Fig. 8

Mechanism diagram of MH regulating S100A8-CAMKK2-AMPK axis against cerebral IR injury. Cerebral IR injury leads to an increase in the expression of S100A8, which inhibits the activity of the CAMKK2/AMPK pathway. This inhibition leads to mitochondrial dysfunction, including oxidative damage, decreased membrane potential, and loss of mitochondrial criste structure, along with an increase in apoptosis-related proteins such as bax and cleaved-caspase3. Consequently, this results in neuronal apoptosis. By contrast, MH down-regulates the high expression of S100A8, thereby enhancing mitochondrial function via activation of the CAMKK2/AMPK signaling pathway. As a result, this inhibits neuronal apoptosis and ameliorates neurological injury during cerebral IR in rats.