Schisandrin B Alleviates Lipid Metabolism Disorders and Apoptosis of MAFLD via Modulation of PPARγ-PCK1 and Caspase-3 Signaling Pathways.

ABSTRACT: Objectives: This study focuses on the regulatory mechanism of Schisandrin B (Sch B) on the lipid metabolism and apoptosis of AML-12 liver cells, with a particular emphasis on its potential therapeutic effect and mechanism of action in preventing and treating metabolic-associated fatty liver disease (MAFLD) by activating the PPARγ signaling pathway. Methods: An MAFLD cell model was established by inducing AML-12 cells with a mixture of oleic acid (OA) and palmitic acid (PA) (2:1). AML-12 cells were divided into a control group, a model group, and 20 μM and 40 μM Sch B groups. The cells were lysed and prepared into the cell suspension, then the cell suspension was centrifuged to obtain its supernatant, and the levels of total cholesterol (TC), triglycerides (TG), alanine aminot

SUBMITTER: Gao M 

PROVIDER: S-EPMC12567207 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature