Kaempferol protects retinal ganglion ceils from high-glucose-induced injury by regulating vasohibin-1.

Kaempferol is a medicinal flavonol derived from the roots of Kaempferia galanga L. Kaempferol can affect cell survival, apoptosis, and anti-oxidation, though its role and underlying mechanism in retinal ganglion cells with high-glucose injury remains unclear. In this study, we explored kaempferol's role in high-glucose injury in cells from the retinal ganglion cell (RGC) line. RGC cells were isolated and then cultured in high glucose (55 mmol/L) for 0 h, 12 h, 24 h, 48 h, or 72 h, and results showed decreased cell viability at 48 h and 72 h. We treated RGC cells with different concentrations of kaempferol (0 μmol/L, 20 μmol/L, 40 μmol/L, 60 μmol/L, 80 μmol/L, or 100 μmol/L) and high-glucose (55 mmol/L) for 48 h. The data indicated inhibited lactate dehydrogenase leakage, apoptosis, caspase-3 activity, and reactive oxygen species (ROS) levels. Moreover, whereas cell viability increased in RGC cells that were incubated with kaempferol (60 μmol/L, 80 μmol/L, or 100 μmol/L) and glucose (55 mmol/L), compared with glucose alone. Kaempferol (60 μmol/L) elevated ERK phosphorylation and vasohibin-1 (VASH1) expression, and inhibition of ERK phosphorylation reversed the effect of kaempferol (60 μmol/L) on VASH1 expression in RGC cells with high-glucose injury. Additionally, interference of VASH1 by VASH1 siRNA markedly reversed the effects of kaempferol (60 μmol/L) on cell viability, caspase-3 activity, and ROS levels in RGC cells with high glucose injury. Taken together, the results suggest that kaempferol protected retinal ganglion cells from high-glucose-induced injury via ERK and VASH1 signaling.