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首页> 外文期刊>Molecules >Inhibition of Lipopolysaccharide-Induced Proinflammatory Responses by Buddleja officinalis Extract in BV-2 Microglial Cells via Negative Regulation of NF-kB and ERK1/2 Signaling
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Inhibition of Lipopolysaccharide-Induced Proinflammatory Responses by Buddleja officinalis Extract in BV-2 Microglial Cells via Negative Regulation of NF-kB and ERK1/2 Signaling

机译:Buddleja officinalis提取物通过负调节NF-kB和ERK1 / 2信号传导抑制Buddleja officinalis提取物在BV-2小胶质细胞中诱导的促炎反应。

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Buddleja officinalis has been traditionally used in the supportive treatment of inflammatory and neuronal diseases in Korea and China. Although several reports have shown the anti-inflammatory effects of Buddleja officinalis, the anti-neuroinflammatory effect has remained unclear. In this study, we aimed to investigate the inhibitory effects of flower buds of B. officinalis Maximowicz water extract (BOWE) on LPS-induced inflammatory processes in BV-2 microglial cells. BOWE dose-dependently inhibited the production of nitric oxide as well as iNOS mRNA expression. Moreover, BOWE prevented IL-1β and IL-6 mRNA expression. However, BOWE had no effect on LPS-induced COX-2 or TNF-a mRNA expression. The extract also had no effect on LPS-stimulated p38 MAPK, JNK, and c-Jun phosphorylation, whereas ERK1/2 phosphorylation was strongly inhibited by BOWE. BOWE also inhibited the LPS-induced degradation of IkB-α, and LPS-induced phosphorylation of p65 NF-kB protein. These data indicate that BOWE inhibited the nitric oxide production and pro-inflammatory gene expression in BV-2 microglial cells, possibly through a negative regulation of the NF-kB and ERK1/2 pathways. Further identification of the direct target molecule(s) of BOWE is required to support its use as an anti-neuroinflammatory agent against the neurodegenerative disorders.
机译:Buddleja officinalis传统上已在韩国和中国用于支持性治疗炎症和神经元疾病。尽管有几篇报道显示了佛手草的抗炎作用,但抗神经炎作用仍不清楚。在这项研究中,我们旨在调查B. officinalis Maximowicz水提取物(BOWE)的花蕾对LPS诱导的BV-2小胶质细胞炎症过程的抑制作用。 BOWE剂量依赖性地抑制一氧化氮的产生以及iNOS mRNA的表达。此外,BOWE阻止了IL-1β和IL-6 mRNA的表达。但是,BOWE对LPS诱导的COX-2或TNF-a mRNA表达没有影响。该提取物也对LPS刺激的p38 MAPK,JNK和c-Jun磷酸化没有影响,而ERK1 / 2磷酸化受到BOWE的强烈抑制。 BOWE还抑制LPS诱导的IkB-α降解,以及LPS诱导的p65 NF-kB蛋白磷酸化。这些数据表明,BOWE可能通过负调节NF-kB和ERK1 / 2途径抑制BV-2小胶质细胞中一氧化氮的产生和促炎基因的表达。需要进一步鉴定BOWE的直接靶分子以支持其用作抗神经退行性疾病的抗神经炎药。

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