Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway 英文参考文献.docVIP

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Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway 英文参考文献.doc

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Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway 英文参考文献

ProtectiveRoleofTaurineagainstArsenic-Induced Mitochondria-DependentHepaticApoptosisviathe InhibitionofPKCd-JNKPathway JoydeepDas,JyotirmoyGhosh,PrasenjitManna,ParamesC.Sil* DivisionofMolecularMedicine,BoseInstitute,Kolkata,India Abstract Background: Oxidative stress-mediated hepatotoxic effect of arsenic (As) is mainly due to the depletion of glutathione (GSH)inliver.Taurine,ontheotherhand,enhancesintracellularproductionofGSH.Littleisknownaboutthemechanismof the beneficial role of taurine in As-induced hepatic pathophysiology. Therefore, in the present study weinvestigated its beneficialroleinAs-inducedhepaticcelldeathviamitochondria-mediatedpathway. Methodology/Principal Findings: Rats were exposed to NaAsO2 (2mg/kg body weight for 6 months) and the hepatic tissue was used for oxidative stress measurements. In addition, the pathophysiologic effect of NaAsO2 (10mM) on hepatocyteswasevaluatedbydeterminingcellviability,mitochondrialmembranepotentialandROSgeneration.Ascaused mitochondrialinjurybyincreasedoxidativestressandreciprocalregulationofBcl-2,Bcl-xL/Bad,Bax,Biminassociationwith increasedlevelofApaf-1,activationofcaspase9/3,cleavageofPARPproteinandultimatelyledtoapoptoticcelldeath.In addition, As markedly increased JNK and p38 phosphorylation with minimal disturbance of ERK. Pre-exposure of hepatocytes to a JNK inhibitor SP600125 prevented As-induced caspase-3 activation, ROS production and loss in cell viability. Pre-exposure of hepatocytes to a p38 inhibitor SB2035, on the other hand, had practically no effect on these events.Besides,AsactivatedPKCdandpre-treatmentofhepatocyteswithitsinhibitor,rottlerin,suppressedtheactivationof JNK indicating that PKCd is involved in As-induced JNK activation and mitochondrial dependent apoptosis. Oral administrationoftaurine(50mg/kgbodyweightfor2weeks)bothpreandposttoNaAsO2exposureorincubationofthe hepatocyteswithtaurine(25mM)werefoundtobeeffectiveincounteractingAs-inducedoxidativestressandapoptosis. Conclusions/Significan