Interleukin-10 mediates the neuroprotection of hyperbaric oxygen therapy against traumatic brain injury in mice

Chen, X.; Duan, Xuening; Xu, Lihua; Zhao, Jianlong; She, Zhou; Chen, W.-W.; Zheng, Zhenlin; Jiang, Guohui

doi:10.1016/j.neuroscience.2013.11.036

Cited by 86 publications

(69 citation statements)

References 34 publications

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“…The neuroprotective effects of HBO treatment in brain injury have been evidenced by the preservation of mitochondrial membrane properties [40], the stimulation of neurogenesis, the attenuation of inflammation [13], as well as a decrease in apoptotic activities [20]. Consistent with previous studies, we found that the loss of neurons and the number of TUNEL-positive neurons in the cerebral cortex surrounding the primary injury site were significantly increased 3 d after TBI but were reduced with HBO treatment.…”

Section: Hbo Effects On Neuropathology and Functional Outcomesupporting

confidence: 90%

“…Several studies have demonstrated that HBO affects neuronal apoptosis by reducing the messenger RNA levels of apoptosisrelated proteins, such as members of the Bcl2 family [11], Bcl2, and Caspase-3, in the perilesioned area in a cerebral contusion rat model [20]. In the present study, we further demonstrated the effects of HBO on the expression of the apoptosisassociated factors TGIF and TGF-b1.…”

Section: Hbo Effects On the Neuronal Apoptosis-associated Factors Tgisupporting

confidence: 76%

“…Neurologic functional outcome after brain injury can be evaluated using the beam-balancing and prehensile traction tests [20], maximal grasp angle on an inclined plane [13,24], modified neurologic severity score [41], and gait analysis [42]. In the present study, gait analysis was performed using TreadScan to evaluate both the spatial and temporal aspects of limb function changes during overground locomotion after TBI.…”

Section: Hbo Effects On Neuropathology and Functional Outcomementioning

confidence: 99%

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Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

Wee¹,

Lim

Chio

et al. 2015

Journal of Surgical Research

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Section: Hbo Effects On Neuropathology and Functional Outcomesupporting

confidence: 90%

Section: Hbo Effects On the Neuronal Apoptosis-associated Factors Tgisupporting

confidence: 76%

Section: Hbo Effects On Neuropathology and Functional Outcomementioning

confidence: 99%

See 1 more Smart Citation

Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

Wee¹,

Lim

Chio

et al. 2015

Journal of Surgical Research

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“…Administration of circulating antibody against proinflammatory cytokine TNF‐α protects rat brain from reperfusion injury (Baratz et al., 2011). Anti‐inflammatory cytokine IL‐10 can mediate the neuroprotection of hyperbaric oxygen therapy against TBI (X. Chen et al., 2014). In this study, we found that EPO could reduce proinflammatory cytokines TNF‐α and IL‐1β, but increase anti‐inflammatory cytokines IL‐10 in the brain tissue.…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin regulates immune/inflammatory reaction and improves neurological function outcomes in traumatic brain injury

Zhou

Zheng

et al. 2017

Brain and Behavior

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IntroductionTraumatic brain injury (TBI) remains a leading cause of disability and death among young people in China. Unfortunately, no specific pharmacological agents to block the progression of secondary brain injury have been approved for clinical treatment. Recently, neuroprotective effects of erythropoietin (EPO) have been demonstrated in addition to its principal function in erythropoiesis, and hence it is viewed as a potential drug for TBI. In this study, we have investigated the neuroprotective effects of EPO associated with immune/inflammatory modulation in a mouse experimental TBI model.Methods EPO (5000 U/kg body weight, i.p.) was injected at 1 hr, 1, 2, and 3 days after TBI, and its effect on cognitive function, brain edema, immune/inflammatory cells including regulatory T cells (Tregs), neutrophils, CD3+ T cells, and microglia, cytokines including interleukin‐10 (IL‐10), transforming growth factor‐β (TGF‐β), interleukin‐1β (IL‐1β), and tumor necrosis factor‐α (TNF‐α) were evaluated at different time points after treatment.Results EPO treatment significantly decreased brain edema and improved cognitive function when compared to Saline‐treated mice (p < .05). EPO treatment also significantly increased Tregs level in spleen and injured brain tissue as well as significantly reduced the infiltration and activation of immune/inflammatory cells (neutrophils, CD3+T cells, and microglia) in the injured hemisphere compared to Saline‐treated control animals (p < .05). In addition, ELISA analysis demonstrated that EPO treatment increased the expression of anti‐inflammatory cytokine IL‐10, but decreased the expression of proinflammatory cytokine IL‐1β and TNF‐α in the injured brain tissue (p < .05).ConclusionsThese findings suggest that EPO could improve neurological and cognitive functional outcomes as well as regulate immune/inflammatory reaction in TBI.

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“…[39][40][41][42][43] Bcl-2 proteins were previously shown to exert a neuroprotective effect by reducing the release of cytochrome c and blocking caspase activation. 44 Bcl-2 is not only involved in the pathway of apoptosis, but also participates in the regulation of the autophagy signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

Li¹,

Wen²,

Wang³

et al. 2017

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Abstract:In the present study, we evaluated the changes in autophagy after hyperbaric oxygen (HBO) treatment for traumatic brain injury (TBI) and investigated whether autophagy takes part in the neuroprotection after HBO treatment. Male Sprague Dawley rats were assigned to four groups randomly: sham injury, sham injury and HBO, TBI, and TBI and HBO. The HBO rats received HBO treatment for 100 min immediately after injury. Rats were sacrificed at 24 h after the brain injury and the levels of cleaved caspase-3 and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells in the injured cortex were measured to determine cell death. The expression levels of autophagy-associated proteins were measured by immunohistochemistry and Western blotting to assess changes in autophagy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell density and cleaved caspase-3 expression were increased 24 h after TBI. These increases were suppressed by post-TBI HBO treatment. Immunohistochemistry and Western blotting of autophagy-associated proteins showed that TBI can induce autophagy and that HBO treatment can further upregulate the expression of autophagy makers, as shown by an increase in LC3, ATG-5, and Beclin-1 expression and reduction in P62 expression. In conclusion, HBO treatment can reduce apoptosis and further upregulate autophagy in the injured cortex after brain injury, and the autophagy pathway may take part in the neuroprotection provided by HBO treatment for TBI.

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Interleukin-10 mediates the neuroprotection of hyperbaric oxygen therapy against traumatic brain injury in mice

Cited by 86 publications

References 34 publications

Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

Erythropoietin regulates immune/inflammatory reaction and improves neurological function outcomes in traumatic brain injury

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

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