Ischemic stroke is the second most common cause of death worldwide and
cerebral ischemia/reperfusion (I/R) injury also leads to serious tissue damage.
Astilbin, a natural bioactive
flavonoid compound, has been reported to have protective effects on neurological diseases. This study aims to investigate the effects of
astilbin on cerebral I/R injury and determine the mechanisms involved. The results demonstrated that, in cerebral I/R rats,
astilbin could attenuate I/R injury in the hippocampal region, decreasing the activity of
lactate dehydrogenase (LDH) and
malondialdehyde (MDA) in the rat brain.
Astilbin also inhibited the I/R-induced upregulation of pro-inflammatory mediators (TNFα, IL-1β, IL-6). Similarly, in
hypoxia/reperfusion (H/R) treated human
neuroblastoma cells,
astilbin could increase the cell viability of SH-SY5Y, decrease the activity of LDH and MDA, and inhibit the H/R-induced upregulation of pro-inflammatory mediators. For the mechanism study, western blot results indicated that
astilbin could inhibit the expression of
Toll-like receptor 4 (TLR4), myeloid differential
protein 88 (MYD88) and phosphorylated NF-κB p65 in H/R treated SH-SY5Y cells. The research indicated that
astilbin ameliorated cerebral I/R injury partly via the TLR4/MyD88/NF-κB pathway.
Astilbin may have potential
therapeutic effects on
cerebral ischemia.