| First Author | Tokinoya K | Year | 2021 |
| Journal | Mol Med Rep | Volume | 23 |
| Issue | 3 | PubMed ID | 33495844 |
| Mgi Jnum | J:309508 | Mgi Id | MGI:6719727 |
| Doi | 10.3892/mmr.2021.11849 | Citation | Tokinoya K, et al. (2021) Effects of renalase deficiency on liver fibrosis markers in a nonalcoholic steatohepatitis mouse model. Mol Med Rep 23(3) |
| abstractText | Progression of nonalcoholic steatohepatitis (NASH) is attributed to several factors, including inflammation and oxidative stress. In recent years, renalase has been reported to suppress oxidative stress, apoptosis and inflammation. A number of studies have suggested that renalase may be associated with protecting the liver from injury. The present study aimed to clarify the effects of renalase knockout (KO) in mice with NASH that were induced with a cholinedeficient highfat diet (CDAHFD) supplemented with 0.1% methionine. Wild type (WT) and KO mice (6weekold) were fed a normal diet (ND) or CDAHFD for 6 weeks, followed by analysis of the blood liver function markers and liver tissues. CDAHFD intake was revealed to increase blood hepatic function markers, lipid accumulation and oxidative stress compared with ND, but no significant differences were observed between the WT and KO mice. However, in the KOCDAHFD group, the Adgre1 and Tgfb1 mRNA levels were significantly higher, and alphaSMA expression was significantly lower compared with the WTCDAHFD group. Furthermore, the Gclc mRNA and phosphorylated protein kinase B (Akt) levels were significantly lower in the KOND group compared with the WTND group. The results of the current study indicated that as NASH progressed in the absence of renalase, oxidative stress, macrophage infiltration and TGFbeta expression were enhanced, while alphaSMA expression in NASH may be partly suppressed due to the decreased phosphorylation of Akt level. |
