检索结果-南通市图书馆

AGK2 pre-treatment protects against thioacetamide-induced acute liver failure via regulating the MFN2-PERK axis and ferroptosis signaling pathway

引用

Hepatobiliary & Pancreatic Diseases International 2024年第1期23卷 43-51页

作者： Qing-Qi Zhang Qian Chen Pan Cao Chun-Xia Shi Lu-Yi Zhang Lu-Wen Wang zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan UniversityWuhan 430060China

Background:Acute liver failure(ALF)is an unpredictable and life-threatening critical *** pathological characteristic of ALF is massive necrosis of hepatocytes and lots of inflammatory cells infiltration which may lead to multiple organ ***:Animals were divided into 3 groups,normal,thioacetamide(TAA,ALF model)and TAA+*** L02 cells were divided into 5 groups,normal,TAA,TAA+mitofusin 2(MFN2)-siRNA,TAA+AGK2,and TAA+AGK2+MFN2-siRNA *** liver histology was evaluated with hematoxylin and eosin staining,inositol-requiring enzyme 1(IRE1),activating transcription factor 6β(ATF6β),protein kinase R(PKR)-like endoplasmic reticulum kinase(PERK)and phosphorylated-PERK(p-PERK).C/EBP homologous protein(CHOP),reactive oxygen species(ROS),MFN2 and glutathione peroxidase 4(GPX4)were measured with Western blotting,and cell viability and liver chemistry were also *** endoplasmic reticulum membranes(MAMs)were measured by ***:The liver tissue in the ALF group had massive inflammatory cell infiltration and hepatocytes necrosis,which were reduced by AGK2 *** comparison to the normal group,apoptosis rate and levels of IRE1,ATF6β,p-PERK,CHOP,ROS and Fe2+in the TAA-induced ALF model group were significantly increased,which were decreased by AGK2 *** levels of MFN2 and GPX4 were decreased in TAA-induced mice compared with the normal group,which were enhanced by AGK2 *** with the TAA-induced L02 cell,apoptosis rate and levels of IRE1,ATF6β,p-PERK,CHOP,ROS and Fe2+were further increased and levels of MFN2 and GPX4 were decreased in the MFN2-siRNA ***2 pre-treatment decreased the apoptosis rate and levels of IRE1,ATF6β,p-PERK,CHOP,ROS and Fe2+and enhanced the protein expression of MFN2 and GPX4 in MFN2-siRNA treated L02 *** observation showed that level of MAMs was promoted in the AGK2 pre-treatment group when compared with the TAA-induced gr

关键词： SIRT2 inhibitor AGK2 Acute liver failure MFN2 Ferroptosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Sirtuin1 attenuates acute liver failure by reducing reactive oxygen species via hypoxia inducible factor 1α

引用

World Journal of Gastroenterology 2022年第17期28卷 1798-1813页

作者： Pan Cao Qian Chen Chun-Xia Shi Lu-Wen Wang zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan UniversityWuhan 430060Hubei ProvinceChina

BACKGROUND The occurrence and development of acute liver failure(ALF)is closely related to a series of inflammatory reactions,such as the production of reactive oxygen species(ROS).Hypoxia inducible factor 1α(HIF-1α)is a key factor that regulates oxygen homeostasis and redox,and the stability of HIF-1αis related to the ROS level regulated by Sirtuin(Sirt)*** activation of Sirt1 will lead to a powerful antioxidant defense system and therapeutic effects in liver ***,little is known about the relationship between HIF-1αand Sirt1 in the process of ALF and the molecular *** To investigate whether HIF-1αmay be a target of Sirt1 deacetylation and what the effects on ALF *** Mice were administrated lipopolysaccharide(LPS)/D-gal and exposed to hypoxic conditions as animal model,and resveratrol was used as an activator of *** cellular model was established with L02 cells stimulated by LPS.N-acetyl-Lcysteine was used to remove ROS,and the expression of Sirt1 was inhibited by *** blotting was used to detect Sirt1 and HIF-1αactivity and related protein *** possible signaling pathways involved were analyzed by immunofluorescent staining,co-immunoprecipitation,dihydroethidium staining,and Western *** Compared with mice stimulated with LPS alone,the expression of Sirt1 decreased,the level of HIF-1αacetylation increased in hypoxic mice,and the levels of carbonic anhydrase 9 and Bcl-2-adenovirus E1B interacting protein 3 increased significantly,which was regulated by HIF-1α,indicating an increase of HIF-1α*** hypoxia,the down-regulation of Sirt1 activated and acetylated HIF-1αin L02 *** inhibition of Sirt1 significantly aggravated this effect and the massive production of *** regulation of ROS was partly through peroxisome proliferatoractivated receptor alpha or AMP-activated protein ***,a Sirt1 activator,effectively relieved ALF aggravated by hypoxia,the production

关键词： Acute liver failure Deacetylation Hypoxia inducible factor 1α Reactive oxygen species Sirtuin1

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Histone deacetylase inhibitor suberoylanilide hydroxamic acid alleviates liver fibrosis by suppressing the transforming growth factor-β1 signal pathway

引用

Hepatobiliary & Pancreatic Diseases International 2018年第5期17卷 423-429页

作者： Yao Wang Lei Zhao Fang-Zhou Jiao Wen-Bin Zhang Qian Chen zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan University Department of Infectious Diseases Union Hospital Tongji Medical College Huazhong University of Science and Technology

Background: Histone deacetylases(HDACs) inhibitors are new anti-fibrotic drugs that inhibit the activity of hepatic stellate cells. The present study focused on the anti-fibrotic function of HDAC inhibitor suberoylanilide hydroxamic acid(SAHA) by suppressing transforming growth factor-β1(TGF-β1) signaling. Methods: Male Sprague-Dawley rats were used to induce liver fibrosis with carbon tetrachloride(CCl 4) and LX2 cell(human hepatic stellate cell line) was stimulated by TGF-β1. Both animals and cells were treated with SAHA. The Smad7 and connective tissue growth factor(CTGF) mRNA levels were detected by real-time polymerase chain reaction(PCR). Western blotting was used to examine the protein levels of CTGF, Histone H3(H3), Smad7, Smad2/3, Acetyl-Histone H3(AH3), HDAC2, α-smooth muscle actin( α-SMA), HDAC6, p-Smad2/3 and HDAC8. In addition, the TGF-β1 and liver enzyme levels from rat serum were detected. Histopathological changes were examined by hematoxylin and eosin(HE), Sirius red and Masson trichrome staining. The α-SMA expression was detected by immumohistochemical staining. Results: Compared with control group, the TGF-β1 and liver enzyme levels from rat serum, together with the mRNA levels of CTGF and protein levels of CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were elevated in fibrotic rats( P < 0.01). But the Smad7 mRNA and AH3 protein levels were notably suppressed in the fibrotic rats( P < 0.01). Pathological examination showed the typical changes of liver fibrosis in the fibrotic rats. After the treatment with SAHA, the levels of liver enzymes, TGF-β1, CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were reduced( P < 0.01) and Smad7 and AH3 protein contents were elevated in liver fibrotic rats( P < 0.01). Moreover, immumohistochemistry showed that SAHA significantly suppressed the α-SMA protein content in fibrotic liver( P < 0.01). Conclusion: The HDAC inhibitor SAHA alleviated liver fibrosis by suppressing the TGF-β1 signaling.

关键词： Acetylation Transforming growth factor-β1 Liver fibrosis Suberoylanilide hydroxamic acid

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Dynamic changes of HBV DNA in serum and peripheral blood mononuclear cells of chronic hepatitis patients after lamivudine treatment

引用

World Journal of Gastroenterology 2006年第25期12卷 4061-4063页

作者： Chang-Zheng Ke Yue Chen zuo-jiong gong Zhong-Ji Meng Li Liu Ze-Jiu Ren zuo-Hua Zhou Department of Infectious Diseases Taihe Hospital Affiliated to Yunyang Medical College Shiyan 442000 Hubei Province China Department of Infectious Diseases Renmin Hospital Affiliated to Wuhan University Wuhan 430060 Hubei Province China Clinical Laboratory Taihe Hospital Affiliated to Yunyang Medical College Shiyan 442000 Hubei Province China

AIM： To study the dynamic changes of hepatits B virus （HBV） DNA in serum and peripheral blood mononuclear cells （PBMCs） of patients after lamivudine therapy. METHODS： A total of 72 patients with chronic HBV infection were included in this study. All patients were confirmed to have the following conditions： above 16 years of age, elevated serum alanine amonotransferase （ALT）, positive hepatitis B e antigen （HBeAg）, positive HBV DNA in serum and PBMCs, negative antibodies against HAV, HCV, HDV, HEV. Other possible causes of chronic liver damages, such as drugs, alcohol and autoimmune diseases were excluded. Seventy-two cases were randomly divided into lamivudine treatment group （n = 42） and control group （n = 30）. HBV DNA was detected both in serum and in PBMCs by fluorescence quantitative polymerase chain reaction （PCR）, during and after lamivudine treatment. RESULTS： In the treatment group, HBV DNA became negative both in serum and in PBMC, of, 38 and 25 out of 42 cases respectively during the 48 wk oflamivudine treatment, the negative rate was 90.5% and 59.5% respectively. In the control group, the negative rate was 23.3% and 16.7% respectively. It was statistically significant at 12, 24 and 48 wk as compared with the control group （P 〈 0.005）. The average conversion period of HBV DNA was 6 wk （2-8 wk） in serum and 16 wk （8-24 wk） in PBMC.CONCLUSION： Lamivudine has remarkable effects on HBV replication both in serum and The inhibitory effect on HBV DNA in PBMCs than that in serum inhibitory in PBMCs. is weaker

关键词： Lamivudine Hepatitis B virus DNA Peripheral blood mononuclear cells

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Ethyl pyruvate prevents inflammatory factors release and decreases intestinal permeability in rats with D-galactosamine-induced acute liver failure

引用

Hepatobiliary & Pancreatic Diseases International 2013年第2期12卷 180-188页

作者： Li-Kun Wang Lu-Wen Wang Xun Li Xiao-Qun Han zuo-jiong gong Department of Infectious Diseases Renmin Hospita of Wuhan University

BACKGROUND: The pathogenesis and progression of acute liver failure (ALF) are closely associated with intestinal endotoxemia because of the high permeability of the intestinal wall. Treatment with ethyl pyruvate (EP) has been shown to protect liver failure effectively. The current study aimed to explore the relationship between proinflammatory cytokines and intestinal permeability, and to investigate whether EP administration might prevent the release of multiple proinflammatory cytokines and decrease intestinal permeability and therefore, protect the liver from injury. METHODS: The ALF model was induced by D-galactosamine in rats. The rats were randomly divided into control (saline i.p.), model (D-galactosamine, 1.2 g/kg, i.p.), prevention [EP injection (40 mg/kg) 2 hours ahead of D-galactosamine] and treatment groups (EP injection 2 hours after D-galactosamine) Samples were obtained at 12 and 24 hours after ALF induction respectively. The histology of liver and intestinal tissue was accessed. Serum alanine aminotransferase, endotoxin, D(-) lactate, diamine oxidase (DAO), tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ) and high mobility group box-1 (HMGB1) were evaluated. The survival of rats was also recorded. RESULTS: The rats in model group showed severe damage to liver tissue and intestinal mucosa 12 and 24 hours after ALF induction. EP significantly improved liver or intestinal injury In addition, serum endotoxin, D(-)-lactate, DAO, TNF-α IFN-γ and HMGB1 levels were significantly increased in the model group compared with the control group. There was a positive correlation between intestinal permeability andproinflammatory cytokines. EP significantly reduced serum endotoxin, D(-)-lactate, DAO, TNF-α, IFN-γ and HMGB1 levels. The median survival time was significantly prolonged in both prevention and treatment groups (126 and 120 hours compared with 54 hours in the model group). CONCLUSIONS: EP has protective and therapeutic effects on intestinal mucos

关键词： acute liver failure ethyl pyruvate intestinal permeability cytokines

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Expression and activity of inducible nitric oxide synthase and endothelial nitric oxide synthase correlate with ethanolinduced liver injury

引用

World Journal of Gastroenterology 2006年第15期12卷 2375-2381页

作者： Guang-Jin Yuan Xiao-Rong Zhou zuo-jiong gong Pin Zhang Xiao-Mei Sun Shi-Hua Zheng Department of Infectious Diseases Renmin Hospital of Wuhan UniversityWuhan 430060 Hubei Province China

AIM： To study the expression and activity of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS） in rats with ethanol-induced liver injury and their relation with liver damage, activation of nuclear factor-KB （NF-κB） and tumor necrosis factor-α （TNF-α） expression in the liver. METHODS： Female Sprague-Dawley rats were given fish oil （0.5 mL） along with ethanol or isocaloric dextrose daily via gastrogavage for 4 or 6 wk. Liver injury was assessed using serum alanine aminotransferase （ALT） activity and pathological analysis. Liver malondialdehyde （MDA）, nitric oxide contents, iNOS and eNOS activity were determined. NF-κB p65, iNOS, eNOS and TNF-α protein or mRNA expression in the liver were detected by immunohistochemistry or reverse transcriptase-polymerase chain reaction （RT-PCR）. RESULTS： Chronic ethanol gavage for 4 wk caused steatosis, inflammation and necrosis in the liver, and elevated serum ALT activity. Prolonged ethanol administration （6 wk） enhanced the liver damage. These responses were accompanied with increased lipid peroxidation, NO contents, iNOS activity and reduced eNOS activity. NF-κB p65, iNOS and TNF-α protein or mRNA expression were markedly induced after chronic ethanol gavage, whereas eNOS mRNA expression remained unchanged. The enhanced iNOS activity and expression were positively correlated with the liver damage, especially the necro-inflammation, activation of NF-KB, and TNF-α mRNA expression. CONCLUSION： iNOS expression and activity are induced in the liver after chronic ethanol exposure in rats, which are correlated with the liver damage, especially the necro-inflammation, activation of NF-KB and TNF-α expression, eNOS activity is reduced, but its mRNA expression is not affected.

关键词： Alcoholic liver disease Inducible nitric oxide synthase Endothelial nitric oxide synthase Nuclear factor-κB

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Sulforaphane,an NRF2 agonist,alleviates ferroptosis in acute liver failure by regulating HDAC6 activity

引用

结合医学学报:英文版 2023年第5期21卷 464-473页

作者： Yan-qiong Zhang Chun-xia Shi Dan-mei Zhang Lu-yi Zhang Lu-wen Wang zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan UniversityWuhan 430060Hubei ProvinceChina

Objective Acute liver failure(ALF)is characterized by severe liver dysfunction,rapid progression and high mortality and is difficult to *** have found that sulforaphane(SFN),a nuclear factor E2-related factor 2(NRF2)agonist,has anti-inflammatory,antioxidant and anticancer effects,and has certain protective effects on neurodegenerative diseases,cancer and liver *** paper aimed to explore the protective effect of SFN in ALF and it possible mechanisms of *** Lipopolysaccharide and D-galactosamine were used to induce liver injury in vitro and in ***2 agonist SFN and histone deacetylase 6(HDAC6)inhibitor ACY1215 were used to observe the protective effect and possible mechanisms of SFN in ALF,*** viability,lactate dehydrogenase(LDH),Fe2+,glutathione(GSH)and malondialdehyde(MDA)were *** expression of HDAC6,NRF2,glutathione peroxidase 4(GPX4),acyl-CoA synthetase long-chain family member 4(ACSL4)and solute carrier family 7 member 11(SLC7A11)were detected by Western blotting and *** Our results show that NRF2 was activated by ***,Fe2+,MDA and ACSL4 were downregulated,while GSH,GPX4 and SLC7A11 were upregulated by SFN in vitro and in vivo,indicating the inhibitory effect of SFN on ***,HDAC6 expression was decreased in the SFN group,indicating that SFN could downregulate the expression of HDAC6 in *** using the HDAC6 inhibitor,ACY1215,SFN further reduced HDAC6 expression and inhibited ferroptosis,indicating that SFN may inhibit ferroptosis by regulating HDAC6 *** SFN has a protective effect on ALF,and the mechanism may include reduction of ferroptosis through the regulation of HDAC6.

关键词： Acuteliverfailure Sulforaphane NRF2 HDAC6 Ferroptosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Ethyl pyruvate protects against experimental acute-on-chronic liver failure in rats

引用

World Journal of Gastroenterology 2012年第40期18卷 5709-5718页

作者： Lu-Wen Wang Li-Kun Wang Hui Chen Cheng Fan Xun Li Can-Ming He zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Institute of Infectious Diseases Hubei Center for Disease Control and Prevention Wuhan 430079 Hubei Prov- ince China

AIM： To investigate the protective effects of ethyl py- ruvate （EP） on acute-on-chronic liver failure （ACLF） in rats. METHODS： An ACLF model was established in rats, and animals were randomly divided into normal, mod- el and EP treatment groups. The rats in EP treatment group received EP （40 mg/kg） at 3 h, 6 h, 12 h and 24 h after induction of ACLF. Serum endotoxin, high mobility group box-1 （HMGB1）, alanine transaminase （ALT）, tumor necrosis factor-α （TNF-α）, interferon-α （IFN-γ）, interleukin （IL）-10 and IL-18 levels, changes of liver histology and HMGB1 expressions in liver tis- sues were detected at 48 h after induction of ACLF. The effects of EP on the survival of ACLF rats were also ***： Serum levels of endotoxin （0.394 ± 0.066 EU/mL vs 0.086±0.017 EU/mL, P 〈 0.001）, HMGB1 （35.42±10,86 μg/L vs 2.14 ± 0.27 μg/L, P 〈 0.001）, ALT （8415.87 ± 3567.54 IU/L vs 38.64 ± 8.82 IU/L, P 〈 0.001）, TNF-α （190.77 ± 12.34 ng/L vs 124.40 ± 4.12 ng/L, P 〈 0.001）, IFN-γ （715.38 ± 86.03 ng/L vs 398.66 ± 32.91 ng/L, P 〈 0.001）, IL-10 （6.85 ± 0.64 ng/L vs 3.49 ± 0.24 ng/L, P 〈 0.001） and IL-18 （85.19 ±3.49 ng/L vs 55.38 ±1.25 ng/L, P 〈 0.001） were significantly increased, and liver tissues presented se- vere pathological injury in the model group compared with the normal group, Howeverr EP administration significantly improved hepatic histopathology and re- duced the serum levels of endotoxin （0.155±0.045 EU/mL vs 0.394 ± 0.066 EU/mL vs P 〈 0.001） and in- flammatory cytokines （11.13 ± 2.58 μg/L vs 35.42 ± 10.86 μg/L for HMGB1, 3512.86 ± 972.67 IU/L vs 8415.87 ± 3567.54 IU/L for ALT, 128.55 ± 5.76 ng/L vs 190.77 ± 12.34 ng/L for TNF-α 438.16 ± 38.10 ng/L vs 715.38 ± 86.03 ng/L for IFN-γ 3.55 ± 0.36 ng/L vs 6.85 ± 0.64 ng/L for IL-10, and 60.35 ± 1.63 ng/L vs 85.19 ± 3.49 ng/L for IL-18, respectively, P 〈 0.001）, and the levels of HMGB1 in liver tissues re- gardless of treatment time after induction of ACLF. EP treatment at the four time points prolonged the me- dian survi

关键词： Acute-on-chronic liver failure Ethyl pyru-vate High mobility group box-1 Inflammatory cyto-kines Histopathology Survival time

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Sodium butyrate protects against toxin-induced acute liver failure in rats

引用

Hepatobiliary & Pancreatic Diseases International 2014年第3期13卷 309-315页

作者： Fan Yang Li-Kun Wang Xun Li Lu-Wen Wang Xiao-Qun Han zuo-jiong gong Department of Infectious Diseases Renmin Hospital of Wuhan University Department of Infectious Diseases Linyi People's Hospital

BACKGROUND: Acute liver failure(ALF) is a serious clinical syndrome with high mortality. Sodium butyrate has been shown to alleviate organ injury in a wide variety of preclinical models of critical diseases. The aim of this study was to investigate the protective effect of sodium butyrate on ALF in ***: All rats were randomly divided into control,model and sodium butyrate treatment groups. Except the control group, the rats were induced ALF animal model by subcutaneous injection of human serum albumin+D- galactosamine+lipopolysaccharide. After induction of ALF,the rats in the treatment group received sodium butyrate(500mg/kg) at 12-hour or 24-hour time point. Fourty-eight hours after ALF induction, the animals were sacrificed and samples were harvested. Serum endotoxin, high mobility group box-1(HMGB1), liver function parameters, tumor necrosis factoralpha(TNF-α) and interferon-gamma(IFN-γ) were *** expression of HMGB1 and nuclear factor-kappa B(NF-κB)p65 protein in liver tissue was detected by Western blotting. The histological changes of liver and intestine were examined. The survival duration was also ***: Serum endotoxin, alanine aminotransferase, HMGB1,TNF-α and IFN-γ were significantly increased and the liver histology showed more severe histopathological injury in the model group compared with the control group(P<0.05).Compared to the model group, sodium butyrate treatment significantly improved the histopathological changes in the liver and intestine, reduced serum endotoxin and inflammatory cytokines, suppressed HMGB1 and NF-кB p65 proteins in liver tissue, and prolonged the survival duration regardless of treatment at 12 hours or 24 hours after induction of ALF(P<0.05).CONCLUSIONS: Sodium butyrate protected the liver from toxin-induced ALF in rats. The mechanisms may be due to direct hepatoprotection and decreased intestinal permeability.

关键词： acute liver failure high mobility group box-1 nuclear factor-kappa B p65 animal model sodium butyrate

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Changes of plasma D(-) -lactate, diamine oxidase and endotoxin in patients with liver cirrhosis

引用

Hepatobiliary & Pancreatic Diseases International 2004年第1期3卷 58-61页

作者： Peng Ruan, zuo-jiong gong and Quan-Rong Zhang Wuhan, China Department of Infectious Diseases, Renmin Hospital Wuhan University Medical College, Wuhan 430060 , China Department of Infectious Diseases Renmin Hospital Wuhan University Jiefang Road Wuhan 430060 China.

BACKGROUND: Plasma D(-)-lactate and diamine oxidase (DAO) can reflect patients' intestinal mucosal condition. We evaluated the changes of plasma D (-)-lactate, DAO and endotoxin activities and their significance in patients with liver cirrhosis. METHODS: Fifty liver cirrhosis patients were enrolled into experimental group and 30 healthy people into control group. The plasma levels of D(-)-lactate, DAO and endo- toxin were detected spectrophotographically. RESULTS: The level of D(-)-lactate was significantly high- er in the experimental group than that in the control group (P<0.01). Significant differences of D (-)-lactate levels were observed in Child-Pugh subgroups of the experimen- tal group (P <0. 01). The level of DAO was significantly higher in the experimental group than that in the control group (P <0.01), but the level of DAO in Child-Pugh sub- group C was significantly lower than that in Child-Pugh subgroup B (P<0.01). The level of endotoxin was signifi- cantly increased in the experimental group except Child Pugh subgroup A (P<0.01). The plasma levels of D(-) lactate, DAO and endotoxin were positively correlated with each other (P<0.01). CONCLUSIONS: The data suggest that both plasma D(-) lactate and DAO activity are sensitive markers for early diagnosis of gut failure and endotoxemia in patients with liver cirrhosis. The impairment of intestinal barrier func- tion may be one of the critical reasons for deterioration of liver cirrhosis.

关键词： liver cirrhosis D(-)-lactate diamine oxidase endotoxin intestinal permeability gut failure

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：