Tectoridin alleviates lipopolysaccharide-induced inflammation via inhibiting TLR4-NF-κB/NLRP3 signaling in vivo and in vitro

Background: Tectoridin, widely extracted and separated from the rhizome of Iris tectorum Maxim, is extensively reported to have affluent bioactivity, but rarely reported to have anti-inflammatory effects. In this study, we aim to investigate the anti-inflammatory effects and the underlying mechanisms of tectoridin. Methods: Here, RAW264.7 macrophages were stimulated with Lipopolysaccharide (LPS) for the inflammation model in vitro. Experimental animals received tectoridin and Dexamethasone (DEX) before LPS injection for endotoxic shock mouse model in vivo. The pro-inflammatory mediators and cytokines in the cell supernatant and serum were detected by ELISA kits. The tissue damages were assessed by biochemical indexes and H&E staining. Immunohistochemistry and Western blot were performed for the detection of proteins. Results: Our data showed that tectoridin attenuated the LPS-up-regulated nitric oxide (NO), interleukin-6 (IL-6), and interleukin-18 (IL-18) from macrophages and tumor necrosis factor-alpha (TNF-alpha); (IL-6) and (IL-1 beta) in the serum levels. Besides, our histopathological study showed that the damages caused by LPS in the lung, liver, and kidney tissues were decreased. Furthermore, our results demonstrated that tectoridin inhibited the activation of TLR4-NF-kappa B/NLRP3 signaling proved by immunohistochemistry assay and Western blot. Conclusion: Taken all together, tectoridin might have the potential ability of anti-inflammatory effects and the possible mechanism may be relevant to its inhibition of TLR4-NF-kappa B/NLRP3 signaling.