AI Article Synopsis
- The study investigated the impact of myocardin-related transcription factor A (MRTF-A) knockout on mice with nonalcoholic steatohepatitis (NASH) induced by a high-fat diet (HFD).
- MRTF-A knockout mice showed significant improvements in body weight, liver function, and reduced liver fibrosis compared to wild-type mice following HFD.
- The findings suggest that MRTF-A knockout may decrease inflammation and macrophage infiltration in the liver, highlighting its potential as a therapeutic target for NASH treatment.
Article Abstract
Objective: To explore the effects of myocardin-related transcription factor A (MRTF-A) knockout on mice with nonalcoholic steatohepatitis (NASH) induced by high-fat diet (HFD).
Methods: Normal-fat diet (NFD) or HFD was fed to MRTF-A-knockout (MRTF-A) and wild-type (WT) mice for 16 weeks. Liver histopathological status was observed using Hematoxylin and Eosin (HE) staining, Oil Red O staining, Sirius Red staining, and Immunohistochemical staining. The mRNA and protein levels in liver tissues were measured through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot.
Results: Compared with WT + HFD group, mice in MRTF-A + HFD group were decreased in body weight, blood glucose, plasma insulin, liver TG and NAFLD activity score (NAS), with liver function recovery. Besides, compared with HFD-fed WT mice, HFD-fed MRTF-A mice were improved in hepatic fibrosis, accompanied by decreased collagen content (%) and down-regulated expressions of , and . In mice fed with HFD, the expression of MCP-1, CCR2, F4/80 and CD68 declined in liver tissues of MRTF-A mice as compared with WT mice. Besides, in hepatic macrophages isolated from HFD-fed mice, the observed increased expression of , , , as well as decreased expression of CCR2. Compared with WT + HFD group, MRTF-A + HFD group mice were decreased regarding NF-κB p65 in liver tissues.
Conclusion: MRTF-A knockout reduced macrophage infiltration, down-regulated NF-κB p65 expression, and ameliorated inflammation and fibrosis of liver tissues in mice, thereby becoming a potential therapeutic target for NASH treatment.
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