High glucose impairs autophagy and mitochondrial homeostasis in human dental pulp cells

This study aimed to investigate the effects of high-glucose exposure on human dental pulp cells and to explore associated changes in autophagy, mitochondrial homeostasis, and AMPK/mTOR signaling. Human dental pulp cells were cultured in vitro and assigned to a control group, a 5 mmol/L low-glucose group, and a 35 mmol/L high-glucose group. Cell viability was assessed using the CCK-8 assay at 24, 48, 72, and 96 h. The expression levels of p-AMPKα, p-mTOR, SQSTM1/p62, LC3B, and β-actin were detected by western blotting. Intracellular reactive oxygen species were measured using DCFH-DA staining, and cellular glutathione and ATP levels were evaluated using assay kits. Compared with the low-glucose group, high-glucose exposure increased p62 expression, reduced LC3B expression, decreased AMPKα phosphorylation, and increased mTOR phosphorylation. High-glucose exposure also increased intracellular reactive oxygen species levels, reduced glutathione content, and decreased ATP levels. These findings suggest that high-glucose exposure impairs autophagy-related activity and disrupts mitochondrial homeostasis in human dental pulp cells, accompanied by changes in AMPK/mTOR signaling.