Baicalin ameliorated neurological damage in animal models of stroke through its antioxidant and anti-apoptotic effects.

Abstract

Importance: Ischemic stroke leads to neuronal cell death due to a lack of oxygen and glucose. Baicalin is a flavonoid that has antioxidant and anti-inflammatory properties.

Objective: The aim of this study is to elucidate the anti-oxidant and anti-apoptotic effects of baicalin in animal models of stroke.

Methods: Vehicle or baicalin (100 mg/kg) was administered intraperitoneally immediately after the middle cerebral artery occlusion (MCAO) surgery. Neurobehavioral tests were conducted 24 h post-MCAO and brain tissue was isolated to assess histopathological changes and apoptosis-associated protein expression. Additionally, reactive oxygen species (ROS) and lipid peroxidation (LPO) assays were performed to evaluate oxidative stress.

Results: MCAO animals exhibited severe neurological deficits, which were significantly alleviated by baicalin treatment. Baicalin mitigated the up-regulation in ROS and LPO levels induced by surgery. MCAO damage led to severe histopathological lesions and an increase in terminal deoxynucleotidyl transferase dUTP nick end labeling-positive reactions, these alterations were alleviated by baicalin treatment. MCAO damage decreases the expression of Bcl-2 and increases the expression of Bax, baicalin alleviates these changes. Baicalin also attenuated the upregulation of caspase-3 expression caused by MCAO injury.

Conclusions and relevance: These results can suggest evidence that baicalin exerts neuroprotective effects by preventing apoptosis during cerebral ischemia. In conclusion, baicalin acts as a potent neuroprotective agent through its antioxidant and anti-apoptotic effects on neuronal cell damage.