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.