Isochlorogenic acid B inhibits enterovirus 71 replication by upregating p53

：Objective To explore the role of p53 in the replication of enterovirus 71 (EV71) and the anti-EV71 replication mechanism of isochlorogenic acid B in extract of honeysuckle. Methods: EV71 strain was isolated and inoculated with RD cells to detect virus titer, CCK-8 to detect cell survival rate and LDH to detect cell damage rate. RD cells were treated with RITA (p53 activator), Pifithin-α (p53 inhibitor) and isochlorogenic acid B, and the expressions of autophagy related proteins p62, LC3, p53 and viral VP1 were detected by Western Blot. Cell survival rate and cell damage rate were detected by CCK-8 and LDH. Results: EV71 strain was isolated and infected with RD cells, the intracellular p53 content decreased, p62 and LC3II content increased. In the RITA treatment group, p53 content increased, p62, LC3II content decreased, virus titer decreased, cell survival rate decreased, and damage rate increased. In Pifithin-α treatment group, intracellular p53 content decreased, p62, LC3II content increased, virus titer increased, cell survival rate decreased, and damage rate increased. In isochlorogenic acid B treatment group, p53 content increased, p62, LC3II content decreased, virus titer decreased, cell survival rate increased, and damage rate decreased. Conclusion: EV71 can affect autophagy and promote self-replication by regulating p53. Isochlorogenic acid B up-regulates p53 to promote autophagy, inhibits EV71 replication in RD cells, and weakens its cytotoxicity, which has a good anti-EV71 effect.