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Increased hepatic expression of insulin-like growth factor-Ⅰreceptor in chronic hepatitis C

World Journal of Gastroenterology 2006年第24期12卷 3821-3828页

作者： José Tadeu Stefano Maria Lúcia Corr(e|^)a-Giannella Cristiane Maria Freitas Ribeiro Ven(a|^)ncio Avancini Ferreira Alves Paulo Celso Bosco Massarollo Marcel Cerqueira Cesar Machado Daniel Giannella-Neto Laboratory for Cellular and Molecular Endocrinology University of Sao Paulo Medical School Brazil Laboratory for Cellular and Molecular Endocrinology University of Sao Paulo Medical School Diabetes UnitDivision of EndocrinologyBrazil Department of Pathology Santa Casa de Misericórdia de Sao Paulo Brazil Department of Pathology University of Sao Paulo Medical School Brazil Laboratory for Experimental Surgery University of Sao Paulo Medical School Brazil

AIM： Although increased insulin-like growth factor-I receptor （IGF-IR） gene expression has been reported in hepatocellular carcinoma, studies assessing IGF-IR in chronic hepatitis C （CHC） and cirrhosis are scarce. We therefore aimed to evaluate IGF-IR and IGF-I rnRNA expression in liver from patient with CHC. METHODS： IGF-IR and IGF-I rnRNA content were determined by semi-quantitative RT-PCR and IGF-IR protein expression was determined by immunohistochemistry in hepatic tissue obtained from patients with CHC before （34 patients） and after （10 patients） therapy with interferon-α and ribavirin. RESULTS： An increase of IGF-IR rnRNA content was observed in hepatic tissue obtained from all CHC patients as well as from 6 cadaveric liver donors following orthopic transplantation （an attempt to evaluate normal livers） in comparison to normal liver, while no relevant modifications were detected in IGF-I mRNA content. The irnrnunohistochemical results showed that the raise in IGF-IR rnRNA content was related both to ductular reaction and to increased IGF-IR expression in hepatocytes. A decrease in IGF-IR rnRNA content was observed in patients who achieved sustained virological response after therapy, suggesting an improvement in hepatic damage. CONCLUSION： The up-regulation of IGF-IR expression in hepatocytes of patients with CHC could constitute an attempt to stimulate hepatocyte regeneration. Considering that liver is the organ with the highest levels of IGF-I, our finding of increased IGF-IR expression after both acute and chronic hepatic damage highlights the need for additional studies to elucidate the role of IGF-I in liver regeneration.

关键词： Chronic hepatitis C Insulin-like growth factorI Insulin-like growth factor I receptor Ductular reaction hepatocyte regeneration Ischemia-reperfusion

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Molecular pathogenesis of acetaminophen-induced liver injury and its treatment options

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2022年第4期23卷 265-285页

作者： Xiaopeng CAI Huiqiang CAI Jing WANG Qin YANG Jun GUAN Jingwen DENG Zhi CHEN State Key Laboratory for Diagnosis and Treatment of Infectious Diseases National Clinical Research Center for Infectious DiseasesCollaborative Innovation Center for Diagnosis and Treatment of Infectious Diseasesthe First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China Department of Clinical Medicine University of AarhusPalle Juul-Jensens Boulevard 828200 Aarhus NDenmark Department of Pathology Key Laboratory of Disease Proteomics of Zhejiang ProvinceZhejiang University School of MedicineHangzhou 310058China Department of Pathology Women’s HospitalZhejiang University School of MedicineHangzhou 310058China

Acetaminophen,also known as N-acetyl-p-aminophenol(APAP),is commonly used as an antipyretic and analgesic *** overdose can induce hepatic toxicity,known as acetaminophen-induced liver injury(AILI).However,therapeutic doses of APAP can also induce AILI in patients with excessive alcohol intake or who are ***,there is a need to understand the potential pathological mechanisms underlying *** this review,we summarize three main mechanisms involved in the pathogenesis of AILI:hepatocyte necrosis,sterile inflammation,and hepatocyte *** relevant factors are elucidated and *** instance,N-acetyl-p-benzoquinone imine(NAPQI)protein adducts trigger mitochondrial oxidative/nitrosative stress during hepatocyte necrosis,danger-associated molecular patterns(DAMPs)are released to elicit sterile inflammation,and certain growth factors contribute to liver ***,we describe the current potential treatment options for AILI patients and promising novel strategies available to researchers and *** review provides a clearer understanding of AILI-related mechanisms to guide drug screening and selection for the clinical treatment of AILI patients in the future.

关键词： Acetaminophen Acetaminophen-induced liver injury hepatocyte necrosis Sterile inflammation hepatocyte regeneration

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Ductular proliferation in liver tissues with severe chronic hepatitis B: An immunohistochemical study

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World Journal of Gastroenterology 2006年第9期12卷 1443-1446页

作者： Yao-Kai Chen Xu-Xia Zhao Jun-Gang Li Song Lang Yu-Ming Wang Institute of Infectious Diseases Southwest Hospital Third Military Medical University Chongqing 400038 China Department of Hepatology Gucheng People's Hospital Gucheng 443003 Hubei Province China

AIM： To clarify the pathogenesis of ductular proliferation and its possible association with oval cell activation and hepatocyte regeneration. METHODS： Immunohistochemical staining and image analysis of the ductular structures in the liver tissues from 11 patients with severe chronic hepatitis B and 2 healthy individuals were performed. The liver specimens were sectioned serially, and then cytokeratin 8 （CK8）, CK19, OV6, proliferating cell nuclear antigens （PCNA）, glutathione-S-transferase （GST）, α-fetal protein （AFP） and albumin were stained immunohistochemically. RESULTS： Typical and atypical types of ductular proliferation were observed in the portal tracts of the liver tissues in all 11 patients. The proliferating ductular cells were positive for CKS, CK19, OV6 and PCNA staining. Some atypical ductular cells displayed the morphological and immunohistochemical characteristics of hepatic oval cells. Some small hepatocyte-like cells were between hepatic oval cells and mature hepatocytes morphometrically and immunohistochemically. CONCLUSION： The proliferating ductules in the liver of patients with severe chronic liver disease may have different origins. Some atypical ductular cells are actually activated hepatic oval cells. Atypical ductular proliferation is related to hepatocyte regeneration and small hepatocyte-like cells may be intermediate transient cells between hepatic oval cells and mature hepatocytes.

关键词： Ductular proliferation Chronic hepatitis B hepatocyte regeneration

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