AMPK mitochondria briefs

Corilagin saves glutathione, membrane potential, and the AMPK-TFAM axis in high-glucose neuroblastoma cells

In SH-SY5Y cells, 50 mM glucose for 24 hours depletes reduced glutathione, raises intracellular and mitochondrial reactive oxygen species, drops membrane potential, fragments the network, and increases cell death. Corilagin pretreatment opposes each of those changes and restores AMPK phosphorylation plus SIRT1, PGC-1α, and TFAM. The named redox species is reduced glutathione, one side of the GSH/GSSG couple. No metal site is identified. The abstract's wider disease framing (diabetic nephropathy, cerebral ischemia) is not the experiment it describes.