Skullcapflavone II protects neuronal damage in cerebral ischemic rats via inhibiting NF-κB and promoting angiogenesis

Background: Cerebral ischemia (CI) is considered as a main cause of cerebral stroke (CS) and poses significant risk to the mankind across the world. In the present study, we intended to investigate the protective effect of Skullcapflavone II (SCP) a flavonoid isolated from S. baicalensis on cerebral ischemia/reperfusion (I/R) injury. Methods: The middle cerebral artery occlusion (MCAO) and reperfusion was used to create ischemic stroke rat model. The rats were treated with (5, 10, and 15 mg/kg) SCP and after the end of the experiment the rats were sacrificed and various biochemical parameters were assed to determine the pharmacological action of SCP. Results: SCP dramatically decreases cerebral edema, infarct volume, and improves neurological manifestation as confirmed by reduced neurological deficit. SCP also improves the survivability of neurons as evidenced by H and E and Nissl staining. The level of oxidative stress in the cerebral cortex of the rats was found reduced after treatment with SCP, as confirmed by increase in GSH and SOD activity with reduction in MDA content. In addition, SCP attenuated inflammation via reducing the level of TNF-alpha, IL-1 beta and IL-6 in brain tissues of rats. SCP increases the expression of Bcl2, cleaved caspase-3 and-9, while decreasing Bax, and NF-kappa B/TLR4. It causes induction of angiogenesis as suggested by increased expression of VEGF, Ang-1 and Tie-2 in cerebral cortex of rat. Conclusions: Our data determined that SCP may provide protective effect on the I/R-induced cerebral ischemia.

Automated summary

This study found that Skullcapflavone II (SCP) has a protective effect on cerebral ischemia/reperfusion injury by reducing cerebral edema, infarct volume, neurological deficits, oxidative stress, inflammation, and increasing angiogenesis.