Baicalin protects mice brain from apoptosis in traumatic brain injury model through activation of autophagy

Abstract

Autophagy is associated with secondary injury following traumatic brain injury (TBI) and is expected to be a therapeutic target. Baicalin, a neuroprotective agent, has been proven to exert multi-functional bioactive effects in brain injury diseases. However, it is unknown if Baicalin influences autophagy after TBI. In the present study, we aimed to explore the effects that Baicalin had on TBI in a mice model, focusing on autophagy as a potential mechanism. We found that Baicalin administration significantly improved motor function, reduced cerebral edema, and alleviated disruption of the blood-brain barrier (BBB) after TBI in mice. Besides, TBI-induced apoptosis was reversed by Baicalin evidenced by Nissl staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and the level of cleaved caspase-3. More importantly, Baicalin enhanced autophagy by detecting the autophagy markers (LC3, Beclin 1, and p62) using western blot and LC3 immunofluorescence staining, ameliorating mitochondrial apoptotic pathway evidenced by restoration of the TBI-induced translocation of Bax and cytochrome C. However, simultaneous treatment with 3-MA inhibited Baicalin-induced autophagy and abolished its protective effects on mitochondrial apoptotic pathway. In conclusion, we demonstrated that Baicalin enhanced autophagy, ameliorated mitochondrial apoptosis and protected mice brain in TBI mice model.