Qi-Wei-Bai-Zhu powder improves inflammatory response via the myd88pathway in neonatal mice infected with human rotavirus.
Qi-Wei-Bai-Zhu powder improves inflammatory response via the myd88pathway in neonatal mice infected with human rotavirus.
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芪味白术散通过 myd88 通路改善感染人轮状病毒的新生小鼠的炎症反应。
DOI：
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Chaolong Chen(陈超龙）
中科院分区：
文献类型：
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作者：
Canrong Wu;Biqiang Sun1（孙必强）;Chaolong Chen(陈超龙）
芪味白术散（QWBZP）作为经典草药方之一，已被证明可以减少人类和啮齿动物感染轮状病毒（RV）的腹泻发生率，降低死亡率并调节细胞因子分泌。我们进行本研究是为了阐明QWBZP如何对新生小鼠的HRV感染发挥有益作用的具体机制。在 HRV 和 QWBZP 处理的新生小鼠和 CD 8 T 细胞中测定了 Toll 样受体 3 (TLR3) 通路中的细胞因子含量和蛋白质表达。结果表明，QWBZP 降低了 HRV 感染小鼠的腹泻发生率和粪便病毒排出量。此外，QWBZP 降低了 HRV 感染小鼠血清和肠道中白细胞介素 (IL)-1β、肿瘤坏死因子-α (TNF-α)、干扰素 (IFN)-α 和 IFN-β 的含量，并增加了 IL-10 的含量。 QWBZP 以及骨髓分化因子 88 (MyD88) 抑制肽下调 MyD88-NFκB 通路并改善细胞因子分泌，但它们不影响 HRV 处理的 CD 8 T 细胞中 TLR3 的表达。此外，QWBZP. 和 MyD88 抑制肽均不对聚 (I:.C) 处理的 CD8 T 细胞中的 NFκB 表达和细胞因子分泌产生任何影响。总之，我们的结果表明，HRV 依赖于 MyD88 激活 TLR3 通路及其下游靶标 NFκB，而 QWBZP 选择性抑制 MyD88，从而进一步灭活 NFκB 通路并随后提高细胞因子的产生，而不影响 TLR3。
Qi-Wei-Bai-Zhu Power (QWBZP), as one of the classic herbal prescription, has been proved to decrease.diarrhea incidence, reduce mortality and regulate cytokines secretion in both human and rodents.infected with Rotavirus (RV). We conducted the present study to elucidate the specific mechanism how.QWBZP exerts its beneficial effects on HRV infection in neonatal mice. Cytokine contents and.expression of proteins in Toll-Like Receptor 3 (TLR3) pathway were determined in HRV and QWBZP.treated neonatal mice and CD 8 T cells. The results showed that QWBZP decreased diarrhea incidence.and fecal virus shedding in HRV-infected mice. Moreover, QWBZP decreased interleukin (IL)-1β,.Tumor Necrosis Factor-α (TNF-α), interferon (IFN)-α and IFN-β contents and increased IL-10 content in.both serum and intestine in HRV-infected mice. QWBZP, as well as myeloid differentiation factor 88.(MyD88) inhibitor peptide, downregulated MyD88-NFκB pathway and improved cytokines secretion,.however, they did not affect TLR3 expression in HRV-treated CD 8 T cells. In addition, neither QWBZP.nor MyD88 inhibitor peptide exerted any effects on NFκB expression and cytokines secretion in poly (I:.C)-treated CD8 T cells. In conclusion, our results indicated that HRV activated TLR3 pathway and its.downstream target NFκB dependent on MyD88, while QWBZP selectively inhibited MyD88 which.further inactivated NFκB pathway and subsequently improved the production of cytokines, without.affecting TLR3.