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alpha-Tocopherol supplementation reduces inflammation and apoptosis in high cholesterol mediated nonalcoholic steatohepatitis

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dc.contributor.authorSÖZEN, AHMET ERDİ
dc.contributor.authorsDemirel-Yalciner, Tugce; Sozen, Erdi; Ozaltin, Esra; Sahin, Ali; Ozer, Nesrin Kartal
dc.date.accessioned2022-03-12T22:55:14Z
dc.date.available2022-03-12T22:55:14Z
dc.date.issued2021
dc.description.abstractInflammation and apoptosis signaling are crucial steps in the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). Alpha-tocopherol, the most active form of vitamin E, is an important modulator of signaling mechanisms, but its involvement to cholesterol-induced NASH pathogenesis remains poorly defined. Herein we have reported a novel effect of alpha-tocopherol in the transition from hepatic steatosis to NASH. High cholesterol diet alone (without alpha-tocopherol) in rabbits elevated NASH development as indicated by increased inflammatory response, apoptotic activity and liver fibrosis. Such elevation results from induction of signaling mechanisms since the expressions of IL1 beta, phospho c-Jun/c-Jun ratio, JNK, caspase 9, CHOP and Bax were increased, and recruitment of macrophage, alpha-smooth muscle actin (alpha-SMA) and COL1A1 into the liver tissue were induced. Alpha-tocopherol supplementation inhibited inflammatory response, apoptosis and fibrosis development without affecting lipid accumulation in high cholesterol-induced NASH. Specifically, alpha-tocopherol lowered the inflammatory level as observed by reduced macrophage infiltration and JNK/c-Jun signaling. Lower inflammatory status co-occurred with the reduction of CHOP and Bax expressions as well as fibrosis-related COL1A1 and alpha-SMA levels. Taken together, alpha-tocopherol supplementation inhibits cholesterol-induced NASH development by lowering JNK/c-Jun/inflammation axis in addition to JNK/CHOP/apoptosis signaling, which might contribute to resistance against NAFLD/NASH transition.
dc.identifier.doi10.1002/biof.1700
dc.identifier.eissn1872-8081
dc.identifier.issn0951-6433
dc.identifier.pubmed34101924
dc.identifier.urihttps://hdl.handle.net/11424/236690
dc.identifier.wosWOS:000658814800001
dc.language.isoeng
dc.publisherWILEY
dc.relation.ispartofBIOFACTORS
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectapoptosis
dc.subjectfibrosis
dc.subjecthigh cholesterol diet
dc.subjectinflammation
dc.subjectNASH
dc.subjectalpha-tocopherol
dc.subjectFATTY LIVER-DISEASE
dc.subjectHEPATIC STELLATE CELLS
dc.subjectOXIDATIVE STRESS
dc.subjectVITAMIN-E
dc.subjectLIPID OXIDATION
dc.subjectC-JUN
dc.subjectEXPRESSION
dc.subjectAUTOPHAGY
dc.subjectNAFLD
dc.subjectACIDS
dc.titlealpha-Tocopherol supplementation reduces inflammation and apoptosis in high cholesterol mediated nonalcoholic steatohepatitis
dc.typearticle
dspace.entity.typePublication
local.avesis.id4babc2d9-8de8-4a7d-a9f5-9947ffe30627
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages11
oaire.citation.endPage413
oaire.citation.issue3
oaire.citation.startPage403
oaire.citation.titleBIOFACTORS
oaire.citation.volume47
relation.isAuthorOfPublication47991a21-cce9-4b87-b091-bede64f8b4e0
relation.isAuthorOfPublication.latestForDiscovery47991a21-cce9-4b87-b091-bede64f8b4e0

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