Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats

Wang, Ying; Yin, Chunyue; Tai, Yanlei; Zhao, Zijun; Hou, Zhiyong; Wang, Qiujun

doi:10.3892/etm.2021.9636

Cited by 13 publications

(9 citation statements)

References 63 publications

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“…The MAC value of sevoflurane was 2.4% or 2.6% in rats or mice respectively, and the ED99 was 1.3MAC (Wang, et al, 2021). Therefore, 3.2% or 3.4% sevoflurane was selected in this study to establish the inhalation anesthesia model.…”

Section: Discussionmentioning

confidence: 99%

“…Most studies on learning and memory are based on the hippocampus as hippocampus is the central administration of learning and memory. Studies on the underlying mechanisms of post‐operative cognition mostly focus on pathways of inflammation (Granger, et al, 2021), apoptosis (Wang, et al, 2021) and Alzheimer’s disease (AD) (Wu, et al, 2018). As main component of senile plaques, amyloid‐β (Abeta) plays a vital role in the whole process of formation and progression of AD.…”

Section: Introductionmentioning

confidence: 99%

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ApoE transiently regulates hippocampus amyloid‐beta deposition to stable learning and memory ability in adult rats exposed in sevoflurane

Zhang

Zhu

2021

Ibrain

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Objective: Post-operative cognitive dysfunction (POCD) is a common central nervous system complication after surgery. Inhaled anesthetic sevoflurane is thought to have harmful effects on the developing and aged nerves, but its efects on adults' nervous system are less studied and the mechanism is not clear. Methods: Male adult rats were divided into control group and sevoflurane group. Rats from sevoflurane group were received 3.2% sevoflurane + carrier gas (1 L/min O 2 +1 L/min air) for 2 h, while control group received carrier gas for 2 h. Each group was subsequently divided into 3 subgroups according to the Day 1, Day 3, Day 7 after sevolurane anesthesia. Morris Water Maze, amyloid-beita (Abeta) and apolipoprotein E (ApoE) mRNA in hippocampus were analyzed. Then, adult ApoE-/-rats were also divided into control group and sevoflurane group. Each group was divided into 3 subgroups according to Day 1, Day 3 and Day 7. Abeta mRNA and protein expression in hippocampus were analyzed. Results: Compared with the control group, hippocampal Abeta mRNA and protein expression in rats from sevolurane group signiicantly increased in hippocampus on Day 7, while ApoE mRNA and protein expression increased on Day 1 and Day 3. There was no diference in times of crossing platforms, time during platform, times across platform quadrant and time percent during platform quadrant between each group. Compared with the control group, hippocampal Abeta and ApoE-/rats in sevolurane group did not change. Conclusion:ApoE modulates hippocampal Abeta deposition and stabilizes learning and memory ability in adult rats after sevolurane exposure, but this efect is not constant.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ApoE transiently regulates hippocampus amyloid‐beta deposition to stable learning and memory ability in adult rats exposed in sevoflurane

Zhang

Zhu

2021

Ibrain

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“…POCD can prolongs hospitalization and rehabilitation time, increases the incidence of disability, and decreases life quality and survival, thus resulting in a heavy economic burden on the health care system [5,[14][15]. Compared with common neurodegenerative diseases and POCD, not only do they share the same characteristic symptoms, at the same time brain structural changes are similar, including cerebral white matter changes, central neuroinflammation, neuronal apoptosis, and so on [16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Roles for c-Abl in postoperative neurodegeneration

Feng¹,

Fu²,

Yao³

et al. 2022

Int. J. Med. Sci.

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The nonreceptor tyrosine kinase c-Abl is inactive under normal conditions. Upon activation, c-Abl regulates signaling pathways related to cytoskeletal reorganization. It plays a vital role in modulating cell protrusion, cell migration, morphogenesis, adhesion, endocytosis and phagocytosis. A large number of studies have also found that abnormally activated c-Abl plays an important role in a variety of pathologies, including various inflammatory diseases and neurodegenerative diseases. c-Abl also plays a crucial role in neurodevelopment and neurodegenerative diseases, mainly through mechanisms such as neuroinflammation, oxidative stress (OS), and Tau protein phosphorylation. Inhibiting expression or activity of this kinase has certain neuroprotective and anti-inflammatory effects and can also improve cognition and behavior. Blockers of this kinase may have good preventive and treatment effects on neurodegenerative diseases. Cognitive dysfunction after anesthesia is also closely related to the abovementioned mechanisms. We infer that alterations in the expression and activity of c-Abl may underlie postoperative cognitive dysfunction (POCD). This article summarizes the current understanding and research progress on the mechanisms by which c-Abl may be related to postoperative neurodegeneration.

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“…Anesthesia induces the activation of pro-apoptotic proteins in the rat hippocampus, which may lead to mitochondrial membrane rupture, further leading to apoptosis [8][9][10]. In addition, anesthetics may induce oxidative stress and inflammation in the brain, resulting in neurotoxicity [2,3,11,12].…”

Section: Introductionmentioning

confidence: 99%

Chrysotoxine attenuates sevoﬂurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway

2021

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Objective: The aim of this study is to investigate the neuroprotective effect of chrysotoxine (CTX) on sevoflurane-treated nerve cells and uncover the potential regulation mechanism. Methods: Nerve cells treated with sevoflurane and CTX were subjected to MTT and apoptotic detection. Cell apoptosis and oxidative stress were detected by flow cytometry (FCM) and ELISA assays. In addition, immunoblot assay was performed to study the signaling pathway affected by CTX treatment. Results: CTX treatment promoted the cell viability and suppressed the apoptosis of sevoflurane-treated SH-SY5Y cells. In addition, CTX inhibited the sevoflurane-induced oxidative stress response and inflammatory response in nerve cells. Mechanically, CTX ameliorated neurotoxicity through activating the PI3K/AKT/GSK signaling pathway. Conclusion: Therefore, CTX can serve as a promising drug target for treating anesthetics-induced neurotoxicity.

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Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats

Cited by 13 publications

References 63 publications

ApoE transiently regulates hippocampus amyloid‐beta deposition to stable learning and memory ability in adult rats exposed in sevoflurane

ApoE transiently regulates hippocampus amyloid‐beta deposition to stable learning and memory ability in adult rats exposed in sevoflurane

Roles for c-Abl in postoperative neurodegeneration

Chrysotoxine attenuates sevoﬂurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway

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