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학술저널
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Li, Xiao-Qiang (Department of Pharmacology, School of Pharmacy, Fourth Military Medical University) Liu, Xiao-Xiao (Department of Pharmacology, School of Pharmacy, Fourth Military Medical University) Wang, Xue-Ying (Department of Pharmacology, School of Pharmacy, Fourth Military Medical University) Xie, Yan-Hua (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University) Yang, Qian (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University) Liu, Xin-Xin (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University) Ding, Yuan-Yuan (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University) Cao, Wei (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University) Wang, Si-Wang (Department of Natural Medicine and Institute of Materia Medica, School of Pharmacy, Fourth Military Medical University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제25권 제3호
발행연도
2017.1
수록면
279 - 287 (9page)

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The chemical property of cinnamaldehyde is unstable in vivo, although early experiments have shown its obvious therapeutic effects on viral myocarditis (VMC). To overcome this problem, we used cinnamaldehyde as a leading compound to synthesize derivatives. Five derivatives of cinnamaldehyde were synthesized: 4-methylcinnamaldehyde (1), 4-chlorocinnamaldehyde (2), 4-methoxycinnamaldehyde (3), ${\alpha}$-bromo-4-methylcinnamaldehyde (4), and ${\alpha}$-bromo-4-chlorocinnamaldehyde (5). Neonatal rat cardiomyocytes and HeLa cells infected by coxsackievirus B3 (CVB3) were used to evaluate their antiviral and cytotoxic effects. In vivo BALB/c mice were infected with CVB3 for establishing VMC models. Among the derivatives, compound 4 and 5 inhibited the CVB3 in HeLa cells with the half-maximal inhibitory concentrations values of $11.38{\pm}2.22{\mu}M$ and $2.12{\pm}0.37{\mu}M$, respectively. The 50% toxic concentrations of compound 4 and 5-treated cells were 39-fold and 87-fold higher than in the cinnamaldehyde group. Compound 4 and 5 effectively reduced the viral titers and cardiac pathological changes in a dose-dependent manner. In addition, compound 4 and 5 significantly inhibited the secretion, mRNA and protein expressions of inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 in CVB3-infected cardiomyocytes, indicating that brominated cinnamaldehyde not only improved the anti-vital activities for VMC, but also had potent anti-inflammatory effects in cardiomyocytes induced by CVB3.

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