Why the study?
Curcumol reduced EMCV replication in vitro, but its antiviral effects and mechanism in vivo remained to be elucidated.
Does curcumol reduce viral load and inflammatory markers in EMCV-infected Kunming mice?
Does curcumol reduce viral load and inflammatory markers in EMCV-infected Kunming mice?
Curcumol alleviates EMCV-induced heart and brain damage in mice by inhibiting the NF-κB/NLRP3 inflammasome pathway, suggesting potential therapeutic value for viral myocarditis and encephalitis.
Introduction Encephalomyocarditis virus (EMCV), a highly significant member of the picornaviridae family, infects a broad range of mammalian hosts and causes severe pathological consequences like encephalitis, myocarditis, and neurologic diseases, etc. In our previous research, curcumol demonstrated a significant reduction in EMCV replication in vitro . However, its antiviral effect in vivo needs to be elucidated. Methods In this study, the mechanism of curcumol against EMCV replication was demonstrated in vivo by establishing an EMCV (100 TCID 50 /20 g) infected mice model. At day 3 post EMCV infection, drug treatment groups were continuously treated with curcumol for 5 days. Results The viral load and expression of interleukins such as IL-1β, IL-6, and TNF-α mRNA levels were significantly decreased in the heart and brain tissues at day 9 of EMCV infection (5 days of curcumol treatment), detected by qPCR. Moreover, Western blot analysis revealed that curcumol considerably elevated the protein levels of IκB and P65, while significantly reducing the levels of P-IκB, P-P65, NLRP3 inflammasome, caspase 1, and IL-1β in cardiac and cerebral tissues. Discussion Conclusively, these results revealed that curcumol inhibits the NF-κB/NLRP3 inflammasome pathway and thus alleviates heart and brain damage induced by EMCV infection in Kunming mice. The present findings provide new insights into the therapeutic potential of curcumol in addressing EMCV-induced pathological conditions.
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Sun et al. (2026) studied this question.
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