鞣花酸通过抑制 TLR2 信号通路在体内和体外发挥抗单纯疱疹病毒 1 脑炎的作用。
Corilagin Protects Against HSV1 Encephalitis Through Inhibiting the TLR2 Signaling Pathways In Vivo and In Vitro.
机构信息
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, People's Republic of China.
Department of Neurology, Wuhan General Hospital of Guangzhou Military Command, Wuhan, 430070, People's Republic of China.
出版信息
Mol Neurobiol. 2015 Dec;52(3):1547-1560. doi: 10.1007/s12035-014-8947-7. Epub 2014 Nov 4.
In this study, we tried to explore the molecular mechanism that Corilagin protected against herpes simplex virus-1 encephalitis through inhibiting the TLR2 signaling pathways in vivo and in vitro. As a result, Corilagin significantly prevented increase in the levels of TLR2 and its downstream mediators following Malp2 or HSV-1 challenge. On the other hand, in spite of TLR2 knockdown, Corilagin could still significantly suppress the expression of P38 and NEMO, phosphor-P38, and nuclear factor kappa B. The mRNA and protein expression of TLR2 and its downstream mediators in the brain tissue were also significantly lowered in mice treated with Corilagin. In addition, Corilagin inhibited expression of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 protein. In conclusion, Corilagin shows the potential to protect against HSV-1-induced encephalitis, and the beneficial effects may be mediated by inhibiting TLR2 signaling pathways.
在这项研究中，我们试图通过体内和体外实验探索柯里拉京通过抑制 TLR2 信号通路来对抗单纯疱疹病毒-1 脑炎的分子机制。结果表明，柯里拉京能显著抑制 Malp2 或 HSV-1 刺激后 TLR2 及其下游介质水平的升高。另一方面，尽管 TLR2 被敲低，柯里拉京仍能显著抑制 P38 和 NEMO、磷酸化 P38 和核因子 kappa B 的表达。用柯里拉京处理的小鼠脑组织中 TLR2 及其下游介质的 mRNA 和蛋白表达也显著降低。此外，柯里拉京抑制肿瘤坏死因子-α（TNF-α）和白细胞介素（IL）-6 蛋白的表达。总之，柯里拉京具有预防 HSV-1 诱导的脑炎的潜力，其有益作用可能是通过抑制 TLR2 信号通路介导的。
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