Diabetic nephropathy (DN) is a serious and common complication of type 1 and 2 diabetes.
Gastrodin has been reported to suppress high
glucose (HG)-induced
inflammation and oxidative stress in vivo and in vitro. However, the effect of
gastrodin on DN has not been fully elucidated. The present study aimed to investigate the underlying mechanism involved in the effect of
gastrodin on podocyte injury caused by DN. Cell viability was evaluated using Cell Counting Kit-8 assay and secretion levels of TNF-α, IL-1β and
IL-6 were measured using ELISA. The levels of
malondialdehyde, activities of
lactate dehydrogenase and
superoxide dismutase were quantified using corresponding assay kits. Additionally, cell apoptosis was analyzed by TUNEL assay, whilst
protein expressions related to
inflammation, apoptosis and the
5'-AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway were measured by western blot analysis. The results showed that
gastrodin increased the viability of
MPC5 cells following HG stimulation.
Gastrodin also alleviated HG-induced
inflammation, oxidative stress and apoptosis in
MPC5 cells. Furthermore,
gastrodin promoted activation of the AMPK/Nrf2 pathway in
MPC5 cells. Treatment with the
AMPK inhibitor, compound C, reversed the inhibitory effects of
gastrodin on
inflammation, oxidative stress and cell apoptosis. To conclude, treatment of
MPC5 cells with
gastrodin can attenuate HG-induced
inflammation, oxidative stress and cell apoptosis by activating the AMPK/Nrf2 signaling pathway. Results from the current study suggest that
gastrodin can be used as an effective therapeutic agent against HG-induced podocyte injury in DN.