SALVIANOLIC ACID B ATTENUATES GLUCOLIPOTOXICITY-INDUCED OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN AML12 HEPATOCYTES VIA MODULATING CRBN/AMPK SIGNALING
TL;DR
It is suggested that SalB protects hepatocytes from glucolipotoxic injury by limiting oxidative damage, preserving mitochondrial function, and restoring CRBN-associated AMPK signaling.
Abstract
Salvianolic acid B (SalB) is a major water-soluble phenolic compound with reported antioxidant and metabolic regulatory properties. We investigated its hepatoprotective effects in AML12 cells exposed to high glucose and palmitic acid (HG-PA), an in vitro model of diabetes-associated non-alcoholic fatty liver disease. SalB showed minimal cytotoxicity and significantly improved cell viability after HG-PA challenge. It reduced mitochondrial reactive oxygen species and 4-hydroxynonenal accumulation, indicating attenuation of oxidative stress and lipid peroxidation. SalB also restored MitoTracker fluorescence and intracellular ATP levels, consistent with improved mitochondrial function and cellular bioenergetics. HG-PA increased cereblon (CRBN) expression and suppressed AMPKα phosphorylation, whereas SalB partially reversed both changes. These findings suggest that SalB protects hepatocytes from glucolipotoxic injury by limiting oxidative damage, preserving mitochondrial function, and restoring CRBN-associated AMPK signaling.