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.