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).