检索结果-南通市图书馆

Sinapic acid ameliorates D-galactosamine/lipopolysaccharideinduced fulminant hepatitis in rats:Role of nuclear factor erythroidrelated factor 2/heme oxygenase-1 pathways

维普期刊数据库博看期刊评论

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2021年第7期27卷 592-608页

作者： Mushtaq Ahmad Ansari Mohammad Raish Yousef A Bin Jardan Ajaz Ahmad Mudassar Shahid SheikhFayaz Ahmad Nazrul Haq Mohammad Rashid Khan Saleh A Bakheet Department of Pharmacology and Toxicology College of PharmacyKing Saud UniversityRiyadh 11451Saudi Arabia Department of Pharmaceutics College of PharmacyKing Saud UniversityRiyadh 11451Saudi Arabia Department of Clinical Pharmacy College of PharmacyKing Saud UniversityRiyadh 11451Saudi Arabia

BACKGROUND Sinapic acid(SA)has been shown to have various pharmacological properties such as antioxidant,antifibrotic,anti-inflammatory,and anticancer activities.Its mechanism of action is dependent upon its ability to curb free radical production and protect against oxidative stress-induced tissue injuries.AIM To study the hepatoprotective effects of SA against lipopolysaccharide(LPS)/Dgalactosamine(D-GalN)-induced acute liver failure(ALF)in rats.METHODS Experimental ALF was induced with an intraperitoneal(i.p.)administration of 8μg LPS and 800 mg/kg D-GalN in normal saline.SA was administered orally once daily starting 7 d before LPS/D-GalN treatment.RESULTS Data showed that SA ameliorates acute liver dysfunction,decreases serum levels of alanine transaminase(ALT),and aspartate aminotransferase(AST),as well as malondialdehyde(MDA)and NO levels in ALF model rats.However,pretreatment with SA(20 mg/kg and 40 mg/kg)reduced nuclear factor kappalight-chain-enhancer of activated B cells(NF-κB)activation and levels of inflammatory cytokines(tumor necrosis factor-αand interleukin 6).Also,SA increased the activity of the nuclear factor erythroid-related factor 2/heme oxygenase-1(Nrf2/HO-1)signaling pathway.CONCLUSION In conclusion,SA offers significant protection against LPS/D-GalN-induced ALF in rats by upregulating Nrf2/HO-1 and downregulating NF-κB.

关键词： Sinapic acid D-galactosamine/lipopolysaccharide Oxidative stress fulminant hepatitis Antioxidant Nuclear factor erythroid-related factor 2/heme oxygenase-1 pathways

Liver synthetic function in predicting the prognosis of pregnancy complicating fulminant hepatitis

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Chinese Medical Journal 2007年第24期120卷 2311-2313页

作者： LI Xiao-mao DENG Liu-zhi SHEN Hui-min YANG Yue-bo LI Meng-xiong CHEN Xiao-wei YIN Yu-zhu ZHOU Shui-sheng Department of Obstetrics and Gynecology Third Affiated Hospital of Sun Yat-sen University Guangzhou 510630 China

Pregnancy complicating fulminant hepatitis is characterized by rapid progress, complicated clinical symptoms, and association with blood coagulation dysfunction, hepatic encephalopathy, hepatorenal syndrome, toxic enteroparalysis and infection. Late pregnancy complicating fulminant hepatitis, which has a high fatality rate, is one of the maior causes of death of gravida and puerperant in China. Searching for exact objective indexes and correct judgement of the prognosis is extremely important to clinical work. The indexes of liver function mainly include （1） indexes for the damage of hepatic cells and its degree such as alanine transaminase （ALT）, etc; （2） indexes for the synthesis function of hepatic cells such as albumin （ALB）, total cholesterol （CHOL）, prothrombin time （PT）, prothrombin activity （PTA）, etc; （3） indexes for the function of liver excretion, metabolism and detoxication such as total bilirubin （TBIL）, total bile acid （TBA）, blood ammonia （NH3）, etc.

关键词： pregnancy fulminant hepatitis liver function prognosis

Dengue induced acute liver failure:A meta summary of case reports

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

World Journal of Virology 2024年第1期13卷 133-142页

作者： Deven Juneja Ravi Jain Prashant Nasa Department of Critical Care Medicine Max Super Speciality HospitalNew Delhi 110017India Department of Critical Care Medicine Mahatma Gandhi Medical College and HospitalJaipur 302022RajasthanIndia Department of Critical Care Medicine NMC Specialty HospitalDubai 7832United Arab Emirates

BACKGROUND Dengue fever is the most common cause of viral hemorrhagic fever,with more than 400 million cases being reported annually,worldwide.Even though hepatic involvement is common,acute liver failure(ALF)is a rare complication of dengue fever.AIM To analyze the demographic profile,symptomology,hospital course and outcomes of patients presenting with ALF secondary to dengue infection by reviewing the published case reports.METHODS A systematic search was performed from multiple databases including PubMed,Reference Citation Analysis,Science Direct,and Google Scholar.The search terms used were"dengue"OR"severe dengue"OR"dengue shock syndrome"OR"dengue haemorrhagic syndrome"OR"dengue fever"AND"acute liver failure"OR"hepatic failure"OR"liver injury".The inclusion criteria were:(1)Case reports or case series with individual patient details;(2)Reported acute liver failure secondary to dengue infection;and(3)Published in English language and on adult humans.The data were extracted for patient demographics,clinical sympto-matology,clinical interventions,hospital and intensive care unit course,need for organ support and clinical outcomes.RESULTS Data from 19 case reports fulfilling the predefined inclusion criteria were included.The median age of patients was 38 years(inter quartile range:Q3-Q126.5 years)with a female preponderance(52.6%).The median days from diagnosis of dengue to development of ALF was 4.5 d.The increase in aspartate aminotransferase was higher than that in alanine aminotransferase(median 4625 U/L vs 3100 U/L).All the patients had one or more organ failure,with neurological failure present in 73.7%cases.42.1%patients required vasopressor support and hepatic enceph-alopathy was the most reported complication in 13(68.4%)cases.Most of the patients were managed conser-vatively and 2 patients were taken up for liver transplantation.Only 1 death was reported(5.3%).CONCLUSION Dengue infection may rarely lead to ALF.These patients may frequently require intensive care and organ support.Even though most of

关键词： Dengue fever Acute liver failure Dengue induced hepatitis Hepatic failure fulminant hepatitis Severe dengue

Neutrophil expressed SRA mediated complement activation contributes to the pathogenesis of fulminant hepatitis via potentiating Fgl2/fibroleukin expression

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neutrophil expressed SRA mediated complement activation cont...

Activated NKT Cells Facilitated Functional Switch of Myeloid-derived Suppressor Cells at Inflammation Sites in fulminant hepatitis Mice

第十一届全国免疫学学术大会

作者： Tang Yuan Xie Mengying Zhou Jia Chen Zhengliang Zuo Daming Department of Immunology School of Basic Medical Science Southern Medical University

Objective:Viral fulminant hepatitis(FH)is a potentially fatal disease,and the underlying pathogenesis remains unclear.Scavenger receptor A(SRA)is a pattern recognition receptor,playing important roles in host defense against foreign microbial infections and maintenance of immune homeostasis,which primarily expressed on myeloid cells.However,the precise role of SRA in FH has not been determined.

关键词： fulminant hepatitis Scavenger receptor A Complement neutrophil neutrophil elastase

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Activated NKT Cells Facilitated Functional Switch of Myeloid...

HMGB1-TLR4-MyD88 Axis Exacerbates Experimental Viral fulminant hepatitis

浙江省免疫学会第十次学术大会

作者： Danxiao Wu Yu Shi Cheng Wang Qiaoyun Liu Hanwen Chen Jianhua Liu Lihuang Zhang Yihua Wu Dajing Xia School of public health Zhejiang University School of Medicine Institute of Immunology Zhejiang University School of Medicine State Key Laboratory for Diagnosis and Treatment of Infectious Diseases Collaborative Innovation Center for Diagnosis and Treatment of Infectious DiseaseThe First Affiliated HospitalZhejiang University School of Medicine The Children's Hospital Zhejiang University School of Medicine Department of Clinical Medicine Zhejiang University City College School of Medicine

Myeloid-derived suppressor cells(MDSCs) confer immunosuppressive properties,but their roles in fulminant hepatitis have not been well defined.In this study,we systematically examined the distribution of MDSCs in bone marrow(BM),hver and spleen was determined,and their functional and differentiation status in an acute fulminant hepatitis mouse model induced by lipopolysaccharide and D-galactosamine(LPS-GaIN).Moreover,the interaction between NKT cells and MDSCs was determined.Our study revealed that BM contained the largest pool of MDSCs during pathogenesis of fulminant hepatitis compared with liver and spleen.MDSCs in liver/spleen expressed higher levels of chemokine receptors such as CCR2,CX3 CR1 and CXCR2.At inflamed tissues such as liver or spleen,activated NKT cells induced differentiation of MDSCs through cell-cell interaction,which markedly dampened the immunosuppressive effects and promoted MDSCs to produce pro-inflammatory cytokines and activate inflammatory cells.Our findings thus demonstrated an unexpected pro-inflammatory state for MDSCs,which is,mediated by the activated NKT cells that precipitated the differentiation and functional evolution of these MDSCs at sites of inflammation.

关键词： myeloid-derived suppressor cell NKT cells fulminant hepatitis

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

HMGB1-TLR4-MyD88 Axis Exacerbates Experimental Viral Fulmina...

Review on hepatitis B virus precore/core promoter mutations and their correlation with genotypes and liver disease severity

第十一届全国免疫学学术大会

作者： Diao Bo Yang Chengying Fei Lei Guo Sheng Zhang Ji Wu Yuzhang Chen Yongwen Institute of Immunology PLAThird Military Medical University

Aim: Viral fulminant hepatitis(FH) is a serious liver disease with high mortality due to excessive inflammation in liver tissues. The lack of knowledge on inflammatory signal dysregulation attributing to FH pathogenesis has been an obstacle for seeking effective interventions.Methods: Mice were injected with MHV-3 via i.p. In some experiments, the virus infected mice were treated with HMGB1 blocking m Abs. Mice were euthanized on the indicated days and the virus titers in liver were determined by plaque assay. Serum FGL2, IL-17, TNF-α, C5 a, IL-1β and HMGB1 levels were measured by ELISA. The expression of HMGB1, FGL2, TNF-α and IL-6 in MHV-3 infected livers was detected by Western-blotting.Results: We report that mice deficiency in My D88(My D88-/-), an adaptor protein that mediates Toll-like receptor(TLR), IL-1R and IL-18 R signaling, are resistant to murine hepatitis virus strain-3(MHV-3)-mediated FH. The expression of multiple pro-inflammatory cytokines and chemokines causing the recruitment of inflammatory macrophages, which produce IL-17, TNF-α and IL-1β, to the livers was severely impaired in My D88-/- mice as compared to wild-type(WT) littermates, resulting in reduced liver pathology, viral replication and prolonged mortality post-infection. The liver infiltration of macrophages was mediated by CXCR5 at a very early time of infection, and CXCR5-/-mice phenocopied My D88-/- mice and exhibited reduced liver damage against MHV-3 infection. Additionally, MHV-3 markedly augments expression of high-mobility group box 1(HMGB1) in infected hepatocytes/macrophages and induces HMGB1 protein migration from the nucleus to the extracellular milieu, where it activates My D88-dependent inflammation by binding to TLR4 receptor. Conversely, TLR4-/- mice or WT animals treated with the HMGB1 blocking antibodies are resistant to MHV-3-caused FH. Conclusion: These results demonstrate that the HMGB1-TLR4-My D88 axis is essential in controlling the pathogenesis of viral FH, and interruption of this signaling pathway sheds light

关键词： MHV-3 viral infection fulminant hepatitis Myd88 HMGB1

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

World Journal of Hepatology 2022年第4期14卷 708-718页

作者： Rajesh Kumar Department of School Education Haryana GovernmentPanchkula 134109HaryanaIndia

Of 350 million people worldwide are chronically infected with hepatitis B virus(HBV)and are at risk of developing cirrhosis and hepatocellular carcinoma(HCC)later in life.HBV is the most diverse DNA virus,and its genome is composed of four open reading frames:Presurface antigen/surface antigen gene(preS/S),precore/core gene(preC/C),polymerase gene(P),and theχgene(χ).HBV produces quasispecies naturally or in response to antiviral agents because of the absence of proofreading activity amid reverse transcription and a high replication rate.The virus has 10 genotypes(A to J)with different geographical distributions.There are various HBV mutations in the HBV genome,including preC/C mutations,preS/S mutations,P gene mutations,andχgene mutations.The core promoter region plays a vital part in the replication,morphogenesis and pathogenesis of the virus.The precore region also plays a crucial role in viral replication.Both core promoter and precore mutations rescue the virus from host immune surveillance and result in the formation of mutated strains that may have altered pathogenicity.preC/C mutations are associated with liver disease progression.Precore mutations stop hepatitis B e antigen(HBeAg)production and basal core promoter mutations downregulate HBeAg production.Mutations in the basal core promoter are also associated with increased HBV replication and an increased incidence of advanced liver diseases such as cirrhosis and HCC.The emergence of antiviral-resistant mutations is the main reason for treatment failure.This review focuses mainly on preC/C promoter mutations and their correlation with genotypes and liver disease severity.Thorough perception and knowledge of HBV genetic variety and mutants could be vital to discover techniques for the prognosis and control of HBV infection.

关键词： hepatitis B virus hepatitis B virus e antigen Hepatocellular carcinoma Basal core promoter Core promoter region Precore region fulminant hepatitis Acute hepatitis

Difficult treatment decisions in autoimmune hepatitis

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2010年第8期16卷 934-947页

作者： Albert J Czaja Division of Gastroenterology and Hepatology Mayo Clinic College of Medicine

Treatment decisions in autoimmune hepatitis are complicated by the diversity of its clinical presentations,uncertainties about its natural history,evolving opinions regarding treatment end points,varied nature of refractory disease,and plethora of alternative immu-nosuppressive agents. The goals of this article are to review the difficult treatment decisions and to provide the bases for making sound therapeutic judgments. The English literature on the treatment problems in au-toimmune hepatitis were identifi ed by Medline search up to October 2009 and 32 years of personal experi-ence. Autoimmune hepatitis may have an acute severe presentation,mild in? ammatory activity,lack autoan-tibodies,exhibit atypical histological changes (centri-lobular zone 3 necrosis or bile duct injury),or have variant features reminiscent of another disease (overlap syndrome). Corticosteroid therapy must be instituted early,applied despite the absence of symptoms,or modified in an individualized fashion. Pursuit of normal liver tests and tissue is the ideal treatment end point,but this objective must be tempered against the risk of side effects. Relapse after treatment withdrawal requires long-term maintenance therapy,preferably with azathioprine. Treatment failure or an incomplete response warrants salvage therapy that can include conventional medications in modified dose or empiricaltherapies with calcineurin inhibitors or mycophenolate mofetil. Liver transplantation supersedes empirical drug therapy in decompensated patients. Elderly and pregnant patients warrant treatment modifications. Difficult treatment decisions in autoimmune hepatitis can be simplified by recognizing its diverse manifestations and individualizing treatment,pursuing realistic goals,applying appropriate salvage regimens,and identifying problematic patients early.

关键词： Autoimmune hepatitis fulminant hepatitis Salvage therapy Treatment end points

Antiviral therapy for hepatitis B virus associated hepatic failure

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Hepatobiliary & Pancreatic Diseases International 2009年第1期8卷 17-24页

作者： Wang, Yu-Ming Tang, Ying-Zi Mil Med Univ 3 Southwest Hosp PLA Inst Infect Dis Chongqing 400038 Peoples R China

BACKGROUND: Chronic hepatitis B virus (HBV) infection remains a major global health issue, and the prognosis of patients with HBV-associated fulminant hepatic failure is extremely poor. The application of antiviral therapies has led to significant improvements in patient outcomes. This article aimed to review the current strategies in antiviral treatment of HBV-associated fulminant hepatic failure. DATA SOURCES: Literature search was conducted using PubMed on the related subjects. Part of the data was from the most recent work of the authors' laboratory. RESULTS: hepatitis B immunoglobulin in prevention of recurrent HBV infection after orthotopic liver transplantation (OLT) has been proven effective. However, its cost is high, and significant side effects have been found to induce viral mutations. Lamivudine has a potent suppression for HBV replication and an excellent safety profile in decompensated cirrhotic patients, but its major drawback is the high rate of drug-resistance. Adefovir is effective for lamivudine-resistance strains in the post-OLT situation, and its drug-resistance rate is relatively low. Combination therapies such as hepatitis B immunoglobulin combined with lamivudine and lamivudine combined with adefovir have been widely adopted for prophylaxis against HBV recurrence of infection after OLT. Entecavir, telbivudine, tenofovir and other newer agents have been widely used in antiviral therapy. CONCLUSIONS: The prognosis of HBV-associated fulminant hepatic failure is being transformed by developments in antiviral therapy. However, it should be noticed that HBV is controlled but never eliminated, and drug-resistance still remains a major issue. Hopefully, newer strategies may help to solve these problems.

关键词： hepatitis B virus fulminant hepatitis orthotopic liver transplantation antiviral therapy