Arctiin suppresses H9N2 avian influenza virus-mediated inflammation via activation of Nrf2/HO-1 signaling.
Arctiin suppresses H9N2 avian influenza virus-mediated inflammation via activation of Nrf2/HO-1 signaling.
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DOI：
10.1186/s12906-021-03462-4
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发表时间：
2021-11-26
影响因子：
3.9
通讯作者：
Pan X
中科院分区：
文献类型：
--
作者：
Zhou B;Wang L;Liang Y;Li J;Pan X
H9N2型禽流感病毒(AIV)感染禽类和哺乳动物宿主，为新出现的高致病性禽流感病毒提供内部基因，这些病毒导致严重肺炎，死亡率高，目前几乎没有药物可用。牛至苷是一种具有生物活性的木脂素糖苷，具有多种药理作用。然而，牛至苷对H9N2病毒感染的作用尚不清楚。在本研究中，我们在体外分析了牛至苷对H9N2病毒感染的影响及其潜在的分子机制。用空斑减数试验(PRA)和子代病毒减数试验检测其对H9N2病毒的抑制作用。采用四甲基偶氮唑盐比色法、定量逆转录聚合酶链式反应、酶联免疫吸附试验、免疫荧光和免疫印迹等方法，进一步了解牛至苷对H9N2病毒感染细胞的抗炎作用及其机制。结果表明，牛至苷对H9N2病毒具有抗病毒活性。牛至苷治疗降低了H9N2病毒触发的促炎细胞因子，如IL-6和肿瘤坏死因子-α。此外，牛至苷显著抑制H9N2病毒介导的COX-2和PGE2的表达。此外，我们还发现Artiin抑制了H9N2病毒介导的RIG-I/JNK MAPK信号通路的激活。有趣的是，牛至苷能明显逆转H9N2病毒诱导的Nrf2的减少，增加Nrf2的核转位，并上调Nrf2信号转导靶基因(HO-1和SOD2)。HO-1抑制剂锌原卟啉可减弱牛至苷对H9N_2病毒诱导的RIG-I/JNK MAPK和促炎介质的抑制作用。上述结果提示，牛至苷对H9N2病毒感染的抗炎作用可能与其激活Nrf2/HO-1，阻断RIG-I/JNK MAPK信号通路有关，有望成为防治H9N2病毒感染的药物。网上版载有补充材料，可在10.1186/s12906-021-03462-4查阅。
H9N2 avian influenza viruses (AIVs) infect avian and mammalian hosts and provide internal genes for new emerging highly pathogenic avian viruses that cause severe pneumonia with high mortality, for which few medications are available. Arctiin, a bioactive lignan glycoside, has been reported to possess multiple pharmacological properties. However, the effect of arctiin on H9N2 virus infection is unclear. In the current study, we analyzed the effect of arctiin on H9N2 virus infection and the underlying molecular mechanism in vitro. The antiviral effect against H9N2 virus was determined by plaque reduction assay (PRA) and progeny virus reduction assay. We employed MTT assay, qRT-PCR, ELISA, immunofluorescence and Western blotting to better understand the anti-inflammatory effect and corresponding mechanism of arctiin on H9N2 virus-infected cells. The results showed that arctiin had antiviral activity against H9N2 virus. Arctiin treatment reduced H9N2 virus-triggered proinflammatory cytokines, such as IL-6, and TNF-α. Moreover, arctiin significantly suppressed H9N2 virus-mediated expression of COX-2 and PGE2. Furthermore, we found that arctiin inhibited H9N2 virus-mediated activation of RIG-I/JNK MAPK signaling. Interestingly, arctiin treatment obviously reversed H9N2 virus-induced reduction of Nrf2, increased the nuclear translocation of Nrf2, and upregulated Nrf2 signaling target genes (HO-1 and SOD2). Zinc protoporphyrin (Znpp)—an HO-1 inhibitor—weakened the inhibitory effect of arctiin on H9N2 virus-induced RIG-I/JNK MAPK and proinflammatory mediators. Taken together, these results suggested that the anti-inflammatory effects of arctiin on H9N2 virus infection may be due to the activation of Nrf2/HO-1 and blocked RIG-I/JNK MAPK signaling; thus, arctiin may be a promising agent for prevention and treatment of H9N2 virus infections. The online version contains supplementary material available at 10.1186/s12906-021-03462-4.
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DOI：
10.1186/1476-9255-8-16
发表时间：
2011-07-07
期刊：
Journal of inflammation (London, England)
影响因子：
--
作者：
Lee S;Shin S;Kim H;Han S;Kim K;Kwon J;Kwak JH;Lee CK;Ha NJ;Yim D;Kim K
通讯作者：
Kim K
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影响因子：
2.7
作者：
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影响因子：
3.7
作者：
Gao W;Sun W;Qu B;Cardona CJ;Powell K;Wegner M;Shi Y;Xing Z
通讯作者：
Xing Z
影响因子：
5.8
作者：
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影响因子：
6.1
作者：
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通讯作者：
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