Calycosin attenuates the inflammatory damage of                     microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-&amp;kappa;B                     signaling pathway

Li, Xiang; Yang, Xiaohong; Lü, Huiling; Wang, Wenbo; Cai, Lixin; Chen, Jian; Wang, Yong

doi:10.3724/abbs.2023125

Cited by 9 publications

(3 citation statements)

References 30 publications

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“…Naringenin is a flavonoid prevalent in citrus fruits that has exhibited antioxidant properties and shown neuroprotective effects in preclinical models of TBI ( Anwar et al, 2021 ; Yousuf et al, 2022 ; Li et al, 2023b ). The primary mechanical injury in TBI triggers secondary injury cascades involving neuroinflammation, oxidative stress, mitochondrial dysfunction, and excitotoxicity.…”

Section: Role Of Phytochemicals In Tbimentioning

confidence: 99%

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

Hasan,

Anwar,

Shamsi

et al. 2024

Front. Pharmacol.

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Traumatic brain injury (TBI) leads to brain damage, comprising both immediate primary damage and a subsequent cascade of secondary injury mechanisms. The primary injury results in localized brain damage, while the secondary damage initiates inflammatory responses, followed by the disruption of the blood-brain barrier, infiltration of peripheral blood cells, brain edema, and the release of various immune mediators, including chemotactic factors and interleukins. TBI disrupts molecular signaling, cell structures, and functions. In addition to physical tissue damage, such as axonal injuries, contusions, and haemorrhages, TBI interferes with brain functioning, impacting cognition, decision-making, memory, attention, and speech capabilities. Despite a deep understanding of the pathophysiology of TBI, an intensive effort to evaluate the underlying mechanisms with effective therapeutic interventions is imperative to manage the repercussions of TBI. Studies have commenced to explore the potential of employing natural compounds as therapeutic interventions for TBI. These compounds are characterized by their low toxicity and limited interactions with conventional drugs. Moreover, many natural compounds demonstrate the capacity to target various aspects of the secondary injury process. While our understanding of the pathophysiology of TBI, there is an urgent need for effective therapeutic interventions to mitigate its consequences. Here, we aimed to summarize the mechanism of action and the role of phytochemicals against TBI progression. This review discusses the therapeutic implications of various phytonutrients and addresses primary and secondary consequences of TBI. In addition, we highlighted the roles of emerging phytochemicals as promising candidates for therapeutic intervention of TBI. The review highlights the neuroprotective roles of phytochemicals against TBI and the mechanistic approach. Furthermore, our efforts focused on the underlying mechanisms, providing a better understanding of the therapeutic potential of phytochemicals in TBI therapeutics.

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Section: Role Of Phytochemicals In Tbimentioning

confidence: 99%

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

Hasan,

Anwar,

Shamsi

et al. 2024

Front. Pharmacol.

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“… 65 Meanwhile, HMGB1 binds to TLR4, enhancing the migration, proliferation and differentiation of immune cells. 66 Consequently, radiation‐induced brain injury triggers the release of DAMPs, promoting the migration of neutrophils, monocytes, and other inherent immune cells, provoking an innate immune response and directly or indirectly triggering an adaptive immune response.…”

Section: Signal Pathways Of Microglia In Radiation‐induced Brain Injurymentioning

confidence: 99%

“…HMGB1 strongly stimulates astrocytes to secrete various chemokines, including neutrophil chemokines (CXCL1, CXCL2, and CCL3) and T‐cell chemokines (CXCL1, CCL2, CCL5, and CCL20) 65 . Meanwhile, HMGB1 binds to TLR4, enhancing the migration, proliferation and differentiation of immune cells 66 . Consequently, radiation‐induced brain injury triggers the release of DAMPs, promoting the migration of neutrophils, monocytes, and other inherent immune cells, provoking an innate immune response and directly or indirectly triggering an adaptive immune response.…”

Section: Signal Pathways Of Microglia In Radiation‐induced Brain Injurymentioning

confidence: 99%

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Wang,

Tian,

Liu

et al. 2024

CNS Neurosci Ther

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BackgroundRadiation‐induced brain injury is a neurological condition resulting from radiotherapy for malignant tumors, with its underlying pathogenesis still not fully understood. Current hypotheses suggest that immune cells, particularly the excessive activation of microglia in the central nervous system and the migration of peripheral immune cells into the brain, play a critical role in initiating and progressing the injury. This review aimed to summarize the latest advances in the cellular and molecular mechanisms and the therapeutic potential of microglia in radiation‐induced brain injury.MethodsThis article critically examines recent developments in understanding the role of microglia activation in radiation‐induced brain injury. It elucidates associated mechanisms and explores novel research pathways and therapeutic options for managing this condition.ResultsPost‐irradiation, activated microglia release numerous inflammatory factors, exacerbating neuroinflammation and facilitating the onset and progression of radiation‐induced damage. Therefore, controlling microglial activation and suppressing the secretion of related inflammatory factors is crucial for preventing radiation‐induced brain injury. While microglial activation is a primary factor in neuroinflammation, the precise mechanisms by which radiation prompts this activation remain elusive. Multiple signaling pathways likely contribute to microglial activation and the progression of radiation‐induced brain injury.ConclusionsThe intricate microenvironment and molecular mechanisms associated with radiation‐induced brain injury underscore the crucial roles of immune cells in its onset and progression. By investigating the interplay among microglia, neurons, astrocytes, and peripheral immune cells, potential strategies emerge to mitigate microglial activation, reduce the release of inflammatory agents, and impede the entry of peripheral immune cells into the brain.

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Demyelination in cuprizone mice is ameliorated by calycosin mediated through astrocyte Nrf2 signaling pathway

Chen,

Wang,

et al. 2024

European Journal of Pharmacology

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Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Cited by 9 publications

References 30 publications

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Demyelination in cuprizone mice is ameliorated by calycosin mediated through astrocyte Nrf2 signaling pathway

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