Effect of baicalin on oxidative stress, inflammation and pancreatic cell apoptosis in streptozotocin-induced diabetic rats

Background: Baicalin is a natural compound with established antioxidant and anti-inflammatory activities. Nevertheless, its specific influence on oxidative damage, inflammatory pathways, and pancreatic ?-cell apoptosis in streptozotocin-induced diabetes remains insufficiently characterized. Objectives: We evaluated the therapeutic role of baicalin to reduce inflammation, oxidative stress and pancreatic cell apoptosis in diabetic rats. Methods: 18 Wistar rats were grouped into a control, diabetic and diabetic rats with administered 100 mg/kg baicalin. Antioxidant capacity (TAC), 8-hydroxy-2?-deoxyguanosine (8-OHdG), malondialdehyde and protein carbonyls were measured. Apoptosis of pancreatic cells was examined and the expression of TNF-?, IL-10, catalase, superoxide dismutase, Caspases-3/9, Bcl2 and Bax was evaluated using Real Time PCR. Results: Baicalin administration significantly improved body weight, blood insulin, glucose levels, hyperlipidemia and TAC level (p < 0.01), while markedly decreased malondialdehyde, protein carbonyls and 8-OHdG contents (p<0.01) in diabetic animals. Baicalin treatment significantly reduced the percentage of pancreatic apoptotic cells compared to diabetic control (8.67 ± 1.17% vs. 14.46 ± 2.39%; p < 0.001). A marked increase was found in Bax, TNF-?, Caspases expression in diabetic control, but IL-10, superoxide dismutase, catalase and Bcl2 expression was markedly decreased (p < 0.001). Baicalin supplementation significantly improved the expression of these genes in pancreatic tissue (p < 0.01). Conclusion: Baicalin protects pancreatic cells and restores insulin production in diabetic subjects by enhancing the antioxidant pool, attenuating oxidative stress, inflammation and pancreatic cell apoptosis in diabetic subjects.