-3/TIMP-1 levels

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Asian Pacific Journal of Tropical Biomedicine 2022年第9期12卷 374-382页

作者： Dina F.Elmaghraby Fatma A.M.Salem Esraa S.A.Ahmed Department of Health Radiation Research National Center for Radiation Research and TechnologyEgyptian Atomic Energy AuthorityCairoEgypt Department of Chemistry Faculty of ScienceHelwan UniversityCairoEgypt Radiation Biology Research National Center for Radiation Research and TechnologyEgyptian Atomic Energy AuthorityCairoEgypt

Objective:To explore the effect of Persea americana supplementation on inflammation,oxidative stress,and lipid profiles in ovariectomized rats fed with a high-fat diet and exposed to radiation.Methods:The control group was sham operated,while groups 2-5 were ovariectomized and fed a high-fat diet.Groups 4 and 5 were exposed toγ-radiation(1 Gy/week for 5 weeks)after ovariectomy.Groups 3 and 5 were treated with 1 mL/250 g/day of Persea americana for one month.Serum levels of estrogen,alanine aminotransferase,aspartate aminotransferase,cholesterol,triglycerides and lipoproteins were measured.Additionally,hepatic oxidative stress,inflammatory and fibrogenic markers were evaluated.Results:Persea americana treatment reduced the oxidative stress markers as well as the levels of triglyceride,total cholesterol,and low-density lipoprotein cholesterol,which in turn lowered hepatic fat accumulation.Moreover,it suppressed hepatic inflammatory mediators(interleukin-6,tumor necrosis factor-α,and C-reactive protein)and downregulated pro-fibrogenic markers(transforming growth factor-βand tissue inhibitor of metalloproteinase-1).Conclusions:Persea americana provides protection against ovariectomy,and gamma radiation-mediated hepatic inflammation not only through its antioxidant,anti-inflammatory,lipid-lowering effect but also by modulating the fibrogenic markers.

关键词： Persea americana γ-Radiation Postmenopausal Oxidative stress Lipid Ovariectomy hepatic inflammation Fibrogenic Rat

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Promotion of nonalcoholic steatohepatitis by RNA N^(6)-methyladenosine reader IGF2BP2 in mice

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Life Metabolism 2022年第2期1卷 161-174页

作者： Bing Zhou Yunchen Luo Nana Ji Fei Mao Liping Xiang Hua Bian Ming-Hua Zheng Cheng Hu Yao Li Yan Lu Shanghai Diabetes Institute Shanghai Key Laboratory of Diabetes MellitusShanghai Clinical Centre for DiabetesShanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism of Zhongshan HospitalFudan UniversityShanghaiChina Department of Endocrinology and Metabolism Shanghai General HospitalShanghai Jiao Tong UniversityShanghaiChina Department of Endocrinology and Metabolism Qingpu Branch of Zhongshan HospitalFudan UniversityWenzhouChina NAFLD Research Center Department of HepatologyThe First Affiliated Hospital of Wenzhou Medical UniversityWenzhouChina Key Laboratory of Diagnosis and Treatment for The Development of Chronic Liver Disease in Zhejiang Province WenzhouChina Department of Endocrinology and Metabolism Fengxian Central Hospital Affiliated to the Southern Medical UniversityShanghaiChina Department of Laboratory Animal Science Shanghai Jiao Tong University School of MedicineShanghaiChina Institute of Metabolism and Regenerative Medicine Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina

Nonalcoholic steatohepatitis(NASH)has emerged as the major cause of end-stage liver diseases.However,an incomplete understanding of its molecular mechanisms severely dampens the development of pharmacotherapies.In the present study,through systematic screening of genome-wide mRNA expression from three mouse models of hepatic inflammation and fibrosis,we identified IGF2BP2,an N6-methyladenosine modification reader,as a key regulator that promotes NASH progression in mice.Adenovirus or adeno-associated virus-mediated overexpression of IGF2BP2 could induce liver steatosis,inflammation,and fibrosis in mice,at least in part,by increasing Tab2 mRNA stability.Besides,hepatic overexpression of IGF2BP2 mimicked gene expression profiles and molecular pathways of human NASH livers.Of potential clinical significance,IGF2BP2 expression is significantly upregulated in the livers of NASH patients.Moreover,knockdown of IGF2BP2 substantially alleviated liver injury,inflammation,and fibrosis in diet-induced NASH mice.Taken together,our findings reveal an important role of IGF2BP2 in NASH,which may provide a new therapeutic target for the treatment of NASH.

关键词： nonalcoholic steatohepatitis m6A reader hepatic inflammation IGF2BP2 TAB2

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Anti-inflammatory and anti-oxidant effects of aloe vera in rats with non-alcoholic steatohepatitis

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World Journal of Hepatology 2020年第7期12卷 363-377页

作者： Naruemon Klaikeaw Jutamas Wongphoom Duangporn Werawatganon Maneerat Chayanupatkul Prasong Siriviriyakul Department of Pathology Faculty of MedicineChulalongkorn UniversityBangkok 10330Thailand Alternative and Complementary Medicine for Gastrointestinal and Liver Diseases Research Unit Department of PhysiologyFaculty of MedicineChulalongkorn UniversityBangkok 10330Thailand

BACKGROUND Aloe vera exerts several biological activities,such as,anti-inflammatory,antioxidant,and antimicrobial effects.It was recently shown to reduce insulin resistance and triglyceride level.We hypothesized that aloe vera would have beneficial effects in alleviating non-alcoholic steatohepatitis(NASH)in rats.AIM To examine the therapeutic effects of aloe vera in NASH rats.METHODS All rats were randomly divided into 3 groups(n=6 in each group).Rats in the control group were fed ad libitum with a standard diet for 8 wk.Rats in the NASH group were fed ad libitum with a high-fat high-fructose diet(HFHFD)for 8 wk.Rats in the aloe vera group were fed ad libitum with a HFHFD and aloe vera in dimethylsulfoxide(50 mg/kg)by gavage daily for 8 wk.Liver samples were collected at the end of the treatment period.RESULTS hepatic malondialdehyde(MDA)levels increased significantly in the NASH group as compared with the control group(377±77 nmol/mg vs 129±51 nmol/mg protein,respectively,Pinflammation and increased hepatocyteapoptosis were observed in the NASH group. Aloe vera treatment attenuatedthese changes in liver histology.CONCLUSIONAloe vera attenuated oxidative stress, hepatic inflammation and hepatocyteapoptosis, thus improving liver pathology in rats with NASH.

关键词： Non-alcoholic steatohepatitis Aloe vera Oxidative stress hepatic inflammation Hepatocyte apoptosis Peroxisome proliferator-activated receptor

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The Prevention of non-alcoholic fatty liver disease in obese mice through Lactobacillus johnsonii BS15 by attenuating inflammation and mitochondrial injury and improving gut environment

The Prevention of non-alcoholic fatty liver disease in obese...

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中国畜牧兽医学会动物微生态学分会第十一次全国学术研讨会...

作者： Hesong Wang Dong-Zeng Jinge Xin Xueqin Ni Dan Yi Kangcheng Pan Bo Jing Animal Microecology Institute College of Veterinary MedicineSichuan Agricultural University Key Laboratory of Animal Disease and Human Health of Sichuan Province

The increasing prevalence of obesity worldwide is associated with a parallel increase in non-alcoholic fatty liver disease(NAFLD).To investigate the effect of Lactobacillus johnsonii BS15 on NAFLD.120 male 1CR mice were randomly divided into four groups and administrated with BS15(2×10 cfu/ 0.2 mL·or 2×10 cfu/ 0.2 mL) or phosphate buffered saline(PBS) throughout a 17-week experimental period.The mice were fed with normal chow diet(NCD) five weeks before the experimental period.Afterward,with the exception of the PBS group.NCD was changed into high-fat diet(HFD) for the remaining experimental period.Results showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte apoptosis.BS15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense system.In addition,BS15 inhibited the insulin resistance;decreased the mRNA levels of acetyl-CoA carboxylase 1,fatty acid synthase,and peroxisome proliferator-activated receptor γ;and increased the expression of the fasting-induced adipose factor in livers.Meanwhile,BS15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD mice.BS15 also reduced the level of serum lipopolysaccharide in NAFLD mice by lowering the intestinal permeability and adjusting gut flora,followed by the downregulation of the TNFα mRNA level in liver and the serum level of C-reactive protein.These findings suggest that BS15 may be effective in preventing NAFLD induced by HFD.

关键词： Lactobacillus johnsonii non-alcoholic fatty liver disease intestinal permeability hepatocyte apoptosis hepatic inflammation oxidative stress

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Preventing non-alcoholic fatty liver disease through Lactobacillus johnsonii BS15 by attenuating inflammation and mitochondrial injury and improving gut environment in obese mice

Preventing non-alcoholic fatty liver disease through Lactoba...

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中国畜牧兽医学会动物微生态学分会第五届第十二次全国学术...

作者： Jinge Xin Dong Zeng Hesong Wang Xueqin Ni Dan Yi Kangcheng Pan Bo Jing Animal Microecology Institute College of Veterinary MedicineSichuan Agricultural University Key Laboratory of Animal Disease and Human Health of Sichuan Province

The increasing prevalence of obesity worldwide is associated with a parallel increase in non-alcoholic fatty liver disease(NAFLD).To investigate the effect of Lactobacillus johnsonii BS 15 on NAFLD,120 male ICR mice were randomly divided into four groups and administrated with BS 15(2×10 cfu/0.2 mL or 2×10 cfu/0.2 mL)or phosphate buffered saline(PBS) throughout a 17-week experimental period.The mice were fed with normal chow diet(NCD) five weeks before the experimental period.Afterward,with the exception of the PBS group,NCD was changed into high-fat diet(HFD) for the remaining experimental period.Results showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte apoptosis.BS15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense system.In addition,BS15 inhibited the insulin resistance;decreased the mRNA levels of acetyl-CoA carboxylase 1,fatty acid synthase,and peroxisome proliferator-activated receptor y;and increased the expression of the fasting-induced adipose factor in livers.Meanwhile,BS 15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD mice.BS 15 also reduced the level of serum lipopolysaccharide in NAFLD mice by lowering the intestinal permeability and adjusting gut flora,followed by the downregulation of the TNFα mRNA level in liver and the serum level of C-reactive protein.These findings suggest that BS15 may be effective in preventing NAFLD induced by HFD.

关键词： Lactobacillus johnsonii non-alcoholic fatty liver disease intestinal permeability hepatocyte apoptosis hepatic inflammation oxidative stress

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