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Hepatic apoptosis is elevated in patients with non-alcoholic steatohepatitis and is correlated with the severity of the disease. Long-chain saturated fatty acids, such as palmitate, induce apoptosis in liver cells. The present study examined adiponectin-mediated protection against saturated fatty acid-induced apoptosis in the human hepatoma cell line, HepG2. | Full-length adiponectin protects hepatocytes from palmitate-induced apoptosis via inhibition of c-Jun NH2 terminal kinase Tae W. Jung1 Yong J. Lee2 Myung W. Lee3 4 Seon M. Kim3 and Tae W. Jung1 1 Samsung BiomedicalInstitute Seoul Korea 2 Division of ClinicalResearch SeoulMedicalCenter Research Institute Korea 3 Department of Family Medicine Brain Korea 21 Project MedicalScience College of Medicine Korea University Seoul Korea 4 Department of Anatomy College of Medicine Korea University Seoul Korea Keywords adiponectin AMPK apoptosis JNK palmitate Correspondence T. W. Jung Samsung Biomedical institute Seoul Korea Annex B235 50 Ilwon-Dong Kangnam-Ku PO Box 135-710 Seoul Korea Fax 82 2 873 8071 Tel 82 2 873 8071 E-mail ohayo2030@hanmail.net Received 24 December 2008 revised 31 January 2009 accepted 10 February 2009 doi 10.1111 j.1742-4658.2009.06955.x Hepatic apoptosis is elevated in patients with non-alcoholic steatohepatitis and is correlated with the severity of the disease. Long-chain saturated fatty acids such as palmitate induce apoptosis in liver cells. The present study examined adiponectin-mediated protection against saturated fatty acid-induced apoptosis in the human hepatoma cell line HepG2. Cells were cultured in a control media i.e. without fatty acids or the same media containing 250 pmol-L-1 of albumin-bound oleate or palmitate for 24 h. The adiponectin concentrations used were 0 1 10 or 100 ig-mL-1 n 4-6 per treatment . Palmitate and thapsigargin but not oleate activated caspase-3 and decreased cell viability in the absence of adiponectin. Adiponectin reduced palmitate- and thapsigargin-induced activation of caspase-3 and cell death in a dose-dependent manner. Phosphatidylinositol 3-kinase and AMP-activated protein kinase inhibitors abolished the effects of adiponectin. Adiponectin-induced inhibition of palmitate- and thapsigar-gin-induced apoptosis was not the result of an augmentation in the unfolded protein response or the increased expression of .
