Fig 5. Effect of AS-IV therapy on the NLRP3 inflammasome pathway in A549 cells infected with influenza virus. (A-D) Real-time PCR analysis was used to analyze the mRNA levels of NLRP3, caspase-1, IL-1β, and IL-18 in different groups. (E-H) The protein expression levels of NLRP3 inflammasome, pro-caspase-1, and cleaved caspase-1 in each group were detected by western blot. (I-J) ELISA was used to detect the expression levels of inflammatory cytokines IL-18 and IL-1β in each group. The values are expressed as the mean ± SD. of three independent experiments. * P< 0.05, ** P < 0.01.
3.4. AS-IV attenuates lung inflammatory lesions in mice caused by poly (I: C)
The above results led us to further investigate whether AS-IV can inhibit viral pneumonia induced by viral RNA mimics poly (I: C) in vivo . The results showed that compared with the NC group, the lung tissue structure of mice in the poly (I: C) group was seriously abnormal, with a large number of alveolar epithelial cells proliferating and alveolar walls thickening, accompanied by a large number of inflammatory cells infiltrating, and pulmonary scores and lung indexes were significantly increased (Fig. 6A-C). Compared with the poly (I: C) group, the increase of lung index in the AS-IV treatment group was reduced by 11.7-19.8%, and AS-IV significantly alleviated the lung tissue structure destruction and inflammatory cell infiltration caused by poly (I: C) infection (Fig. 6A-C).