Baicalein Protects Against Ischemia-Reperfusion Injury in a Rat Model of Ischemic Stroke: Role of STAT-1 Phosphorylation
Dong-Ick Shin1, Hyeyoung Kwon2, Ho-seong Han3
1Neurology, Chungbuk National University Hospital, Chungbuk National University, 2Chungbuk National University, KHY Clinic, 3Yuseong Sun Hospital
Objective:
This study investigates the neuroprotective effects of baicalein, a flavonoid derived from Scutellaria baicalensis, in reducing ischemia-reperfusion (I-R) injury in the brain. It also examines baicalein's role in reducing STAT-1 phosphorylation, which is associated with neuronal apoptosis in ischemic stroke.
Background:
Ischemia-reperfusion injury is a major complication following ischemic stroke, leading to neuronal death. Phosphorylated STAT-1 has been shown to promote apoptotic pathways in neurons after I-R injury. Although baicalein has demonstrated neuroprotective properties in various models, its specific effects on I-R injury and STAT-1 phosphorylation have not been fully explored. This study aims to address these gaps by evaluating baicalein’s protective mechanisms in a rat model of cerebral I-R injury.
Design/Methods:
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.
Results:
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).
Conclusions:
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.
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