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首页> 外文期刊>Applied Biological Chemistry >Physalis alkekengi L. var. francheti alleviates neuronal cell death caused by activated microglia in vitro
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Physalis alkekengi L. var. francheti alleviates neuronal cell death caused by activated microglia in vitro

机译:physalis alkekengi l. var。 柏雷切蒂减轻了由活化的微胶质增生的神经元细胞死亡

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Microglia are the macrophages that reside in the brain. Activated microglia induces further activation of astrocytes and neuronal cells for mounting an immune response. However, activated microglia release neurotoxic mediators causing neuroinflammation, which is associated with chronic etiology of neurodegenerative diseases. We investigated the effect of ethanol extract of Physalis alkekengi L. var. francheti fruit (PAFE) on neuronal cell death mediated by activated microglia. PAFE decreased NO production and IL-6 secretion in LPS-stimulated BV-2 and primary microglial cells without reducing cell viability. Consistently, treatment with PAFE decreased iNOS and COX-2 expression and ERK phosphorylation in LPS-stimulated BV-2 cells. Finally, apoptosis of N2a cells grown in conditioned media prepared from LPS-stimulated BV-2 cells containing PAFE was inhibited via downregulation of the Bax/Bcl-2 ratio. Taken together, PAFE alleviates neuronal cell death by reducing neurotoxic mediators such as NO and IL-6 from activated microglia. Therefore, it could be a potential candidate to treat neurodegenerative diseases caused by chronic neuroinflammation.
机译:微胶质细胞是存在于大脑中的巨噬细胞。活性微胶质细胞进一步激活星形胶质细胞和神经元细胞以安装免疫应答。然而,活化的微胶质细胞释放神经毒性介质,导致神经引起的神经炎症,这与神经变性疾病的慢性病因有关。我们研究了乙醇提取物的乙醇提取物的作用。群果子(封装)在神经元细胞死亡介导的被活性的微胶质细胞介导。在LPS刺激的BV-2和初级微胶质细胞中,Pafe在没有降低细胞活力的情况下在LPS刺激的BV-2和初级微胶质细胞中减少了没有生产和IL-6分泌物。始终如一地,在LPS刺激的BV-2细胞中,用缩放蛋止和COX-2表达和ERK磷酸化进行治疗。最后,通过Bax / Bcl-2比的下调抑制了由​​含有诱饵的LPS刺激的BV-2细胞制备的条件培养基中生长的N2A细胞的凋亡。连胜,通过减少神经毒性介质,减少神经毒性介质,例如从活性微胶质细胞中获得神经毒性介质,缩放神经元细胞死亡。因此,它可能是治疗慢性神经炎症引起的神经变性疾病的潜在候选者。

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