Diabetic nephropathy (DN), a microvascular complication of diabetes, has emerged as an important health problem worldwide. There is strong evidence to suggest that oxidative stress, inflammation, and fibrosis play a pivotal role in the progression of DN. Apigenin has been shown to possess antioxidant, anti-inflammatory, anti-apoptotic, anti-fibrotic, as well as anti-diabetic properties. Hence, we evaluated whether apigenin halts the development and progression of DN in streptozotocin (STZ)-induced diabetic rats. Male albino Wistar rats were divided into control, diabetic-control, apigenin treatment groups (5-20 mg/kg p.o. respectively), apigenin per se (20 mg/kg p.o.) and ramipril treatment group (2 mg/kg p.o.). A single injection of STZ (55 mg/kg i.p) was administered to all the groups, except control and per se groups, to induce type 1 diabetes mellitus. Rats with fasting blood glucose > 250mg/dl were included in the study and randomized to different groups. Thereafter, the protocol was continued for 8 months in all the groups. Apigenin (20 mg/kg) treatment attenuated renal dysfunction, oxidative stress and fibrosis (decreased TGF-β1, fibronectin and type IV collagen) in the diabetic rats. It also significantly prevented MAPK activation which inhibited inflammation (reduced TNF-α, IL-6 and NF-B expression) and apoptosis (increased expression of Bcl-2 and decreased Bax and Caspase-3). Furthermore, histopathological examination demonstrated reduced inflammation, collagen deposition and glomerulosclerosis in the renal tissue. In addition, all these changes were comparable to those produced by ramipril. Hence, apigenin ameliorated renal damage due to DN by suppressing oxidative stress, fibrosis and by inhibiting MAPK pathway.