Hepatic　ischemia　and　reperfusion　(I/R)　injury　is　a　major　cause　of　liver　damage　during　liver　transplantation,　resection　surgery,　shock,　and　trauma.　It　has　been　reported　that　TXNIP　expression　was　upregulated　in　a　rat　model　of　hepatic　I/R　injury.　However,　the　role　of　TXNIP　in　the　hepatic　I/R　injury　is　little　known.　In　our　study,　we　investigated　the　biological　role　of　TXNIP　and　its　potential　molecular　mechanism　in　the　human　hepatic　cell　line　(HL7702　cells).　Using　oxygen-glucose　deprivation　and　reoxy-genation　(OGD/R)　to　create　a　cell　model　of　hepatic　I/R　injury,　we　found　that　the　mRNA　and　protein　expression　levels　of　TXNIP　were　upregulated　in　HL7702　cells　exposed　to　OGD/R.　TXNIP　overexpression　remarkably　promoted　OGD/R-induced　cell　apoptosis　and　lactate　dehydrogenase　(LDH)　release,　both　of　which　were　significantly　decreased　by　TXNIP　knockdown.　The　production　of　malondialdehyde　(MDA)　was　also　increased　by　TXNIP　overexpression,　but　was　reduced　by　TXNIP　knockdown.　Moreover,　TXNIP　overexpression　significantly　upregulated　the　phosphorylation　of　p38　and　JNK,　which　was　remarkably　inhibited　by　TXNIP　knockdown.　Additionally,　p38-specific　inhibitor　SB203580　abrogated　the　effect　of　TXNIP　overexpression　on　OGD/R-induced　cell　injury.　Taken　together,　these　results　indicated　that　TXNIP　knockdown　alleviated　hepatocyte　I/R　injury　through　preventing　p38/JNK　pathway　activation.　Thus,　TXNIP　might　offer　a　novel　potential　therapeutic　target　for　the　treatment　of　hepatic　I/R　injury.　(C)　2018　Elsevier　Inc.　All　rights　reserved.