Cellular and molecular neurobiology
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Cell. Mol. Neurobiol. · Aug 2015
Anesthetic Propofol Attenuates Apoptosis, Aβ Accumulation, and Inflammation Induced by Sevoflurane Through NF-κB Pathway in Human Neuroglioma Cells.
Anesthetics have been reported to promote Alzheimer's disease neuropathogenesis by inducing amyloid beta (Aβ) protein accumulation and apoptosis. The aim of this study was to evaluate the effect of propofol on the apoptosis, Aβ accumulation, and inflammation induced by sevoflurane in human neuroglioma cells. Human neuroglioma cells were treated with or without sevoflurane and then co-incubated with or without propofol. ⋯ Moreover, the level of nuclear factor-kappa B (NF-κB) was tested by Western blot and immunofluorescence assay. We found that the activation of NF-κB pathway was suppressed by propofol. The results suggest that propofol can effectively attenuate the apoptosis, Aβ accumulation, and inflammation induced by sevoflurane in human neuroglioma cells through NF-κB signal pathway.
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Cell. Mol. Neurobiol. · Aug 2015
Time Course of Behavioral Alteration and mRNA Levels of Neurotrophic Factor Following Stress Exposure in Mouse.
Stress is known to affect neurotrophic factor expression, which induces depression-like behavior. However, whether there are time-dependent changes in neurotrophic factor mRNA expression following stress remains unclear. In the present study, we tested whether chronic stress exposure induces long-term changes in depression-related behavior, serum corticosterone, and hippocampal proliferation as well as neurotrophic factor family mRNA levels, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), and ciliary neurotrophic factor (CNTF), in the mouse hippocampus. ⋯ Anhedonia-like behavior in the sucrose preference test and NGF mRNA levels were decreased following 15 days of stress. NGF mRNA levels were significantly higher 1 week after stress exposure. The current data demonstrate that chronic stress exposure induces prolonged BDNF and NGF mRNA changes and increases corticosterone levels and depression-like behavior in the FST, but does not alter other neurotrophic factors or performance in the sucrose preference test.
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Cell. Mol. Neurobiol. · May 2015
Wogonin inhibits LPS-induced inflammatory responses in rat dorsal root ganglion neurons via inhibiting TLR4-MyD88-TAK1-mediated NF-κB and MAPK signaling pathway.
Recent studies showed that the activation of toll-like receptor 4 (TLR4) on dorsal root ganglion (DRG) neurons might underlie neuropathic and inflammatory pain states. This study was undertaken to investigate the effects of wogonin, a flavonoid with potent anti-inflammatory properties on the inflammatory reaction and TLR4 dependent pathways in lipopolysaccharide (LPS)-treated DRG neurons. ⋯ Moreover, wogonin significantly suppressed the release of pro-inflammatory mediators in LPS-induced DRG neurons, including cyclooxygenase-2, inducible nitric oxide synthases, interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha. Our results suggested that pre-treatment with wogonin could attenuate the TLR4-mediated inflammatory response in LPS-induced DRG neurons, thus might be beneficial for the treatment of neuropathic and inflammatory pain.
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Cell. Mol. Neurobiol. · May 2015
Cysteamine alleviates early brain injury via reducing oxidative stress and apoptosis in a rat experimental subarachnoid hemorrhage model.
Oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The aim of this study was to assess whether cysteamine prevents post-SAH oxidative stress injury via its antioxidative and anti-apoptotic effects. ⋯ Meanwhile, cysteamine treatment reduced post-SAH elevated the reactive oxygen species level, the concentration of malondialdehyde, 3-nitrotyrosine, and 8-hydroxydeoxyguanosine and increased the glutathione peroxidase enzymatic activity, the concentration of glutathione and brain-derived neurotrophic factor in brain cortex at 48 h after SAH. These results indicated that administration of cysteamine may ameliorate EBI and provide neuroprotection after SAH in rat models.
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Cell. Mol. Neurobiol. · May 2015
Administration of antagomir-223 inhibits apoptosis, promotes angiogenesis and functional recovery in rats with spinal cord injury.
MicroRNAs (miRNAs) are recently described as a class of short non-coding RNAs, which play important roles in post-transcriptional gene regulation and involved in many physiological and pathological processes. MicroRNA-223 (miR-223) has been showed highly elevated in the injured spinal cord. However, the potential role and underlying mechanisms of miR-223 in spinal cord injury (SCI) were incompletely understood. ⋯ Moreover, inhibition of miR-223 promoted angiogenesis, as evidenced by the increased CD31 expression and microvascular density. Taken together, our results indicate that inhibition of miR-223 with antagomir-223 exerts protective role in functional recovery, angiogenesis, and anti-apoptosis during SCI. Thereby, miR-223 may be a promising target of therapy for SCI.