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2016•China Journal of Chinese Materia MedicaRequires access

Inhibitory effects of acteoside on LPS-induced inflammatory response on BV-2 microglial cells

Xiaomin Song, Li‐Xi Liao, Xin Dong, Jun Li, Ke‐Wu Zeng, Pengfei Tu

Open publisher page 4 citations

Abstract

To investigate the inhibitory effects of acteoside (ACT) on BV-2 microglial cells and the potential mechanism,LPS was used to treat BV-2 cells with or without ACT (12.5,25,50 μmol•L ⁻¹). Then, the expressions of inflammatory factors (NO,TNF-α,IL-6) and inflammation related proteins (iNOS,COX-2,p-IKKβ,IKKβ,p-ⅠκB,ⅠκB) were detected. In addition,the nuclear translocation of NF-κB was explored. The results showed that ACT could significantly suppress the inflammatory response against LPS stimulation by decreasing the expressions of NO,IL-6,TNF-α,iNOS,COX-2 and the phosphorylations of IKKβ and IκB. Moreover,the nuclear translocation of NF-κB p65 was inhibited by ACT. Taken together, ACT could significantly inhibit the inflammatory response of BV-2 microglial cells which were induced by LPS via inhibition of NF-κB signaling pathway.

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What this paper is about

To investigate the inhibitory effects of acteoside (ACT) on BV-2 microglial cells and the potential mechanism,LPS was used to treat BV-2 cells with or without ACT (12.5,25,50 μmol•L ⁻¹). Then, the expressions of inflammatory factors (NO,TNF-α,IL-6) and inflammation related proteins (iNOS,COX-2,p-IKKβ,IKKβ,p-ⅠκB,ⅠκB) were detected. In addition,the nuclear translocation of NF-κB was explored. The results showed that ACT could significantly suppress the inflammatory response against LPS stimulation by decreasing the expressions of NO,IL-6,TNF-α,iNOS,COX-2 and the phosphorylations of IKKβ and IκB. Moreover,the nuclear translocation of NF-κB p65 was inhibited by ACT. Taken together, ACT could significantly inhibit the inflammatory response of BV-2 microglial cells which were induced by LPS via inhibition of NF-κB signaling pathway.

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Available abstract

To investigate the inhibitory effects of acteoside (ACT) on BV-2 microglial cells and the potential mechanism,LPS was used to treat BV-2 cells with or without ACT (12.5,25,50 μmol•L ⁻¹). Then, the expressions of inflammatory factors (NO,TNF-α,IL-6) and inflammation related proteins (iNOS,COX-2,p-IKKβ,IKKβ,p-ⅠκB,ⅠκB) were detected. In addition,the nuclear translocation of NF-κB was explored. The results showed that ACT could significantly suppress the inflammatory response against LPS stimulation by decreasing the expressions of NO,IL-6,TNF-α,iNOS,COX-2 and the phosphorylations of IKKβ and IκB. Moreover,the nuclear translocation of NF-κB p65 was inhibited by ACT. Taken together, ACT could significantly inhibit the inflammatory response of BV-2 microglial cells which were induced by LPS via inhibition of NF-κB signaling pathway.

Key concepts: Chemistry, NF-κB, Inflammation, IκB kinase, Inhibitory postsynaptic potential, Chromosomal translocation, Stimulation, Tumor necrosis factor alpha

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