Abstract
BackgroundIsoflurane-induced neuroapoptosis and cognitive impairment has been previously reported. Hydrogen sulfide (H2S) has been shown to be a neuromodulator that is thought to have anti-apoptotic, anti-inflammatory, and anti-oxidative benefits. However, it is not known if H2S is protective against anesthesia-induced apoptosis and cognitive defects.MethodsIn this study, postnatal day 7 (P7) Sprague-Dawley rats were randomly divided into four groups: control group (normal saline), H2S group (NaHS 28 μM/kg), isoflurane group (normal saline +0.75% isoflurane) and H2S preconditioning group (NaHS 28 μM/kg + 0.75% isoflurane). After exposure to isoflurane for 6 h, half the numbers of rats in each group were euthanized, and the hippocampus and cerebral cortex were dissected and examined for apoptosis by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) technique and western blot. After 6 weeks, the remaining rats were subjected to a Morris water maze (MWM) test for behavioral assessment.ResultsThe TUNEL assay and western blot showed that when rats were preconditioned with NaHS, neuroapoptosis decreased significantly both in hippocampus and cerebral cortex compering with the isofulrane group. The MWM showed that P7 rats administration of NaHS improved cognitive impairments induced by isoflurane.ConclusionsThe current study demonstrates that H2S attenuates isoflurane-induced neuroapoptosis and improves cognitive impairments in the developing rat brain.
Highlights
Isoflurane-induced neuroapoptosis and cognitive impairment has been previously reported
Hydrogen sulfide (H2S) mitigates neuronal apoptosis induced by 0.75% isoflurane No signs of abdominal pain or discomfort were observed after administration of NaHS or normal saline, and none of the rats died
After exposure to 0.75% isoflurane for 6 h, transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were quantitated in all assessed brain samples (Fig. 1A), and compared with the CON group, neuronal apoptosis was higher (Fig. 1A: d, e, f ) in both the hippocampus and cerebral cortex
Summary
Isoflurane-induced neuroapoptosis and cognitive impairment has been previously reported. Hydrogen sulfide (H2S) has been shown to be a neuromodulator that is thought to have anti-apoptotic, antiinflammatory, and anti-oxidative benefits. It is not known if H2S is protective against anesthesia-induced apoptosis and cognitive defects. It is principally an agonist for the γ-aminobutyric acid (GABA) type A receptor [8], thereby altering synaptic function [9]. It has been reported that immature rats exposed to isoflurane have persistent memory and learning impairments, which are associated with widespread caspase-3 activation and neuronal apoptosis [3, 6, 11]
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