| Literature DB >> 27588101 |
Jian Sun1, Xiao-Ling Chen2, Jin-Yu Zheng3, Jian-Wei Zhou4, Zheng-Liang Ma5.
Abstract
Exposure to general anesthesia may cause severe neurotoxicity in developing brain due to neuronal apoptosis. Astragaloside IV (AS IV) has antioxidant and antiapoptosis properties; however, its effects on anesthesia-induced neuroapoptosis have not been studied. In the present study, we determined whether AS IV pre-treatment is able to reduce isoflurane exposure-induced neuroapoptosis in rats. New born rats were pre-treated with AS IV or solvent by oral gavage for three days, then exposed to isoflurane. The results showed that pre-treatment of AS IV significantly inhibited isoflurane-induced neural apoptosis in the hippocampus of new born rats, and such protection was accompanied by reduced levels of caspase-3, nuclear factor-κB activation and phosphorylated c-Jun N-terminal kinase, extracellular signal-regulated kinase and increased levels of B-cell lymphoma-2, glycogen synthase kinase-3β, Klotho and phosphorylated protein kinase B. Furthermore, AS IV pre-treatment significantly alleviated isoflurane-induced oxidative stress and proinflammatory cytokine release in the rat hippocampus and serum. In summery, the results of the study demonstrated that AS IV is able to protect developing brain from anesthesia-induced neuroapoptosis via anti-oxidant and anti-inflammatory activities.Entities:
Keywords: anesthesia; astragaloside IV; inflammation; neurotoxicity; oxidative stress
Year: 2016 PMID: 27588101 PMCID: PMC4998115 DOI: 10.3892/etm.2016.3519
Source DB: PubMed Journal: Exp Ther Med ISSN: 1792-0981 Impact factor: 2.447