The Extract of Camellia japonica L. Protects Against Mice Cerebral Ischemia/Reperfusion Injury via Promoting the H₂S-BKCa Pathway

Background and Purpose The effect and mechanism of the extract of Camellia japonica L. (ECJ) on brain injury following cerebral ischemia/reperfusion (I/R) were demonstrated in the present study. Methods We detected mice’s brain damage after cerebral I/R and tested neuronal injury following oxygen-glucose deprivation/re-oxygenation (OGD/R) to evaluate the neuroprotection of ECJ. Besides, we tested the expressions of hydrogen sulfide (H 2 S) synthase cystathionine-β-synthase (CBS) and α subunit of large-conductance Ca 2+ -activated K + channels (BKα) both in brain tissues and culture neurons. Importantly, the roles of iberiotoxin (IbTX), BK Ca channel inhibitor, and CBS inhibitor aminooxyacetic acid (AOAA) on ECJ-mediated neuroprotection were assessed to explore the neuroprotective mechanism of ECJ. Results ECJ treatment could alleviate the mice’s brain injury following cerebral I/R and reduce the neuronal damage caused by OGD/R in vitro, which was inhibited by IbTX and AOAA. In addition, ECJ could increase the expression of CBS and the α subunit of BK Ca channel (BKα) in mice brain tissues and the culture neurons, as well as improve the H 2 S production. Furthermore, exogenous H 2 S donor NaHS also improved the BKα expression in OGD/R neurons. Importantly, NaHS alleviated the neuronal injury in vitro, which was inhibited by IbTX as well. Conclusion ECJ can protect against mouse cerebral I/R injury, the mechanism of which is correlated with promoting the CBS/H 2 S-BK Ca pathway.