Annexin A7 Levels Increase in Rats With Traumatic Brain Injury and Promote Secondary Brain Injury

Gao, Fan; Li, Di; Qin, Rui; Ni, Haibo; Liu, Huixiang; Jiang, Feng; Tao, Liyuan; Gao, Rong; Dang, Baoqi

doi:10.3389/fnins.2018.00357

Cited by 11 publications

(13 citation statements)

References 22 publications

(23 reference statements)

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“…In this model, ANXA7 knockdown in vivo showed rescue effects on neuronal death, blood–brain barrier damage, brain edema, neurobehavioral deficient, and inflammatory response. Similar results were also obtained after subarachnoid hemorrhage-induced brain injury [ 383 ] and correlate with elevated AnxA7 levels in traumatic brain injury [ 384 ], making AnxA7-based therapies a potentially novel and alternative approach in the treatment of cerebrovascular disease ( Table 7 a).…”

Section: Anxa7supporting

confidence: 73%

Annexin Animal Models—From Fundamental Principles to Translational Research

Grewal

Rentero

Enrich

et al. 2021

IJMS

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Routine manipulation of the mouse genome has become a landmark in biomedical research. Traits that are only associated with advanced developmental stages can now be investigated within a living organism, and the in vivo analysis of corresponding phenotypes and functions advances the translation into the clinical setting. The annexins, a family of closely related calcium (Ca2+)- and lipid-binding proteins, are found at various intra- and extracellular locations, and interact with a broad range of membrane lipids and proteins. Their impacts on cellular functions has been extensively assessed in vitro, yet annexin-deficient mouse models generally develop normally and do not display obvious phenotypes. Only in recent years, studies examining genetically modified annexin mouse models which were exposed to stress conditions mimicking human disease often revealed striking phenotypes. This review is the first comprehensive overview of annexin-related research using animal models and their exciting future use for relevant issues in biology and experimental medicine.

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Section: Anxa7supporting

confidence: 73%

Annexin Animal Models—From Fundamental Principles to Translational Research

Grewal

Rentero

Enrich

et al. 2021

IJMS

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“…Many investigations indicated that secondary damage result in neuronal apoptosis is the main reason of poor outcome after TBI which is progressive from hours to days . Many pathological process were reported to be related to the neuronal apoptosis in the secondary damage . So, relieve of neuronal apoptosis was the fundamental therapy purpose of TBI.…”

Section: Introductionmentioning

confidence: 99%

Alpha lipoic acid inhibits oxidative stress‐induced apoptosis by modulating of Nrf2 signalling pathway after traumatic brain injury

Xia

Zhai

Wang

et al. 2019

J Cellular Molecular Medi

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Alpha lipoic acid (ALA) is a powerful antioxidant which has been widely used in the treatment of different system diseases, such as cardiovascular and cerebrovascular diseases. But, there are few studies that refer to protective effects and potential mechanisms on traumatic brain injury (TBI). This study was carried out to investigate the neuroprotective effect following TBI and illuminate the underlying mechanism. Weight drop‐injured model in rats was induced by weight‐drop. ALA was administrated via intraperitoneal injection after TBI. Neurologic scores were examined following several tests. Neurological score was performed to measure behavioural outcomes. Nissl staining and TUNEL were performed to evaluate the neuronal apoptosis. Western blotting was engaged to analyse the protein content of the Nuclear factor erythroid 2‐related factor 2 (Nrf2) and its downstream protein factors, including hemeoxygenase‐1 (HO‐1) and quinine oxidoreductase‐1 (NQO1). ALA treatment alleviated TBI‐induced neuron cell apoptosis and improved neurobehavioural function by up‐regulation of Nrf2 expression and its downstream protein factors after TBI. This study presents new perspective of the mechanisms responsible for the neuronal apoptosis of ALA, with possible involvement of Nrf2 pathway.

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“…Many investigators have indicated that secondary damage, which is progressive from hours to days, results in neuronal apoptosis and is the primary reason for poor TBI outcomes . Many pathologic processes were reported to be related to neuronal apoptosis during the secondary damage . So, relieving neuronal apoptosis has been instituted as a fundamental therapy for TBI.…”

Section: Introductionmentioning

confidence: 99%

“…2 Many pathologic processes were reported to be related to neuronal apoptosis during the secondary damage. 3,4 So, relieving neuronal apoptosis has been instituted as a fundamental therapy for TBI. However, despite much research on possible mechanisms, an effective treatment has not been found.…”

Section: Introductionmentioning

confidence: 99%

Breviscapine provides a neuroprotective effect after traumatic brain injury by modulating the Nrf2 signaling pathway

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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Breviscapine (BVP) has been widely used in the treatment of several systemic diseases, including those of the cardiovascular and cerebrovascular systems. But, few studies have looked at the neuroprotective effects of BVP and its potential effect in treating traumatic brain injury (TBI). The present study investigated the neuroprotective effect of BVP following TBI and illuminated the underlying mechanism. The weight drop‐induced closed diffuse traumatic brain injury method was used to induce TBI in rats. BVP was injected intraperitoneally 30 minutes after TBI. Neurologic scores were performed to measure behavioral outcomes. Nissl staining and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling (TUNEL) assays were performed on histopathologic tissue sections to evaluate neuronal apoptosis. The nuclear factor erythroid 2‐related factor 2 (Nrf2) and its related downstream proteins, including heme oxygenase‐1 (HO‐1) and quinine oxidoreductase‐1 (NQO1) were detected with Western blots. BVP treatment alleviated or attenuated TBI‐induced neuron cell apoptosis and improved neurobehavioral functions through the upregulated expression of Nrf2 and its related downstream proteins. This study, using the drug, BVP, we present new mechanisms responsible for neuronal apoptosis in TBI with possible involvement of the Nrf2 pathway.

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Annexin A7 Levels Increase in Rats With Traumatic Brain Injury and Promote Secondary Brain Injury

Cited by 11 publications

References 22 publications

Annexin Animal Models—From Fundamental Principles to Translational Research

Annexin Animal Models—From Fundamental Principles to Translational Research

Alpha lipoic acid inhibits oxidative stress‐induced apoptosis by modulating of Nrf2 signalling pathway after traumatic brain injury

Breviscapine provides a neuroprotective effect after traumatic brain injury by modulating the Nrf2 signaling pathway

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