| objective： To investigate the effect of corilagin on Toll-like receptor 3(TLR3)/nuclear factor-κb (NF-κb) signaling pathway and cell apoptosis in a murine model of viral myocarditis (VMC) infected by CVB3. Methods: viral myocarditis model was established by CVB 3 infected murine macrophages (RAW264.7) and divided into control group, CVB 3 group, CVB 3 + corilagin (25 μg · ml -1) group and CVB 3 + TLR3 inhibitor Chloroquine (Synonyms: Chloroquine) group, 25 μm, CVB3 + corilagin (25 μg · ML-1) + TLR3 agonist CU-CPT17e (10 μm) , CVB3 + poly (I: C)(positive control group) , 5 μg · ML-1 were used to construct the cell model, the mRNA expression of TLR3, TRIF, TRAF6, MAPK and Nemo was detected by Real-time PCR, and the expression of TLR3, TRIF, TRAF6, MAPK and Nemo was analyzed by QPCR (relative quantification, 2-δδct) . Western-blot was used to detect the relative expression of the proteins. After β-actin was homogenized, the nuclear transcription of NF-ΚB was detected by EMSA. Results: Corilagin could decrease the level of IL-6 and increase the level of IFN-β in VMC. Corilagin could stimulate the expression of TLR3, TRIF, TRAF6, MAPK, NEMO mRNA and reduce the expression of NF-κb in VMC induced by CVB3.Conclusion: Corilagin can attenuate the cardiac inflammatory response induced by CVB3 infection by up-regulating the expression of TLR3 and downstream signaling pathways, and promote the release of interferon, the anti-viral effect of Corilagin on VMC may provide a basis for further elucidating the molecular mechanism of Corilagin in the treatment of VMC. |
