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 β-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-α, 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-α, 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.