Effect of Early Normobaric Hyperoxia on Blast-Induced Traumatic Brain Injury in Rats

Li, Yanteng; Lv, Wenying; Cheng, Gang; Wang, Shuwei; Liu, Bang-xin; Zhao, Hulin; Wang, Hongwei; Zhang, Leiming; Dong, Chao; Zhang, Jianning

doi:10.1007/s11064-020-03123-x

Cited by 9 publications

(9 citation statements)

References 24 publications

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“…In the present study, Ea stimulation increased MAP2 and GALC expression and decreased GFAP expression, implying that Ea promotes the survival of neurons and oligodendrocytes and inhibits astrocyte hyperplasia in rats subjected to ICH. In addition, serum concentrations of the MBP, NSE, and S100B proteins, common indicators of the severity of hemorrhagic brain injury [23,24], are often used as diagnostic and prognostic biomarkers for brain injury [25][26][27]. We found that Ea treatment downregulated these proteins in the serum, indicating that Ea treatment relieved brain injury in rats after ICH.…”

Section: Discussionmentioning

confidence: 76%

Electroacupuncture Therapy Effectively Protects the Rat Brain after Intracerebral Hemorrhage

Huang,

Fan,

Chen

et al. 2024

Neural Plasticity

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Objective. Electroacupuncture (Ea) is a useful complementary and alternative therapy for intracerebral hemorrhage (ICH). However, the neurobiological basis for the Ea treatment of ICH is still unclear. The primary aim of the present study was to explore whether Ea prevents brain edema, apoptosis, excitotoxicity, and neuroinflammation in rats after hemorrhagic stroke. Methods. Rats were randomly divided into Sham, Control, and Ea groups. We used modified neurological severity score (mNSS) and gait analysis to estimate neurological function in rats, and PET/CT to assess glucose uptake and the hemorrhagic focus volume. Measurement of the brain water content and TUNEL staining were used to evaluate brain edema and cell apoptosis, respectively. The serum myelin basic protein (MBP), neuron-specific enolase (NSE), calcium-binding protein B (S100B), and tumor necrosis factor-α (TNF-α) concentrations were examined with ELISA. The expression levels of the CD68, GALC, Arg-1, iNOS, NR2A, Glu2R, AQP4, MAP2, GFAP, AQP9, Bcl-2, Bax, and Glu proteins around the hematoma were detected via immunohistochemistry staining. Western blot was used to analyze the levels of the AQP4, AQP9, Bax, Bcl-2, iNOS, and Arg-1 proteins. Results. Ea treatment improved neurological function and reduced the hemorrhagic area and brain water content in rats after ICH. The serum concentrations of MBP, NSE, S100B, and TNF-α all decreased significantly in the Ea group compared with the Control group. Expression levels of the Glu, NR2A, AQP4, AQP9, Bax, GFAP, iNOS, and CD68 proteins in brain tissue surrounding the hematoma were obviously suppressed in ICH rats following Ea treatment. Moreover, Ea stimulation increased the levels of the MAP2, GALC, Glu2R, Arg-1, and Bcl-2 proteins, but reduced the number of TUNEL-positive cells in rats after ICH. Conclusion. The results of this study suggest that Ea may exert neuroprotective effects by suppressing brain edema, apoptosis, excitotoxicity, and neuroinflammation.

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Section: Discussionmentioning

confidence: 76%

Electroacupuncture Therapy Effectively Protects the Rat Brain after Intracerebral Hemorrhage

Huang,

Fan,

Chen

et al. 2024

Neural Plasticity

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“…4C) (46,87,89,93), but not after smTBI (Fig. 4B) (55,94,96,101). Notably, one study reported increased t-Tau and p-Tau levels up to one year following rmTBI in tauopathy-prone transgenic TghTau/PS1 mice expressing human tau (97).…”

Section: Discussionmentioning

confidence: 88%

“…t-Tau and p-Tau may hold potential as pharmacodynamic markers, although the evidence is somewhat limited. Some interventions, such as oxygen therapy, have been associated with a temporary reduction in t-Tau protein levels, indicating possible neuroprotective effects (94). Dietary interventions also seem to prevent post-traumatic increases in t-Tau (73,103).…”

Section: Discussionmentioning

confidence: 99%

“…The pharmacodynamic value of t-Tau was assessed in 5 preclinical studies (41,73,82,94,103), and in one study for p-Tau (41). Notably, TBI-induced circulating t-Tau and p-Tau levels were decreased following early normobaric hyperoxia and hyperbaric oxygen treatment (94), turmeric supplementation (103), and supplementation with omega-3 fatty acids and vitamin D3 (73). However, two studies reported no changes in circulating t-Tau and p-Tau in spite of reported neuroprotective effects of etanercept and lithium chloride (82) and LEV (41) in the experimental TBI models.…”

Section: T-tau and P-taumentioning

confidence: 99%

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Translating from mice to humans: using preclinical blood-based biomarkers for the prognosis and treatment of traumatic brain injury

Lisi,

Moro,

Mazzone

et al. 2023

Preprint

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Rodent models are important research tools for studying the pathophysiology of traumatic brain injury (TBI) and developing potential new therapeutic interventions for this devastating neurological disorder. However, the failure rate for the translation of drugs from animal testing to human treatments for TBI is 100%, perhaps due, in part, to distinct timescales of pathophysiological processes in rodents versus humans that impedes translational advancements. Incorporating clinically relevant biomarkers in preclinical studies may provide an opportunity to calibrate preclinical models to human TBI biomechanics and pathophysiology. To support this important translational goal, we conducted a systematic literature review of preclinical TBI studies in rodents measuring blood levels of clinically used NfL, t-Tau, p-Tau, UCH-L1, or GFAP, published in PubMed/MEDLINE up to June 13th, 2023. We focused on blood biomarker temporal trajectories and their predictive and pharmacodynamic value and discuss our findings in the context of the latest clinical TBI biomarker data. Out of 369 original studies identified through the literature search, 71 met the inclusion criteria, with a median quality score on the CAMARADES checklist of 5 (interquartile range 4-7). NfL was measured in 17 preclinical studies, GFAP in 41, t-Tau in 17, p-Tau in 7, and UCH-L1 in 19 preclinical studies. Data in rodent models show that all blood biomarkers exhibited injury severity-dependent elevations, with GFAP and UCH-L1 peaking within hours after TBI, NfL peaking within days after TBI and remaining elevated up to 6 months post-injury, whereas t-Tau and p-Tau levels were gradually increased many weeks after TBI. Blood NfL levels emerges as a prognostic indicator of white matter loss after TBI, while both NfL and GFAP hold promise for pharmacodynamic studies of neuroprotective treatments. Therefore, blood-based preclinical biomarker trajectories could serve as important anchor points that may advance translational research in the TBI field. However, further investigation into biomarker levels in the subacute and chronic phases will be needed to more clearly define pathophysiological mechanisms and identify new therapeutic targets for TBI.

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“…NBO plays a neuroprotective role against traumatic brain injury (TBI) and stroke, 37 , 38 but the relevant mechanisms involved in this process have not been elucidated. In this study, our clinical and experimental results demonstrated that NBO treatment markedly reduces neurological deficits and brain damage following ICH in both patients and animals, confirming the neuroprotective functions of NBO after ICH.…”

Section: Discussionmentioning

confidence: 99%

Normobaric hyperoxia alleviates complement C3‐mediated synaptic pruning and brain injury after intracerebral hemorrhage

Wu,

Chen,

Zhao

et al. 2024

CNS Neurosci Ther

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BackgroundIntracerebral hemorrhage (ICH) is a common cerebrovascular disease, and the complement cascade exacerbates brain injury after ICH. As the most abundant component of the complement system, complement component 3 (C3) plays essential roles in all three complement pathways. However, the effects of C3 on neurological impairment and brain injury in ICH patients and the related mechanism have not been fully elucidated. Normobaric hyperoxia (NBO) is regarded as a treatment for ICH patients, and recent clinical studies also have confirmed the neuroprotective role of NBO against acute ICH‐mediated brain damage, but the underlying mechanism still remains elusive.AimsIn the present study, we investigated the effects of complement C3 on NBO‐treated ICH patients and model mice, and the underlying mechanism of NBO therapy in ICH‐mediated brain injury.ResultsHemorrhagic injury resulted in the high plasma C3 levels in ICH patients, and the plasma C3 levels were closely related to hemorrhagic severity and clinical outcomes after ICH. BO treatment alleviated neurologic impairments and rescued the hemorrhagic‐induced increase in plasma C3 levels in ICH patients and model mice. Moreover, the results indicated that NBO exerted its protective effects of on brain injury after ICH by downregulating the expression of C3 in microglia and alleviating microglia‐mediated synaptic pruning.ConclusionsOur results revealed that NBO exerts its neuroprotective effects by reducing C3‐mediated synaptic pruning, which suggested that NBO therapy could be used for the clinical treatment of ICH.

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Effect of Early Normobaric Hyperoxia on Blast-Induced Traumatic Brain Injury in Rats

Cited by 9 publications

References 24 publications

Electroacupuncture Therapy Effectively Protects the Rat Brain after Intracerebral Hemorrhage

Electroacupuncture Therapy Effectively Protects the Rat Brain after Intracerebral Hemorrhage

Translating from mice to humans: using preclinical blood-based biomarkers for the prognosis and treatment of traumatic brain injury

Normobaric hyperoxia alleviates complement C3‐mediated synaptic pruning and brain injury after intracerebral hemorrhage

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