Cefminox sodium alleviates the high-fat high-sugar-fed mice's hepatic fatty accumulation via multiple pathways

The increasing global prevalence of nonalcoholic fatty liver disease (NAFLD) starves for effective therapy, but no agent has been approved yet. We sought to evaluate the therapy of cefminox sodium (CMNX) on fatty accumulation in animal and cell models and explore the underlying mechanisms. The results revealed that CMNX reduced the gain of the liver and alleviated fatty accumulation both in high-fat high-sugar diet (HFHSD) mice's livers and WRL-68 cells. In HFHSD mice's livers and FFAs exposure hepatic cells, ACC1, SREBP-1c, and CYP2E1 were enhanced expression, which were reversed by CMNX treatment. In addition, PPAR gamma, PPAR alpha, PCK1, and ACSL4 expressions were increased in CMNX-treated WRL-68 cells. These findings suggest that CMNX improves fatty accumulation in HFHSD mice/hepatic cells by restraining fatty acid synthesis and facilitating fatty acid oxidation.

Automated summary

The study demonstrated that cefminox sodium (CMNX) has a therapeutic effect on fatty accumulation in animal and cell models. CMNX reduced fatty liver in mice on a high-fat high-sugar diet and alleviated fatty accumulation in liver cells. The mechanism behind this effect involves inhibition of fatty acid synthesis and facilitation of fatty acid oxidation.