Published online Sep 19, 2023. doi: 10.5498/wjp.v13.i9.620
Peer-review started: May 19, 2023
First decision: June 1, 2023
Revised: July 4, 2023
Accepted: July 28, 2023
Article in press: July 28, 2023
Published online: September 19, 2023
Autophagy is associated with hippocampal injury after status epilepticus (SE), and is considered a potential mechanism with curative value. Baicalin, an emerging multi-therapeutic drug that has been demonstrated to exert neuroprotective effects in patients with nervous system diseases because of its antioxidant property.
We investigate the influence of Baicalin on the improvement of LiCl-Pilocarpine-induced rat SE.
We intended to investigate the potential role of autophagy in LiCl-pilocarpine-induced SE.
Nissl staining showed that Baicalin attenuates hippocampal injury and reduces the number of neuronal deaths in the hippocampus. Besides, the expression intensity of cleaved caspase-3 and apoptosis in hippocampal CA1 following SE were reversed by Baicalin, as proven by western blotting and terminal deoxynucleotidyl transferase dUTP nick end labelling assay. Furthermore, western blotting and immunofluorescence staining were used to measure the expression of autophagy markers (p62/SQSTM1, Beclin 1, and LC3) and apoptotic pathway markers (cleaved caspase-3 and Bcl-2).
Baicalin significantly upregulated autophagic activity and downregulated mitochondrial apoptotic pathway markers. Conversely, 3-methyladenine, a commonly used inhibitor of autophagy, was simultaneously administered to inhibit the autophagy induced by Baicalin, abrogating the latter’s protection on the mitochondria apoptotic level.
We illustrated that Baicalin induced activation of autophagy alleviates apoptotic death and protects the hippocampus of SE rats.
The improvement of LiCl-Pilocarpine-induced rat SE by Baicalin was validated.