25 March 2017 : Laboratory Research
Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro
Qian Dai1ABCDF*, Di Zhang1AEF, Hua Yu12E, Wei Xie1D, Rong Xin1B, Lei Wang1B, Xiaohui Xu12B, Xiaomei He1C, Junzhi Xiong1C, Halei Sheng1C, Le Zhang1D, Kebin Zhang1ADG, Xiaomei Hu12ADEFDOI: 10.12659/MSM.899804
Med Sci Monit 2017; 23:1448-1455
Abstract
BACKGROUND: At present, the treatment of coxsackievirus-induced myocarditis remains difficult. Berberine (BBR), an isoquinoline alkaloid isolated from traditional medicine herbs, exhibits significant anti-viral efficacy against various viruses. However, the underlying mechanism by which BBR controls CVB3 infection has not yet been reported. The purpose of this study was to investigate the anti-viral efficacy of BBR against CVB3 infection and its mechanism.
MATERIAL AND METHODS: In our experiments, the protein levels of VP1 and MAPKs signal pathway were measured by Western blot. The mRNA level of VP1 was measured by RT-PCR. The virus titers were determined by TCID50 assay.
RESULTS: We found that BBR treatment significantly decreased CVB3 replication in HeLa cells. In addition, the BBR treatment reduced the phosphorylation levels of JNK and p38 MAPK upon CVB3 infection in both HeLa cells and primary rat myocardial cells.
CONCLUSIONS: Taken together, these results suggest that BBR inhibits CVB3 replication through the suppression of JNK and p38 MAPK activation, shedding new light on the investigation of therapeutic strategies against CVB3-induced viral myocarditis.
Keywords: Berberine, JNK Mitogen-Activated Protein Kinases, Virus Replication
Editorial
01 December 2024 : Editorial
Editorial: The 2024 Revision of the Declaration of Helsinki and its Continued Role as a Code of Ethics to Guide Medical ResearchDOI: 10.12659/MSM.947428
Med Sci Monit 2024; 30:e947428
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