3.7 Inhibition of NLRP3 is indispensable of TBⅡ-mediated protective effects against DSS-induced colitis
Given that TBⅡ could protect against LPS+ATP-induced damage of epithelial barrier and inflammatory response via the mechanism of NLRP3 inhibition in cell model, prompting us to ask whether TBⅡ might have a similar pattern for alleviation of DSS-induced colitis in mice. Therefore, to further verify the role of NLRP3 on TBⅡ-mediated protection against DSS-induced colitis in mice, NLPR3-/- mice were used (Figure S3a). Under DSS treatment, compared with WT mice, NLRP3-/- mice exhibited an ameliorative effect on DSS-induced colitis, as shown by slower weight loss (Figure 8A), lower DAI score (Figure 8B), and significantly improved colon shortening (Figure 8C). Moreover, the serum SOD and GSH levels of NLPR3-/- mice were higher than those of WT mice, and MDA levels were lower than those of WT mice (Figure 8D). Besides, NLRP3-/- mice showed less colon tissue damage under DSS than WT mice (Figure 8E). As expected as the results of Figure 1, TBⅡ notably alleviated DSS-induced colitis, as evidenced by improvement of colon shortening, decreased diarrhea and bleeding higher serum GSH and SOD levels, lower serum MDA levels, and lower inflammatory infiltration and colon histopathological injury (Figure 8 and Figure S3B). However, TBⅡ-mediated amelioration was no longer enhanced in NLPR3-/-mice (Figure 8 and Figure S3B). Collectively, our results suggest the critical role of NLPR3 in the ameliorative effects exerted by TBⅡ.