Articles: traumatic-brain-injuries.
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Secondary brain insult induced by traumatic brain injury (TBI), including excitotoxicity, oxidative stress, inflammatory response, and neuronal degeneration, is sensitive to therapeutic interventions; therefore, searching for neuroprotective agents represents a promising therapeutic strategy for TBI treatment. Luteolin, a member of the flavonoid family, has recently been proven to modulate autophagy. However, whether it activates autophagy after TBI thereby alleviating the secondary insult is not yet understood. ⋯ In line with these observations, luteolin decreased mRNA and protein expressions of pro-inflammatory factors IL-1b and TNF-a. At last, luteolin reduced neuronal degeneration, and alleviated brain edema and blood-brain barrier (BBB) disruption. In conclusion, these results implied that luteolin protected mice brain from traumatic brain injury by inhibiting inflammatory response, and luteolin-induced autophagy might play a pivotal role in its neuroprotection.
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mild traumatic brain injury (mTBI) can produce lasting memory deficits even in the absence of cell loss. We investigated changes in hippocampal firing patterns during exploration and during a novel object recognition (NOR) task. ⋯ memory deficits after mTBI are associated with decreased intrinsic burst activity and impaired context-specific firing patterns in the hippocampus during object exploration.
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A secondary and often lethal consequence of traumatic brain injury is cellular edema that we posit is due to astrocytic swelling caused by transmembrane water fluxes augmented by vasopressin-regulated aquaporin-4 (AQP4). We therefore tested whether vasopressin 1a receptor (V1aR) inhibition would suppress astrocyte AQP4, reduce astrocytic edema, and thereby diminish TBI-induced edematous changes. V1aR inhibition by SR49059 significantly reduced brain edema after cortical contusion injury (CCI) in rat 5h post-injury. ⋯ In CCI-vehicle, sham and CCI-SR49059 groups, fluorescence intensity of GFAP was 349±38, 56±5, and 244±30, respectively, V1aR was 601±71, 117.8±14, and 390±76, and AQP4 was 818±117, 158±5, and 458±55 (n=3/group). The results support that edema was predominantly cellular following CCI and documented that V1aR inhibition with SR49059 suppressed injury-induced up regulation of GFAP, V1A and AQP4, blunting edematous changes. Our findings suggest V1aR inhibitors may be potential therapeutic tools to prevent cellular swelling and provide treatment for post-traumatic brain edema.
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Ginseng, the root of Panax ginseng C.A. Meyer, is a traditional medicinal herb that has been widely used in Asia for the treatment of many diseases through its effects of reinforcing vitality, strengthening the bodily resistance to pathogenic factors, engendering body liquids and allaying thirst, relieving uneasiness of the body and mind and benefiting intelligence, reducing body weight and prolonging life. Ginsenosides are the most important biologically active substances in ginseng. Many reports have suggested that ginsenosides could exert prominent neuroprotective and neurotrophic effects, promote neural stem/progenitor cell (NSC) proliferation and promote neurite outgrowth and neuronal network formation. The present study aimed to investigate whether treatment with ginsenosides could facilitate NSC proliferation in the hippocampal formation after traumatic brain injury (TBI) and contribute to the recovery of neurological functions including learning and memory. ⋯ GTS treatment in rats after a TBI alleviated the secondary brain injury and ameliorated the neurological functions with an effective dose limit of 5-80 mg/kg. GTS regulated the expression of nerve growth-related factors and improved the proliferation of neural stem/progenitor cells, which might facilitate neural regeneration and tissue repair, and might contribute to the recovery of neurological functions, including learning and memory. These effects of GTS might provide a foundation for the use of ginseng as a medicinal herb to enhance intelligence, reduce the aging process and prolong life in the traditional medicine.
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Journal of neurosurgery · Sep 2014
Review Meta AnalysisThe efficacy of erythropoietin in treating experimental traumatic brain injury: a systematic review of controlled trials in animal models.
Erythropoietin (EPO) shows promise as a neuroprotective agent in animal models of traumatic brain injury (TBI). However, clinical trials of the efficacy of EPO treatment in patients with TBI yield conflicting results. The authors conducted a systematic review and meta-analysis to assess the effect of EPO in experimental animal models of TBI, the goal being to inform the design of future clinical trials. ⋯ Despite limitations of this systematic review that may have influenced the findings, the authors conclude that EPO might be beneficial in treating experimental TBI in terms of reducing lesion volume and improving neurobehavioral outcome. However, this review also indicates that more well-designed and well-reported animal studies are needed.