Galangin protects against oxidative damage and attenuates inflammation and apoptosis via modulation of NF-κB p65 and caspase-3 signaling molecules in a rat model of diabetic nephropathy.

Abstract

Oxidative tissue injury and inflammatory response are the main regulators of diabetic nephropathy (DN). The potential protective effect of galangin (Gal), a powerful flavonoid with several promising bioactivities, on hyperglycemia-induced kidney injury in a rat model of DN has been investigated in this study. A rat model of diabetes was induced by intraperitoneal injection of 50 mg kg⃛1 streptozotocin (STZ). Rats were treated orally with Gal (15 mg kg⃛1 d⃛1) for 8 weeks. Diabetic animals demonstrated elevated levels of glucose and glycosylated hemoglobin along with reduced insulin levels. Hyperglycemia was associated with a remarkable increase in malondialdehyde and protein carbonyl along with a significant decrease in reduced glutathione, superoxide dismutase and catalase in the kidney of rats. Diabetic rats showed a remarkable increase in blood creatinine and blood urea nitrogen (BUN) and urine albumin. Additionally, diabetic rats demonstrated increased nuclear factor kappaB (NF-κB) p65 expression and pro-inflammatory cytokines (tumor necrosis factor-α, interleukin 1β and interleukin 6) levels in the renal tissue. Gal ameliorated hyperglycemia, oxidative stress and inflammation and increased antioxidants in the kidney of diabetic rats. In addition, Gal decreased Bax and caspase-3 and increased Bcl-2 in the kidney of diabetic animals. In conclusion, Gal improved renal function and ameliorated oxidative stress, inflammation and apoptosis in the kidney of diabetic rats. Gal might have therapeutic potential for the treatment of DN, which deserves exploration in upcoming studies.