The results suggested that inhibition of BECN1 suppresses accumulation of lipid peroxidation by increasing system X<sub>c</sub><sup>-</sup> activity in EBI after SAH, and BECN1 may be a new effective target for EBI treatment after SAH.
Compared with the SAH group, we observed normal morphology in the hippocampus and better learning and memory ability in the rats in the drug group, accompanied by downregulated ROCK2 expression and increased beclin-1 and LC3-II expression.
In addition, the normal autophagic flux induced by EGCG at both the initiation and formation stages regulated Atg5 and Beclin-1 after SAH for the timely elimination of damaged mitochondria.