Hirsutanol A exhibits neuroprotective activities against sevoflurane-induced neurotoxicity in aged rats.
Abstract
The neurotoxicity of the inhaled anesthetic, sevoflurane, has been documented in a number of studies. In this study, we conducted experiments to investigate whether Hirsutanol A (HA), a sesquiterpene compound from the fungus, Chondrostereum sp., can provide protection from sevoflurane-induced neurological toxicity in aged rats, and analyzed the underlying mechanisms. The cognitive dysfunction of rats following sevoflurane exposure was evaluated by behavioral tests. The neuronal cell survival was determined by Nissl staining. In addition, human neuroblastoma H4 cells were exposed to sevoflurane to establish an in vitro model. Apoptotic marker expression in hippocampal tissue was determined by western blotting. Cell apoptosis in vitro was also examined by TUNEL assay and flow cytometry. The expression and translocation of Nrf2 were examined by both western blot and immunofluorescence staining. Our results show that HA significantly attenuated sevoflurane-induced cognitive impairment in aged rats. In addition, HA treatment decreased sevoflurane-induced neuronal apoptosis in the hippocampus and alleviated Aβ accumulation. Our results also show that the neuroprotective effect of HA is associated with the activation of Nrf2 signaling...Continue Reading
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Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis