Saikosaponin D suppresses enterovirus A71 infection by inhibiting autophagy View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-12

AUTHORS

Chang Li, Lihong Huang, Wei Sun, Ying Chen, Ming-Liang He, Jianbo Yue, Heather Ballard

ABSTRACT

The dysregulation of autophagy, an evolutionarily conserved lysosomal degradation process, has been implicated in a wide variety of human diseases, and thus, small chemicals that modulate autophagy have therapeutic potential. Here, we assessed the ability of active components isolated from Bupleurum falcatum, a popular Chinese herb, to modulate autophagy. We found that saikosaponin D (SsD) and A (SsA) but not C (SsC) potently and reversibly inhibited the fusion of autophagosomes and lysosomes, resulting in the accumulation of autophagosomes, an increased lysosomal pH, and TFEB nuclear translocation. RAB5A knockdown or the expression of a dominant-negative RAB5 mutant significantly reduced the ability of SsD or SsA to block autophagy. Enterovirus A71 (EV-A71), the cause of hand-foot-mouth disease, has been shown to induce autophagy. We found that SsD potently inhibited EV-A71 RNA replication and subsequent viral protein synthesis, thereby preventing EV-A71-induced cell death. ATG5 knockdown inhibited EV-A71 viral protein synthesis, whereas autophagy induction by rapamycin promoted synthesis. Taken together, our data indicate that SsD and SsA are potent late-stage autophagy inhibitors that can be used to prevent EV-A71 infection. More... »

PAGES

4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41392-019-0037-x

DOI

http://dx.doi.org/10.1038/s41392-019-0037-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112285927

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30820356


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