Astragaloside IV attenuates IL-1β secretion by enhancing autophagy in H1N1 infection.

Excessive secretion of inflammatory factors (cytokine storm) plays a significant role in H1N1-induced acute pneumonia, and autophagy acts as a cell-intrinsic mechanism to regulate inflammation. Astragaloside IV (AS-IV), originating from the astragalus root, possesses multiple pharmacological activities, such as anti-inflammation. However, the influences of AS-N on H1N1-induced autophagy and inflammation have remained elusive. It has been reported that H1N1 infection leads to the accumulation of autophagosomes but obstructs autophagosomes incorporating into lysosomes, whereas the present study showed that AS-N enhanced autophagy activation in H1N1 infection. Furthermore, we found that AS-N promoted H1N1-triggered formation of autophagosomes and autolysosomes. Additionally, it was noted that AS-N did not affect viral replication, mRNA level of interleukin-1 beta (IL-1 beta) and pro-IL-1 beta protein level, but significantly decreased secretion of IL-1,8, and chloroquine (CQ as an inhibitor of autophagy) increased secretion of IL-1 beta in H1N1 infection. In conclusion, AS-N stimulates the formation of autophagosomes and the fusion of autophagosomes and lysosomes in H1N1 infection and may lead to decreased IL-1 beta secretion.