TAILIEUCHUNG - Báo cáo khoa học: Hepatic stimulator substance mitigates hepatic cell injury through suppression of the mitochondrial permeability transition

Hepatic stimulator substance (HSS) has been shown to protect liver cells from various toxins. However, the mechanism by which HSS protects hepatocytes remains unclear. In this study, we established BEL-7402 cells that stably express HSS and analyzed the protective ability of HSS on cells through mitochondrial permeability (MP). | Hepatic stimulator substance mitigates hepatic cell injury through suppression of the mitochondrial permeability transition Yuan Wu1 z Jing Zhang1 z Lingyue Dong1 Wen Li1 Jidong Jia2 and Wei An1 1 Department of CellBiology and MunicipalKey Laboratory for Liver Protection and Regulation of Regeneration CapitalMedicalUniversity Beijing China 2 Liver Unit Beijing Friendship Hospital CapitalMedicalUniversity Beijing China Keywords apoptosis hepatic stimulator substance mitochondria mitochondrialmembrane potential mitochondrial permeability transition Correspondence W. An Department of CellBiology MunicipalKey Laboratory for Liver Protection and Regulation of Regeneration CapitalMedicalUniversity Beijing 100069 China Fax 86 10 83911480 Tel 86 10 83911480 E-mail anwei@ These authors contributed equally to this work Received 12 October 2009 revised 18 December 2009 accepted 23 December 2009 doi Hepatic stimulator substance HSS has been shown to protect liver cells from various toxins. However the mechanism by which HSS protects hepatocytes remains unclear. In this study we established BEL-7402 cells that stably express HSS and analyzed the protective ability of HSS on cells through mitochondrial permeability MP . After administration of carbonyl cyanide m-chlorophenylhydrazone CCCP a specific agent that leads to depolarization of the mitochondrial transmembrane potential the apoptosis rate of HSS-expressing cells was significantly reduced as measured using Hoechst staining and flow cytometry. The mitochondrial membrane transition and cytochrome c leakage were significantly inhibited in the HSS-expressing cells as compared with the untransfected cells and as a consequence the cellular ATP content in the HSS-expressing cells was relatively preserved. Additionally decreased caspase-3 activity was observed in the HSS-expressing cells treated with CCCP as compared with the vector-transfected cells and cells expressing mutant HSS. .

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