Subarachnoid hemorrhage (SAH) caused brain damage accounts for more than 20 % death of patients with cerebrovascular diseases. We aimed to investigate the effects of Astragaloside IV (AS-IV) on SAH-induced brain damage and its underlying mechanism. SAH rat model was established and treated with or without AS-IV. Brain injury and function were evaluated by neurological score, brain water content, Nissl staining, and behavioral experiments using Morris water maze. The protein expression related to SAH caused inflammation and neuron apoptosis were assessed. As expected, after 24 h of SAH, Garcia score, beam balance score and the number of intact neurons were significantly reduced in SAH rats compared to sham rats, but AS-IV treatment dramatically elevated the two scores and the number of intact neuron number. Brain water content that increased after SAH was also declined in AS-IV treated rats compared to untreated rats. In addition, SAH rats treated with AS-IV also showed better neurological outcomes than untreated SAH rats including shorter escape time and swimming distance, longer quadrant stay in the Morris water maze and increased fall latency from the rod rotating. In addition, in the SAH rats, the anti-apoptosis pathway phosphoinositide 3-kinase (PI3K)/ protein kinase B (Akt) was activated while nuclear factor-κB (NF-κB) signaling was markedly repressed by AS-IV. Several apoptosis associated genes including FoxO1, Bim, Bax and a typical apoptosis marker cleaved-caspase-3 were all downregulated by AS-IV. In conclusion, this study found a protective role of AS-IV in SAH-induced brain injury through regulating PI3K and NF-κB signaling pathways.
Keywords: Apoptosis; Inflammation; Phosphoinositide 3-kinase (PI3K); Protein kinase B (Akt); Subarachnoid hemorrhage (SAH).
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