Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain-derived neurotrophic factor (BDNF) protein levels increase in rats treated with a regimen of delayed, mild hypothermia that improve neurological recovery after asphyxial cardiac arrest. BDNF transcription in rat brain involves at least five different BDNF exons (exons I-V) that produce four different varieties of mRNA, each containing exon V paired with one of exons I-IV. This study examined whether these different BDNF transcripts are differentially affected by cardiac arrest and by therapeutic hypothermia in rat hippocampus using a reverse transcription and PCR-based method. At 24 h after asphyxial cardiac arrest, transcripts containing exons I and III increased. In rats treated with hypothermia after cardiac arrest, transcripts containing exon III were further increased. No significant alterations in transcripts from exons II or IV were observed, though there was a trend for hypothermia to decrease message from these exons. These data suggest that hypothermia after cardiac arrest produces exon-specific changes in BDNF transcription.
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PMID:Delayed hypothermia preferentially increases expression of brain-derived neurotrophic factor exon III in rat hippocampus after asphyxial cardiac arrest. 1585 65

Hypoxia-ischemia (H/I) brain injury results in various degrees of damage to the body, and the immature brain is particularly fragile to oxygen deprivation. Hypothermia and erythropoietin (EPO) have long been known to be neuroprotective in ischemic brain injury. Brain-derived neurotrophic factor (BDNF) has recently been recognized as a potent modulator capable of regulating a wide repertoire of neuronal functions. This review was based on studies concerning the involvement of BDNF in the protection of H/I brain injury following a search in PubMed between 1995 and December, 2011. We initially examined the background of BDNF, and then focused on its neuroprotective mechanisms against ischemic brain injury, including its involvement in promoting neural regeneration/cognition/memory rehabilitation, angiogenesis within ischemic penumbra and the inhibition of the inflammatory process, neurotoxicity, epilepsy and apoptosis. We also provided a literature overview of experimental studies, discussing the safety and the potential clinical application of BDNF as a neuroprotective agent in the ischemic brain injury.
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PMID:The neuroprotective roles of BDNF in hypoxic ischemic brain injury. 2464 14

Stroke poses a serious health and economic burden, and the lack of treatment options necessitates a viable therapy. Hypothermia represents a promising stroke therapy, yet side effects of full-body cooling, such as pneumonia, limit its clinical application. Selective endovascular cooling (SEC), via infusion of cold saline through the intraarterial artery, represents an attractive alternative by locally cooling the brain while preserving body temperature. However, the mechanisms underlying SEC are poorly understood. Brain-derived neurotrophic factor (BDNF) is a widely recognized promotor of neuroplasticity and biomarker of stroke outcomes, as well as its association with inflammation, such as IL-10. Stroke-induced neuroinflammation exacerbates damage and stems from peripheral organs, namely the spleen. The spleen has emerged as a therapeutic target for stroke, yet the effect of SEC on the splenic inflammatory response is unknown. Here, we aimed to elucidate the local and peripheral mechanisms driving SEC as a neuroprotective stroke therapy by examining brain BDNF and splenic IL-10 expression. Animals that received SEC prior to stroke displayed elevated brain BDNF expression ipsilaterally and contralaterally across the cortex, striatum, and hippocampus. SEC also upregulated splenic IL-10, suggesting alteration of the peripheral inflammatory response. The oxygen-glucose deprivation in vitro model of stroke further demonstrated that "cold" rat splenocytes protected rat primary neurons by upregulating BDNF and IL-10. Altogether these data support BDNF- and IL-10-based mechanisms underlying the neuroprotective potential of SEC therapy for stroke, and further advance the concept of exploiting the pathological link between brain and spleen as therapeutic targets.
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PMID:Selective endovascular cooling for stroke entails brain-derived neurotrophic factor and splenic IL-10 modulation. 3141 65