Fig. 5. PHI ameliorated inflammation via the NLRP3 inflammasome pathway. (A) The gene expression level of cytokines in colonic homogenates. (B and C) The protein levels of cytokines in colonic homogenates and serum. (D) The gene expression level of Nlrp3 and Caspase 1. (E) The protein expression of NLRP3 inflammasome and its upstream pathway. Compared with the model control group *p <0.05, **p <0.01, ***p <0.001, n = 3-4.
Given the remarkable effect of PHI on IL-1β, and NLRP3 inflammasome was reported to be an important protein complex for IL-1β production, we detected the expression level of NLRP3 inflammasome relative proteins. As shown in Fig. 5D-E, the expression of both NLRP3 and Caspase1 was increased dramatically with DSS induction, which was restrained in PHI-treated group.
In summary, the present study demonstrated that PHI improved UC by inhibiting the activation of NLRP3 inflammasome through the TLR4/MyD88/NF-κB pathway. These findings have important implications for the development of future UC treatments