Pharmacological potential of wogonin in rotenone induced mice model of Parkinson's disease via targeting GSK-3β.

Wogonin, a naturally occurring flavonoid derived from Scutellaria species and widely used in traditional East Asian medicine for its anti-inflammatory and antioxidant effects. Although wogonin has demonstrated efficacy against oxidative stress and inflammation, its mechanistic role in Parkinson's disease (PD) remains incompletely understood. The present study investigated the neuroprotective potential of wogonin in a rotenone-induced mice model of PD, with particular emphasis on modulation of glycogen synthase kinase-3β (GSK-3β), a key kinase implicated in dopaminergic neurodegeneration. Swiss albino mice (n = 30) were randomly divided into five groups (six animals each): normal control (0.9% NaCl), rotenone (2 mg/kg, i.p.), wogonin (10 mg/kg, i.p.), wogonin (20 mg/kg, i.p.), and lithium chloride (LiCl; 300 mg/kg, p.o.). Treatments were administered for 21 days. Behavioral assessments, including rotarod, open field, string and narrow beam walk tests were conducted on days 0, 7, 14, and 21. On day 22nd, animals were sacrificed for biochemical, neuroinflammatory and neurotransmitter analysis. Wogonin treatment significantly improved motor coordination, balance and grip strength compared with rotenone treated mice. Biochemical analysis revealed reduced malondialdehyde and nitrite levels along with increased glutathione levels in wogonin treated groups. Enzyme-linked immunosorbent assay demonstrated significant reductions in interleukin-6, caspase-3 and GSK-3β levels accompanied by restoration of striatal dopamine content. In conclusion, wogonin attenuated motor dysfunction, oxidative stress and neuroinflammation in a rotenone induced PD model through inhibition of GSK-3β signaling, highlighting its therapeutic potential against PD.