ArticleExperimental and therapeutic medicine2021
Apoptosis inhibition is involved in improvement of sevoflurane-induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Anesthetic Techniques and Postoperative Cognitive Dysfunction in Older Adults: Current Evidence and Perioperative Strategies.Medicina (Kaunas, Lithuania) · 2026Review
- The role of sevoflurane in postoperative cognitive dysfunction.Medical gas research · 2024Article
- Specific antagonist of receptor for advanced glycation end‑products attenuates delirium‑like behaviours induced by sevoflurane anaesthesia with surgery in aged mice partially by improving damage to the blood‑brain barrier.Experimental and therapeutic medicine · 2023Article
- Behavioral and Molecular Effects of Thapsigargin-Induced Brain ER- Stress: Encompassing Inflammation, MAPK, and Insulin Signaling Pathway.Life (Basel, Switzerland) · 2022Article
- Electro-Acupuncture Pretreatment Ameliorates Anesthesia and Surgery-Induced Cognitive Dysfunction Via Inhibiting Mitochondrial Injury and nEuroapoptosis in Aged Rats.Neurochemical research · 2022Article
- Sevoflurane exposure causes neuronal apoptosis and cognitive dysfunction by inducing ER stressFrontiers in aging neuroscience · 2022Article
- Roles for c-Abl in postoperative neurodegeneration.International journal of medical sciences · 2022Review
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Sevoflurane, a commonly used anesthetic agent has been confirmed to induce cognitive impairment in aged rats. Normobaric hyperoxia preconditioning has been demonstrated to induce neuroprotection in rats. The present study aimed to determine whether normobaric hyperoxia preconditioning could ameliorate cognitive deficit induced by sevoflurane and the possible mechanism by which it may exert its effect. A total of 66, 20-month-old male Sprague-Dawley rats were randomly divided into 3 groups (n=22 each): Rats in the control (C) and sevoflurane anesthesia (S) groups received no normobaric hyperoxia preconditioning before sevoflurane exposure, rats in the normobaric hyperoxia pretreatment (HO) group received normobaric hyperoxia preconditioning before sevoflurane exposure (95% oxygen for 4 continuous h daily for 6 consecutive days). The anesthesia rats (S and HO groups), were exposed to 2.5% sevoflurane for 5 h, while the sham anesthesia rats (C group) were exposed to no sevoflurane. The neurobehavioral assessment was performed using a Morris water maze test, the expressions of the apoptosis proteins were determined using western blot analysis, and the apoptosis rate and cytosolic calcium concentration were measured by flow cytometry. Normobaric hyperoxia preconditioning improved prolonged escape latency and raised the number of platform crossings induced by sevoflurane in the Morris water maze test, increased the level of bcl-2 protein, and decreased the level of bax and active caspase-3 protein, the apoptosis rate and cytosolic calcium concentration in the hippocampus 24 h after sevoflurane exposure. The findings of the present study may imply that normobaric hyperoxia preconditioning attenuates sevoflurane-induced spatial learning and memory impairment, and this effect may be partly related to apoptosis inhibition in the hippocampus. In conclusion, normobaric hyperoxia preconditioning may be a promising strategy against sevoflurane-induced cognitive impairment by inhibiting the hippocampal neuron apoptosis.
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