Rats were pre-treated with baicalein (10 mg/kg and 30 mg/kg) for ten days prior to inducing ischemia via middle cerebral artery occlusion (MCAO), followed by reperfusion. Outcome measures included infarct volume, neuron-specific enolase (NSE) levels, STAT-1 phosphorylation, and oxidative stress markers, such as thiobarbituric acid reactive substances (TBARS) to assess malondialdehyde levels.

Baicalein pretreatment significantly reduced infarct volumes (17.45% ± 2.4%, 9.04% ± 1.94% vs. 25.93% ± 1.25%; p < 0.01) compared to the vehicle group. NSE release was also decreased (2.34 ng/mL ± 0.89, 1.12 ng/mL ± 0.51 vs. 6.39 ng/mL ± 1.14; p < 0.01), as was TBARS production (1.62 ng/mL ± 0.32, 1.07 ng/mL ± 0.32 vs. 2.38 ng/mL ± 0.23; p < 0.05). Additionally, baicalein inhibited STAT-1 phosphorylation (0.0251 and 0.0238 vs. 0.0376 in the vehicle group).

Baicalein pretreatment provides significant neuroprotection against ischemia-reperfusion injury, as demonstrated by reduced infarct size, oxidative stress, and neuronal damage. Its inhibitory effect on STAT-1 phosphorylation suggests a mechanism for its neuroprotective action, positioning baicalein as a potential therapeutic candidate for ischemic stroke.