Involvement of Nrf-2/HO-1 pathway in sevoflurane-induced cognitive improvement in rats with traumatic brain injury

Cui, Li; Yu, Tianyu; Gong, Lirong; Mu, Rui; Zhang, Yuan; Yu, Jianbo

doi:10.1016/j.bbr.2021.113200

Cited by 6 publications

(4 citation statements)

References 34 publications

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“…Further research has highlighted the critical role of Nrf2 and Hemeoxygenase-1 (HO-1) in facilitating the effects of compounds like astaxanthin or hydrogen-rich saline solutions, which are known to reduce ROS production and prevent neuronal apoptosis [88,89]. This underscores the therapeutic potential of targeting the Nrf2/HO-1 pathway to protect against synaptic and cognitive dysfunction following a TBI [90].…”

Section: Antioxidant Strategies In Traumatic Brain Injury (Tbi) Therapymentioning

confidence: 99%

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

Silvestro,

Raffaele,

Quartarone

et al. 2024

IJMS

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A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to the brain: primary and secondary. Secondary damage is particularly critical as it involves complex processes unfolding after the initial injury. These processes can lead to cell damage and death in the brain. Understanding how these processes damage the brain is crucial for finding new treatments. This review examines a wide range of literature from 2021 to 2023, focusing on biomarkers and molecular mechanisms in TBIs to pinpoint therapeutic advancements. Baseline levels of biomarkers, including neurofilament light chain (NF-L), ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), Tau, and glial fibrillary acidic protein (GFAP) in TBI, have demonstrated prognostic value for cognitive outcomes, laying the groundwork for personalized treatment strategies. In terms of pharmacological progress, the most promising approaches currently target neuroinflammation, oxidative stress, and apoptotic mechanisms. Agents that can modulate these pathways offer the potential to reduce a TBI’s impact and aid in neurological rehabilitation. Future research is poised to refine these therapeutic approaches, potentially revolutionizing TBI treatment.

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Section: Antioxidant Strategies In Traumatic Brain Injury (Tbi) Therapymentioning

confidence: 99%

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

Silvestro,

Raffaele,

Quartarone

et al. 2024

IJMS

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“…Nrf2 is a basic leucine zipper transcription factor that plays a vital role in regulating cellular responses to oxidative stress (He et al., 2019 ; Lei et al., 2020 ; L. Zhang & Wang, 2018 ). Accumulating evidence has suggested that Nrf2 is activated after TBI to exert antioxidative effects (Li et al., 2021 ; H. Wang et al., 2020 ). Under basal physiological conditions, Nrf2 is sequestered in the cytoplasm and is degraded by binding to its suppressor Keap1 (H. Wang et al., 2020 ).…”

Section: Discuctionmentioning

confidence: 99%

“…Zhang & Wang, 2018). Accumulating evidence has suggested that Nrf2 is activated after TBI to exert antioxidative effects (Li et al, 2021;. Under basal physiological conditions, Nrf2 is sequestered in the cytoplasm and is degraded by binding to its suppressor Keap1 (H. Wang et al, 2020).…”

Section: Discuctionmentioning

confidence: 99%

Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway

et al. 2022

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Background Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mild hypothermia (32–35°C) has been found to show neuroprotective effects against TBI. However, the specific mechanism is still elusive. In the current study, we explored the relationship between oxidative damage after TBI and treatment with mild hypothermia as well as the underlying molecular mechanisms. Methods We used the closed cortex injury model to perform the brain injury and a temperature monitoring and control system to regulate the body temperature of mice after injury. Adult male C57BL/6 mice were adopted in this study and divided into four experimental groups. Tissue samples were harvested 24 h after injury. Results First, our results showed that treatment with mild hypothermia significantly improved neurobehavioral dysfunction and alleviated brain edema after TBI. Moreover, treatment with mild hypothermia enhanced the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase and reduced the accumulation of lipid peroxidation malondialdehyde. Importantly, the expression and activation of the nuclear factor erythroid 2‐related factor 2‐antioxidant response element (Nrf2‐ARE) pathway were upregulated by mild hypothermia after TBI. Finally, treatment with hypothermia significantly decreased the cell apoptosis induced by TBI. Conclusion Our results showed that the protective effects of mild hypothermia after TBI may be achieved by the upregulation of the Nrf2‐ARE pathway and revealed Nrf2 as a potentially important target to improve the prognosis of TBI.

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“…There is no denying that sevoflurane exposure is associated with neurodegeneration; however, there are study tips in cerebral ischemia‐reperfusion injury, traumatic brain injury, sevoflurane by inhibiting the activation of microglia, reduce rats tissue excessive oxidative stress and inflammation, and protection of injury of rats. 54 , 55 Does this suggest that sevoflurane can activate microglia to exert anti‐inflammatory effects and reduce brain damage in the existing brain tissue damage, while in normal brain tissue, exposure to sevoflurane leads to the accumulation of neurotoxic substances and mediates microglia are activated for a long time, increase the expression of inflammatory factors through various inflammatory signaling pathways, release inflammatory mediators to cause oxidative stress, damage nerve tissue, and eventually develop into neurodegenerative diseases.…”

Section: Sevoflurane and Neurodegenerative Diseasesmentioning

confidence: 99%

Current status of sevoflurane anesthesia in association with microglia inflammation and neurodegenerative diseases

Huang

2022

Ibrain

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Sevoflurane is one of the most commonly used volatile anesthetics in clinical practice and is often used in pediatric anesthesia and intraoperative maintenance. Microglia exist in the central nervous system and are innate immune cells in the central nervous system. Under external stimulation, microglia are divided into two phenotypes: proinflammatory (M1 type) and anti‐inflammatory (M2 type), maintaining the stability of the central nervous system through induction, housekeeping, and defense functions. Sevoflurane can activate microglia, increase the expression of inflammatory factors through various inflammatory signaling pathways, release inflammatory mediators to cause oxidative stress, damage nerve tissues, and eventually develop into neurodegenerative diseases. In this article, the relationship between sevoflurane anesthesia and microglia inflammation expression and the occurrence of neurodegenerative diseases is reviewed as follows.

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Involvement of Nrf-2/HO-1 pathway in sevoflurane-induced cognitive improvement in rats with traumatic brain injury

Cited by 6 publications

References 34 publications

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway

Current status of sevoflurane anesthesia in association with microglia inflammation and neurodegenerative diseases

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