Key result
Resveratrol effectively inhibited Enterovirus 71 replication in rhabdosarcoma cells with an IC50 of 21.36 μg/ml and reduced pro-inflammatory cytokine secretion by blocking the IKKs/NF-κB pathway.
Why the study?
Does resveratrol inhibit EV71 replication and pro-inflammatory cytokine secretion in EV71-infected rhabdosarcoma cells?
Does resveratrol inhibit EV71 replication and pro-inflammatory cytokine secretion in EV71-infected rhabdosarcoma cells?
Effect estimate: IC50 21.36 μg/ml
Resveratrol demonstrates potent antiviral and anti-inflammatory effects against EV71 infection in vitro by blocking the IKKs/NF-κB signaling pathway.
Resveratrol merits preclinical testing for EV71; leaves open whether in vitro effects translate to animal models or patients.
Polydatin and resveratrol, as major active components in Polygonum cuspidatum, have anti-inflammatory, antioxidant and antitumor functions. However, the effect and mechanism of polydatin and resveratrol on enterovirus 71 (EV71) have not been reported. In this study, resveratrol revealed strong antiviral activity on EV71, while polydatin had weak effect. Neither polydatin nor resveratrol exhibited influence on viral attachment. Resveratrol could effectively inhibit the synthesis of EV71/VP1 and the phosphorylation of IKKα, IKKβ, IKKγ, IKBα, NF-κB p50 and NF-κB p65, respectively. Meanwhile, the remarkably increased secretion of IL-6 and TNF-α in EV71-infected rhabdosarcoma (RD) cells could be blocked by resveratrol. These results demonstrated that resveratrol inhibited EV71 replication and cytokine secretion in EV71-infected RD cells through blocking IKKs/NF-κB signaling pathway. Thus, resveratrol may have potent antiviral effect on EV71 infection.
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Zhang et al. (2015) studied Enterovirus 71 (EV71) infection. Resveratrol vs. Untreated EV71-infected cells was evaluated on Inhibition of EV71 replication (IC50) (IC50 21.36 μg/ml). Resveratrol effectively inhibited Enterovirus 71 replication in rhabdosarcoma cells with an IC50 of 21.36 μg/ml and reduced pro-inflammatory cytokine secretion by blocking the IKKs/NF-κB pathway.
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