SAFFLOWERINHIBITSCOXSACKIEVIRUS B3 INFECTION OF MYOCARDIAL MICROVASCULAR ENDOTHELIAL CELLSVIA THE TOLL-LIKE RECEPTOR 4/NUCLEAR FACTOR KAPPA B SIGNA- LING PATHWAY

YING FAN, HONG JIANG

Renmin Hospital of Wuhan University

Introduction: Infections caused by different pathogens can lead to cardiovascular diseases such as acute/chronic myocarditis. Coxsackievirus B3 (CVB3) is the most common causative agent of myocarditis, which can result in dilated cardiomyopathy. Here we investigated the mechanism by which safflower yellow B (SYB) inhibitsthe CVB3 infection of myocardial microvascular endothelial cells.

Materials and methods: CVB3 infected myocardial microvascular endothelial cells was detected by TCID50. The CVB3 acti- vated the TLR4/NF-B pathway in myocardial microvascular endothelial cells was detected by Western blotting. And the which saf- flower yellow B (SYB) inhibitsthe CVB3 infection of myocardial microvascular endothelial cells was detected by Western blotting.

Results: SYB inhibited CVB3 infection via the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. Furthermore, the median tissue culture infective dose of CVB3 was higher in infected cells than in thosetreated withSYB.

Conclusion: We showed that SYB inhibited the CVB3 infection of myocardial microvascular endothelial cellsviathe TLR4/NF- κB signaling pathway. These findings may lead to new insights on the treatment of CVB3-induced myocarditis by SYB.