Abstract
Chronic hyperglycemia leads to myosin light chain kinase (MLCK) upregulation and induces neuronal damage. However, the underlying molecular mechanism of neuronal damage in hyperglycemia has not yet been fully elucidated. In the present study, hippocampal neuronal cells were cultured and treated with a high glucose concentration (45 mmol/l). The results demonstrated that high glucose induced shrinking of the synapses, nuclear shape irregularity and microfilament damage. Filamentous actin (F‑actin) filaments were rearranged, cell apoptosis rate was increased and the protein expression of MLCK and phosphorylated (p)‑MLC was upregulated. The MLCK inhibitor ML‑7 largely reversed the alterations in the microfilament cytoskeleton, inhibited F‑actin depolymerization, reduced apoptosis and downregulated MLCK and p‑MLC protein expression. Overall, these results indicated that high glucose upregulated MLCK to promote F‑actin depolymerization, which induced microfilament cytoskeleton rearrangement in hippocampal neuronal cells.