Phillyrin alleviates high glucose-induced oxidative stress and inflammation in HBZY-1 cells through inhibition of the PI3K/Akt signaling pathway.

This article investigates the protective effects of phillyrin, a major lignin compound from Forsythia suspensa, on high glucose (HG)-induced injury in HBZY-1 glomerular mesangial cells, which are key effector cells in diabetic nephropathy (DN). The study demonstrates that phillyrin inhibits HG-induced cell proliferation, extracellular matrix accumulation, oxidative stress, and inflammation, while promoting apoptosis and autophagy. Mechanistically, phillyrin activates the nuclear factor-E2-related factor 2 (Nrf2) antioxidant pathway and suppresses the phosphatidylinositol 3 kinase (PI3K)/serine/threonine kinase (Akt)/mechanistic target of rapamycin (mTOR) and nuclear factor kappa B (NF-κB) signaling pathways. These findings suggest that phillyrin may be a promising therapeutic candidate for preventing or treating DN by modulating oxidative stress, inflammation, and cellular homeostasis in renal mesangial cells.