YDZG inhibits NLRP3 inflammasome activation in lung tissue.
Since YDZG exhibited NLRP3 inhibitory activity in vitro , the effects of YDZG on LPS-induced mechanism in the lungs of the ALI animal model were examined. IL-1β release was measured in BALF, serum, and lung homogenate by ELISA. Significantly, YDZG suppressed IL-1β expression in BALF (Figure 8A), serum (Figure 8B), and lung homogenate (Figure 8C), respectively. To determine whether YDZG could inhibit activation of the NLRP3 inflammasome in ALI mice, the level of NLRP3 and caspase-1 p20 was measured in lung homogenate by western blot analysis. Results indicated that LPS increased NLRP3 and caspase-1 p20 expression in the lung homogenate of ALI mice, which was reversed by YDZG (Figure 8D), suggesting that administration of YDZG could effectively attenuate activation of the NLRP3 inflammasome. In addition, using immunohistochemistry assay (Figure 8E), we examined the effects of YDZG on LPS-induced NLRP3 expression in situ of lung tissues. Corresponding to results of ELISA and western blotting assay, LPS induced the increase of NLRP3 expression in lung tissue, while YDZG inhibited NLRP3 expression. Taken together, our data demonstrated that YDZG prevented LPS-induced ALI through suppression of NLRP3 inflammasome activation.