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Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects.

机译:缓激肽对神经胶质细胞的多功能作用与潜在的抗炎作用有关。

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摘要

Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca(2+)-dependent signal cascades. Among them, production of prostaglandin E(2) (PGE(2)), via B(1) receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B(2) receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy.
机译:据报道激肽产生并作用于损伤和炎症部位。尽管有许多报道称它们可能引发特定的炎症反应,但是缓激肽(BK)在神经胶质细胞介导的大脑中具有抗炎作用。在本综述中,我们试图描述神经胶质细胞对BK的复杂反应和立即反应。胶质细胞表达BK受体,并诱导Ca(2+)依赖信号级联。其中,通过原代培养的小胶质细胞中的B(1)受体产生前列腺素E(2)(PGE(2)),对脂多糖(LPS)诱导释放的肿瘤坏死因子-α(TNF- α)通过增加细胞内环状单磷酸腺苷(cAMP)。此外,BK通过星形胶质细胞中的B(2)受体上调神经营养因子的产生,例如神经生长因子(NGF)。这些结果表明,BK可能通过对神经胶质细胞的多种功能在大脑中具有抗炎和神经保护作用。这些观察结果可能有助于了解激肽在中枢神经系统中的作用的悖论,并且可能对治疗策略有用。

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