Baicalein is a flavonoid that has been shown to offer neuroprotection in kinds of brain injury models. A study investigated the effects of baicalein on early brain injury (EBI) in rats following SAH. SAH was inducted in male Sprauge-Dawley rats by injection of fresh non-heparinized arterial blood into the prechiasmatic cistern. Baicalein (30 or 100mg/kg) or vehicle were administrated 30min after injury. Neurological deficit, brain edema, blood-brain barrier (BBB) permeability and neural cell apoptosis were assessed. To explore the further mechanisms, the change of toll like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) signaling pathway and the levels of apoptosis associated proteins were also examined. Our study showed that treatment with baicalein (30mg/kg) significantly improved neurological function at 24h after SAH and reduced brain edema at both 24h and 72h after SAH. Baicalein also significantly reduced neural cell death, BBB permeability. These changes were associated with the remarkable reductions of TLR4 expression, IκB-α degradation, NF-κB translocation to nucleus, as well as the expressions of matrix metalloproteinase-9, tight junctions protein, interleukin-1β and tumor necrosis factor- ɑ. These findings suggest that baicalein may ameliorate EBI after SAH potentially via inhibition of inflammation-related pathway 1).
Findings suggest that baicalein prevents cisplatin-induced apoptosis through inhibition of the mitochondrial depolarization in human glioma cells 2).