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Mesenchymal Stem Cells Alleviate Acute Liver Failure through Regulating hepatocyte apoptosis and Macrophage Polarization

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Journal of Clinical and Translational Hepatology 2024年第6期12卷 571-580页

作者： Yachao Tao Yonghong Wang Menglan Wang Hong Tang Enqiang Chen Center of Infectious Diseases West China HospitalSichuan UniversityChengduSichuanChina Division of Infectious Diseases State Key Laboratory of BiotherapySichuan UniversityChengduSichuanChina

Background and Aims:Acute liver failure(ALF)is a life-threatening clinical problem with limited treatment *** of human umbilical cord mesenchymal stem cells(hUC-MSCs)may be a promising approach for *** study aimed to explore the role of hUC-MSCs in the treat-ment of ALF and the underlying ***:A mouse model of ALF was induced by lipopolysaccharide and d-galactosamine *** therapeutic effects of hUC-MSCs were evaluated by assessing serum enzyme activity,histological appearance,and cell apoptosis in liver *** apoptosis rate was analyzed in AML12 *** levels of inflammatory cytokines and the phenotype of RAW264.7 cells co-cultured with hUC-MSCs were *** C-Jun N-terminal kinase/nuclear factor-kappa B signal-ing pathway was ***:The hUC-MSCstreatment decreased the levels of serum alanine aminotransferase and aspartate aminotransferase,reduced pathological damage,alleviated hepatocyte apoptosis,and reduced mortality in *** hUC-MSCs co-culture reduced the apoptosis rate of AML12 cells in ***,lipopolysaccharide-stimulated RAW264.7 cells had higher levels of tumor necrosis factor-α,interleukin-6,and interleukin-1β and showed more CD86-positive cells,whereas the hUC-MSCs co-culture reduced the levels of the three inflammatory cytokines and increased the ratio of CD206-positive *** hUC-MSCs treatment inhibited the activation of phosphorylated(p)-C-Jun N-terminal kinase and p-nuclear factor-kappa B not only in liver tissues but also in AML12and RAW264.7 cells co-cultured with ***:hUC-MSCs could alleviate ALF by regulating hepatocyte apoptosis and macrophage polarization,thus hUC-MSC-based cell therapy may be an alternative option for patients with ALF.

关键词： Human umbilical cord mesenchymal stem cells Acute liver failure hepatocyte apoptosis Hepatitis Macrophage polarization LPS/D-GalN

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Profile of hepatocyte apoptosis and bile lakes before and after bile duct decompression in severe obstructive jaundice patients

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Hepatobiliary & Pancreatic Diseases International 2010年第5期9卷 520-523页

作者： Toar JM Lalisang Raden Sjamsuhidajat Nurjati C Siregar Akmal Taher Department of Surgery Department of Anatomical Pathology Faculty of Medicine University of Indonesia Department of Urology Cipto Mangunkusumo Hospital

BACKGROUND:Excessive hepatocyte apoptosis and bile lakes in severe obstructive jaundice might impair liver *** decompression of the bile duct has been reported to improve liver functions in animal studies,the mechanism of obstruction differs from that in *** study aimed to determine the profiles of hepatocyte apoptosis and bile lakes following bile duct decompression in patients with severe obstructive jaundice in the clinical ***:We conducted a 'before and after study' on severe obstructive jaundice patients as a model of inhibition of the excessive process by bile duct *** of liver biopsies were taken before and after decompression of the bile duct and then stained by terminal deoxynucleotide transferase-mediated dUTP nick end-labeling(TUNEL) to identify hepatocyte apoptosis and by hematoxilin-eosin(HE) to identify bile *** measurements were independently done by 2 ***:Twenty-one severe obstructive jaundice patients were *** all patients,excessive hepatocyte apoptosis and bile lakes were *** decompression,the hepatocyte apoptosis index decreased from 53.1(SD 105) to 11.7(SD 13.6)(Phepatocyte apoptosis and bile lakes in cases of severe obstructive jaundice,similar to the findings in animal studies.

关键词： hepatocyte apoptosis bile lakes TUNEL obstructive jaundice bile duct decompression

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IGFBPrP1 induces liver fibrosis by inducing hepatic stellate cell activation and hepatocyte apoptosis via Smad2/3 signaling

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World Journal of Gastroenterology 2014年第21期20卷 6523-6533页

作者： Yun Zhang Qian-Qian Zhang Xiao-Hong Guo Hai-Yan Zhang Li-Xin Liu Department of Gastroenterology and Hepatology First Hospital of Shanxi Medical University Department of Gastroenterology and Hepatology First Hospital of Shanxi Medical University Experimental Centre of Science and Research The First Clinical Hospital of Shanxi Medical University Key Laboratory of Cell Physiology Provincial Department of the Ministry of EducationShanxi Medical University

AIM: To investigate the role and mechanism of insulin-like growth factor binding protein-related protein 1 (IGFBPrP1) in the development of liver fibrosis.

关键词： Insulin-like growth factor binding protein-related protein 1 Liver fibrosis Hepatic stellate cells hepatocyte apoptosis Smad pathway

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Euptox A induces hepatocyte apoptosis through caspase-and reactive oxygen species-mediated mitochondrial pathways in mice

Euptox A induces hepatocyte apoptosis through caspase-and re...

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第十四届生物毒素毒理学术大会暨第一届生物毒素——从生存适应到转化医学专题学术会议

作者： Quan Mo Liwen Hu Wei Sun Zhihua Ren Yanchun Hu Key laboratory of Animal Disease and Human Health of Sichuan Province College of Veterinary MedicineSichuan Agricultural University Xichang College

As the main toxin of Eupatorium adenophorum(***),Euptox A(9-oxo-10,11-dehydroageraphorone) is known to cause animals’ *** this study,we examined the effects of Euptox A on mouse liver cells and its underlying *** found that euptox A induced liver cell apoptosis and cell cycle arrest in a dose-dependent manner,and the affected cells were characterized by the appearance of DNA fragmentation,cellular shrinkage,and chromatin *** A induced apoptosis of hepatocytes by activating the mitochondrial pathway with downregulation of B-cell lymphoma 2(Bcl-2),upregulation of Bcl-2-associated X protein(Bax),changes in mitochondrial membrane potential(△Ψm),release of cytochrome c(Cyc c) and apoptosisinducing factor(AIF),cleavage of poly ADP-ribose polymerase(PARP),and activation of caspase-9 *** further discovered that euptox A increased the accumulation of reactive oxygen species(ROS) in a dose-dependent *** results indicate that euptox A induces hepatocyte apoptosis by activating the mitochondrial apoptosis pathway,which was associated with AIF release,caspase activation,and ROS *** findings provide new insights into the hepatotoxic mechanisms of euptox A in mice.

关键词： euptox A hepatocyte apoptosis mitochondrial pathway caspases ROS

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Hepatoprotective effects of cathepsin B inhibitor on acute hepatic failure induced by lipopolysaccharide/D-galactosamine in mice

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Hepatobiliary & Pancreatic Diseases International 2013年第1期12卷 80-86页

作者： Bing-Zhu Yan Li-Yan Chen Lan Kang Xiao-Ren Wang Man-Ru Bi Wei Wang Bao-Shan Yang Department of Infectious Diseases Second Clinical HospitalHarbin Medical University

BACKGROUND:Increasing evidence suggests that the inactivation of cathepsin B attenuates hepatocyte apoptosis and liver *** study aimed to investigate the protective effects of a cathepsin B inhibitor(CA-074me) on lipopolysaccharide(LPS)/D-galactosamine(D-GalN)-induced acute hepatic failure(AHF) in ***:Mice were intraperitoneally injected with a combination of LPS/D-GalN to induce AHF with or without CA-074me *** cumulative survival rates were calculated 48 hours after the induction of *** well as changes in biochemical indicators and liver histology,hepatocyte apoptosis was assessed using a TUNEL *** tumor necrosis factor-α(TNF-α) production,caspase-3,caspase-8,and caspase-9 activity was *** cytochrome c and Bcl-2 expression were measured by Western ***:The marked elevation in serum aminotransferase activity and prothrombin time found in LPS/D-GalN-treated mice was significantly improved by pretreatment with *** efficacy of CA-074me was also confirmed by histological analysis and TUNEL *** survival rate significantly improved in LPS/D-GalN-induced mice given CA-074me compared with untreated ***/D-GalNinduced caspase-3 and caspase-9 activation was remarkably suppressed by ***,the increased levels of serum TNF-α and elevated caspase-8 activity in AHF mice were not significantly reduced by ***,CA074me sharply reduced the increased expression of cytosolic cytochrome c and markedly augmented Bcl-2 ***:These results suggest that CA-074me has a protective effect in acute hepatic failure induced by LPS/D-GalN.

关键词： acute hepatic failure cathepsin B inhibitor hepatocyte apoptosis caspases cytochrome c

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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 *** was recently shown to reduce insulin resistance and triglyceride *** hypothesized that aloe vera would have beneficial effects in alleviating non-alcoholic steatohepatitis(NASH)in *** To examine the therapeutic effects of aloe vera in NASH *** 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 *** in the NASH group were fed ad libitum with a high-fat high-fructose diet(HFHFD)for 8 *** 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 *** samples were collected at the end of the treatment *** 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,Phepatocyte ballooning, lobular inflammation and increased hepatocyteapoptosis were observed in the NASH group. Aloe vera treatment attenuatedthese changes in liver *** 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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Dengue hemorrhagic fever and the liver

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World Journal of Hepatology 2021年第12期13卷 1968-1976页

作者： Wattana Leowattana Tawithep Leowattana Department of Clinical Tropical Medicine Faculty of Tropical MedicineMahidol UniversityBangkok 10400BangkokThailand Department of Medicine Faculty of MedicineSrinakharinwirot UniversityBangkok 10110BangkokThailand

Dengue hemorrhagic fever(DHF)is one of the most rapidly emerging infections of tropical and subtropical regions *** affects more rural and urban areas due to many factors,including climate *** most people with dengue viral infection are asymptomatic,approximately 25%experience a selflimited febrile illness with mild to moderate biochemical *** dengue diseases develop in a small proportion of these patients,and the common organ involvement is the *** hepatocellular injury was found in 60%-90%of DHF patients manifested as hepatomegaly,jaundice,elevated aminotransferase enzymes,and critical condition as an acute liver failure(ALF).Even the incidence of ALF in DHF is very low(0.31%-1.1%),but it is associated with a relatively high mortality rate(20%-68.3%).The pathophysiology of liver injury in DHF included the direct cytopathic effect of the DENV causing hepatocytes apoptosis,immunemediated hepatocyte injury induced hepatitis,and cytokine *** hypoperfusion is another contributing factor in dengue shock *** reduction of morbidity and mortality in DHF with liver involvement is dependent on the early detection of warning signs before the development of ALF.

关键词： Dengue hemorrhagic fever Dengue viral infection Liver involvement Liver injury Acute liver failure hepatocyte apoptosis Cytokine storm Severe dengue disease

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Coexistence of hyperlipidemia and acute cerebral ischemia/reperfusion induces severe liver damage in a rat model

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World Journal of Gastroenterology 2012年第35期18卷 4934-4943页

作者： Wei-Hong Gong Wen-Xia Zheng Jun Wang Shi-Hui Chen Bo Pang Xia-Min Hu Xiao-Lu Cao Department of Pharma-cology College of Medicine Wuhan University of Science andTechnology Wuhan 430065 Hubei Province China

AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its ***:Rats were divided into 4 groups:control,HL,I/R and HL+I/*** the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/*** alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological *** apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) *** expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western *** tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status *** hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting ***:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 ***,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were

关键词： Hyperlipidemia High-fat diet Cerebral isch-emia/reperfusion Liver damage hepatocyte apoptosis Cytochrome P450 2E1

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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研讨会

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 *** mice were fed with normal chow diet(NCD) five weeks before the experimental ***,with the exception of the PBS group,NCD was changed into high-fat diet(HFD) for the remaining experimental *** showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte ***15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense *** 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 ***,BS 15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD *** 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 *** 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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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暨第五届会员代表大会

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 *** mice were fed with normal chow diet(NCD) five weeks before the experimental ***,with the exception of the PBS *** was changed into high-fat diet(HFD) for the remaining experimental *** showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte ***15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense *** 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 ***,BS15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD ***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 *** 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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