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-IV 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-IV enhanced autophagy activation in H1N1 infection. Furthermore, we found that AS-IV promoted H1N1-triggered formation of autophagosomes and autolysosomes. Additionally, it was noted that AS-IV did not affect viral replication, mRNA level of interleukin-1 beta (IL-1β) and pro-IL-1β protein level, but significantly decreased secretion of IL-1β, and chloroquine (CQ, as an inhibitor of autophagy) increased secretion of IL-1β in H1N1 infection. In conclusion, AS-IV stimulates the formation of autophagosomes and the fusion of autophagosomes and lysosomes in H1N1 infection and may lead to decreased IL-1β secretion.

中文翻译：

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黄芪甲苷IV通过增强H1N1感染的自噬作用来减弱IL-1β分泌。

炎性因子的过度分泌（细胞因子风暴）在H1N1引起的急性肺炎中起重要作用，自噬是调节炎症的细胞内在机制。源自黄芪根的黄芪甲苷IV（AS-IV）具有多种药理活性，例如抗炎作用。但是，AS-IV对H1N1诱导的自噬和炎症的影响仍然难以捉摸。据报道，H1N1感染导致自噬体的积累，但阻碍自噬体掺入溶酶体中，而本研究表明AS-IV增强了H1N1感染中的自噬激活。此外，我们发现AS-IV促进了H1N1触发的自噬小体和自溶酶体的形成。此外，还注意到AS-IV不会影响病毒复制，IL-1β（IL-1β）和pro-IL-1β蛋白水平的mRNA水平，但IL-1β的分泌显着减少，而氯喹（CQ，作为自噬的抑制剂）增加了H1N1感染中IL-1β的分泌。总之，AS-IV刺激H1N1感染中自噬体的形成以及自噬体和溶酶体的融合，并可能导致IL-1β分泌减少。