Open AccessMiR ‐451a ameliorates alcoholic hepatitis via repressing HDAC8 ‐mediated proinflammatory response
Author(s) -
Du Bo,
Tan XiaoHong,
Cheng Ling,
Wang Feng,
Zhang HaiFeng
Publication year - 2020
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12272
Subject(s) - proinflammatory cytokine , medicine , hdac8 , cancer research , inflammation , immunology , histone deacetylase , gene , biology , histone , biochemistry
Alcoholic hepatitis (AH) is identified as an inflammatory syndrome with high morbidity and mortality as a result of severe hepatocellular dysfunction and liver injury. Accumulated studies indicated that miRNAs are involved in AH. The potential effect of miR‐451a in AH mice was examined in the current study. A mice AH model was established and the miR‐451a expression in AH mice compared with the sham group was tested by real‐time polymerase chain reaction (qRT‐PCR). AH mice were injected with pre‐miR‐451a lentivirus for miR‐451a overexpression and histone deacetylase (HDAC8) lentivirus for HDAC8 overexpression in AH mice. The underlying mechanisms were explored by searching the potential target genes of miR‐451a in miRanda database and then we confirmed this. We found that miR‐451a expression was significantly decreased in AH mice compared with the sham group. Moreover, miR‐451a overexpression alleviated alcohol‐induced liver inflammation and injuries of AH mice. Additionally, further mechanism exploration disclosed that HDAC8 was a target of miR‐451a. The protective effect of miR‐451a on AH in AH mice was abolished by HDAC8 overexpression. In summary, miR‐451a ameliorates AH via repressing HDAC8‐mediated proinflammatory response.