Neryl acetate modulates JNK signaling in streptozotocin-induced diabetic nephropathy

Diabetic nephropathy (DN) is a major complication of diabetes mellitus and a leading cause of chronic kidney disease. Oxidative stress and inflammation play key roles in DN progression and are associated with activation of the c-Jun N-terminal kinase (JNK) pathway. This study evaluated the nephroprotective effects of neryl acetate (NA) in streptozotocin-nicotinamide (STZ-NAD)-induced diabetic rats. Diabetes was induced in Wistar rats, followed by treatment with NA (25, 50, and 75 mg/kg). DN rats showed significant hyperglycemia, renal dysfunction, dyslipidemia, increased oxidative stress, and elevated inflammatory cytokines (p < 0.0001). NA treatment produced dose-dependent improvements, with 50 and 75 mg/kg significantly reducing blood glucose, improving renal function, restoring antioxidant enzyme levels, and suppressing pro-inflammatory cytokines, comparable to glimepiride. Histopathological findings confirmed marked recovery of renal architecture. These findings suggest that NA may attenuate oxidative stress and inflammation, thereby modulating upstream activators of JNK signaling and reducing renal injury. In conclusion, NA exhibits significant nephroprotective effects and may represent a promising therapeutic candidate for diabetic nephropathy.