Key result
Emodin reduced Coxsackievirus B4 entry and replication in vitro (EC50 12.06 μM) and dose-dependently increased survival and decreased myocardial virus titers in infected mice.
Why the study?
Does emodin inhibit Coxsackievirus B4 infection in vitro and in vivo?
Does emodin inhibit Coxsackievirus B4 infection in vitro and in vivo?
Effect estimate: EC50 12.06 μM
Emodin demonstrates antiviral activity against Coxsackievirus B4 in vitro and in vivo, suggesting potential as a post-exposure prophylactic agent.
Emodin shows anti-CVB4 activity in mice; leaves open clinical translation for viral myocarditis pending human trials.
The lack of effective therapeutics for Coxsackievirus B₄ (CVB₄) infection underscores the importance of finding novel antiviral compounds. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is one of the natural anthraquinone derivatives obtained from the root and rhizome of Polygonum cuspidatum. In the present study, the possibility of using emodin as a potential antiviral to treat CVB₄ infection was explored in vitro and in mice. Emodin reduced CVB₄ entry and replication on Hep-2 cells in a concentration- and time-dependent manner, with a 50% effective concentration (EC₅₀) of 12.06 μM and selectivity index (SI) of 5.08, respectively. The inhibitory effect of emodin for CVB₄ entry and replication was further confirmed by a quantitative real time PCR (qPCR) assay. The results further showed that the mice orally treated with different dosages of emodin displayed a dose dependent increase of survival rate, body weight and prolonged mean time of death (MTD), accompanied by significantly decreased myocardial virus titers and pathologic scores/lesions. Moreover, emodin could inhibit CVB₄-induced apoptosis in vitro and in vivo. Our results indicated that emodin could be used as potential antiviral in the post-exposure prophylaxis for CVB₄ infection.
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Liu et al. (2013) studied Coxsackievirus B4 (CVB4) infection. Emodin was evaluated on CVB4 entry and replication (EC50 12.06 μM). Emodin reduced Coxsackievirus B4 entry and replication in vitro (EC50 12.06 μM) and dose-dependently increased survival and decreased myocardial virus titers in infected mice.
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