Plantamajoside inhibits high glucose-induced oxidative stress, inflammation, and extracellular matrix accumulation in rat glomerular mesangial cells through the inactivation of Akt/NF-κB pathway.

Plantamajoside (PMS) is a phenylpropanoid glycoside that possesses anti-diabetic activity. However, the effect of PMS on diabetic nephropathy (DN) has not been investigated. This study aimed to evaluate the role of PMS in DN and the potential mechanism. The rat glomerular mesangial cells ((MCs) (HBZY-1 cells) were cultured under high glucose (HG) condition or normal condition with or without the treatment of PMS. The results showed that PMS ameliorated the cell injury that was induced by HG in HBZY-1 cells. The HG-caused increases in reactive oxygen species (ROS) and malondialdehyde (MDA) production and decrease in superoxide dismutase (SOD) activity were prevented by PMS. The qRT-PCR and ELISA assays demonstrated an anti-inflammatory activity of PMS, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6 in HG-induced HBZY-1 cells. Moreover, the increased levels of fibronectin (FN) and collagen type IV (Col IV) in HBZY-1 cells caused by HG were also reduced by PMS treatment. Furthermore, PMS significantly suppressed HG-induced activation of Akt/NF-κB signaling in HBZY-1 cells. Taken together, these findings indicated that PMS alleviated HG-induced injury in HBZY-1 cells through suppressing oxidative stress, inflammatory response, and extracellular matrix (ECM) accumulation the inactivating Akt/NF-κB pathway. Thus, PMS might possess potential capacity for the treatment of DN.