Dioscin Attenuates Interleukin 1β (IL-1β)-Induced Catabolism and Apoptosis via Modulating the Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling in Human Nucleus Pulposus Cells

Longhui Wang; Yuntao Gu; Hai Zhao; Rong Chen; Wensheng Chen; Hao Qi; Weisong Gao

doi:10.12659/MSM.923386

25 August 2020 : Clinical Research

Dioscin Attenuates Interleukin 1β (IL-1β)-Induced Catabolism and Apoptosis via Modulating the Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling in Human Nucleus Pulposus Cells

Longhui Wang^1DEF, Yuntao Gu^1BE, Hai Zhao^1CEF, Rong Chen^1BD, Wensheng Chen^1BF, Hao Qi^1BE, Weisong Gao^1ABG*

DOI: 10.12659/MSM.923386

Med Sci Monit 2020; 26:e923386

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Figure 6 Dioscin suppressed IL-1β-induced release of proinflammatory factors via regulation of the NF-κB pathway in human NP cells. (A, B) Relative mRNA level of (A) IL-6 and (B) TNF-α were examined by PCR. (C–F) Western blotting and quantitative analysis of TLR4, p65, and IκBα. The results are presented as the means ±SD. * P<0.05 relative to the control group; # P<0.05 relative to the IL-1β group, n=5.

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Dioscin Attenuates Interleukin 1β (IL-1β)-Induced Catabolism and Apoptosis via Modulating the Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling in Human Nucleus Pulposus Cells

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