Abstract: Objective To explore the effects of emodin in myocardial protection in mice with viral myocarditis (VMC) and
explore molecular mechanisms. Methods Fifty-five male 4-week-old BALB/c mice were randomly divided into control group
(n=15), model group (n=20), and emodin group (n=20). The mice in model and emodin groups were inoculated with 0.1 ml
Eagle’s solution containing coxsackievirus B3 intraperitoneally, and those in the control group were given only 0.1 ml Eagle’s
solution. From the day of inoculation, the mice in emodin group received intragastric administration with 0.1 ml of 3 mg/ml
emodin solution once daily for 21 consecutive days, and those in the control and model groups received 0.1 ml distilled water
only. On day 7 after inoculation, 5 mice from each group were sacrificed to determine the viral titers in the cardiac tissues. All
the mice were sacrificed on day 22 for measurement of the heart weight and histopathological inspection of the heart with HE
staining. The mRNA and protein expression levels of myocardial interleukin-23 (IL-23) and interleukin-17 (IL-17) were
detected by real-time quantitative PCR and Western blotting, respectively, and serum IL-23 and IL-17 levels were examined
using enzyme linked immunosorbent assay (ELISA). Th17 cell frequencies were analyzed by flow cytometry. The expression
levels of myocardial nuclear factor-κB (NF-κB) p65 in the cardiomyocyte nuclei were examined using Western blotting, and
myocardial interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) contents were detected by ELISA. Results The
mortality, myocardial histopathologic scores and virus titers in emodin group were all significantly lower than those in the
model group (P<0.05). The heart-to-body weight ratio, myocardial IL-23 and IL-17 expressions, serum IL-23 and IL-17 levels,
Th17 cell frequencies, cardiomyocyte nuclear NF-κB p65 expression, and myocardial contents of IL-1β, IL-6 and TNF-α were
all significantly increased in the model group as compared to the control group (P<0.01) but reduced significantly in emodin group as compared to model
group (P<0.05). Conclusion Emodin can protect against VMC by inhibiting IL-23/IL-17 inflammatory axis, Th17 cell proliferation and viral replication in
mice.