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.