TAILIEUCHUNG - Báo cáo khoa học: Role of Kupffer cells in pathogenesis of sepsis-induced drug metabolizing dysfunction

The present study aimed to determine the role of Kupffer cells (KCs) in cytochrome P450 (CYP) isozyme activity and the expression of its gene during polymicrobial sepsis. For ablation of KCs, rats were pretreated with gadolinium chloride (GdCl3 ) at 48 and 24 h before cecal ligation and punc-ture (CLP). The depletion of KCs was confirmed by measuring the mRNA level of the KC marker gene CD163. | IFEBS Journal Role of Kupffer cells in pathogenesis of sepsis-induced drug metabolizing dysfunction Tae-Hoon Kim Sang-Ho Lee and Sun-Mee Lee Schoolof Pharmacy Sungkyunkwan University Suwon South Korea Keywords CYP450 HMGB1 Kupffer cells sepsis Toll-like receptor Correspondence . Lee Schoolof Pharmacy Sungkyunkwan University 300 Cheoncheon-dong Jangan-gu Suwon-si Gyeonggi-do 440-746 South Korea Fax 82 31 292 8800 Tel 82 31 290 7712 E-mail sunmee@ These authors contributed equally to this work Received 2 December 2010 revised 19 April 2011 accepted 28 April 2011 doi The present study aimed to determine the role of Kupffer cells KCs in cytochrome P450 CYP isozyme activity and the expression of its gene during polymicrobial sepsis. For ablation of KCs rats were pretreated with gadolinium chloride GdCl3 at 48 and 24 h before cecal ligation and puncture CLP . The depletion of KCs was confirmed by measuring the mRNA level of the KC marker gene CD163. Serum aminotransferase levels and lipid peroxidation showed an increase and hepatic glutathione content showed a decrease at 24 h after CLP. These changes were prevented by GdCl3 pretreatment. Catalytic activities of CYP1A1 1A2 and 2E1 showed a significant reduction at 24 h after CLP but were prevented by GdCl3. A reduction in the levels of CYP2E1 protein and CYP2B1 and CYP2E1 mRNA expression was prevented by GdCl3. Phosphorylation of CYP1A1 1A2 markedly increased 24 h after CLP which was prevented by GdCl3. The increased serum level of high mobility group box 1 hepatic level of Toll-like receptors 2 and 4 and inducible nitric oxide synthase protein expression were prevented by GdCl3. In addition elevated serum concentrations of tumor necrosis factor-a and interleukin-6 and increased hepatic mRNA levels of tumor necrosis factor-a and interleukin-6 were decreased by depletion of KCs. Our findings suggest that ablation of KCs protects against hepatic drug-metabolizing dysfunction by

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