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. 2018 Oct 3;14(12):1732–1744. doi: 10.7150/ijbs.24232

Figure 7.

Figure 7

NSM00191 significantly improved the inflammatory response in vivo. (A-B) NSM00191 significantly inhibited the expression of NF-κB downstream targets. The DBA/1 mice (A, n=12) and TNF-α-overexpressing mice (B, n=12) were divided into two groups. One group of mice was treated with DMSO; the other group mice were treated with 20 μM NSM00191 for 7 days. Then, the joint tissues were collected, and their RNAs were isolated. The RNAs from each treatment mice were equally combined and subjected into qRT-PCR analyses to examine the expression of TNF-α, IL-6, MCP-1, CCL5, COX-2, VCAM-1, CD40 and MHC-1. (C) NSM00191 inhibited the interaction between TRADD and TRAF2 in vivo. The joint samples used in A and B were subjected to Western blot analysis to determine the protein levels of TNFR1, TRADD, TRAF2, IKK2 and p65. GAPDH was used as a loading control. (D) NSM00191 decreased the p65 levels in vivo. One pair of joint samples used in A and B were subjected to IHC staining to determine the protein levels of TNFR1, TRADD, TRAF2, IKK and p65.