MicroRNA-124 modulates neuroinflammation in acute methanol poisoning rats via targeting Kruppel-like factor-6

Microglia activation-stimulated neuroinflammation exerts functionally in neurodegenerative diseases like brain injury. Acute methanol poisoning (AMP) is a crucial cause of death and morbidity that possibly leads to neuroinflammation. Studies have manifested that miRNAs can modulate microglia activation to mediate neuroinflammation. Nevertheless, the role of miR-124 in AMP-stimulated neuroinflammation is uncertain. This research was to explore the action of miR-124 in AMP-stimulated neuroinflammation and its molecular mechanism. The study findings indicated that AMP accelerated microglia activation and stimulated inflammation and oxidative stress in brain tissue of rats. MiR-124 expression was lowered in AMP rats, while KLF6 expression was elevated. Elevated miR-124 or repressed KLF6 increased the number of CD206(+) cells and decreased the number of CD68(+) cells, as well as restrained inflammation and NF-kappa B phosphorylation and induced superoxide dismutase, Nrf2/HO-1, and M2 polarization. MiR-124 modulated microglia activation via targeting KLF6. AMP repressed neuronal viability and enhanced neuronal apoptosis. Suppression of miR-124 further promoted AMP-induced damage to neurons, while inhibition of KLF6 turned around this phenomenon. Anyway, our study demonstrated that miR-124 accelerates M2 polarization via targeting KLF6 to ameliorate AMP-stimulated neuronal damage.

Automated summary

This study investigated the role of miR-124 in AMP-stimulated neuroinflammation and its molecular mechanism. The findings showed that miR-124 can modulate microglia activation via targeting KLF6, accelerating M2 polarization and alleviating neurodegeneration induced by AMP.