Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro.
Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro.
复制标题
小檗碱通过抑制 c-Jun N 末端激酶 (JNK) 和 p38 MAPK 体外激活来限制柯萨奇病毒 B 3 型复制
DOI：
10.12659/msm.899804
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发表时间：
2017-03-25
期刊：
影响因子：
--
通讯作者：
Hu X
中科院分区：
文献类型：
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作者：
Dai Q;Zhang D;Yu H;Xie W;Xin R;Wang L;Xu X;He X;Xiong J;Sheng H;Zhang L;Zhang K;Hu X
背景目前，柯萨奇病毒性心肌炎的治疗仍然困难。小檗碱（BBR）是一种从中药中分离得到的异喹啉类生物碱，对多种病毒具有显著的抗病毒作用。然而，BBR控制CVB 3感染的潜在机制尚未报道。本研究旨在探讨BBR对柯萨奇病毒B3（CVB 3）感染的抗病毒作用及其机制。材料/方法采用Westernblot方法检测VP 1和MAPKs信号通路的蛋白水平。RT-PCR法检测VP 1 mRNA水平。通过TCID 50测定法测定病毒滴度。结果BBR处理可显著降低CVB 3在HeLa细胞中的复制。此外，BBR处理降低了HeLa细胞和原代大鼠心肌细胞中CVB 3感染后JNK和p38 MAPK的磷酸化水平。结论BBR通过抑制JNK和p38 MAPK的活化抑制CVB 3的复制，为研究CVB 3诱导的病毒性心肌炎的治疗策略提供了新的思路。
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/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.