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Expression of interleukin-9 and its upstream stimulating factors in rats with ischemic stroke

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Abstract

To investigate the temporal expressions of IL-9 and its related cytokines after middle cerebral artery occlusion in rats. IL-9 and its related cytokines in ischemia brain and blood were tested after rats were subjected to transient focal ischemia. Comparing with sham-operated group, the levels of IL-4, TGF-β, PU.1, IRF4, OX40, NIK, RelB-p52 and IL-9 in experimental groups were significantly higher after middle cerebral artery occlusion. The results showed that expressions of IL-9 and its upstream stimulating factors increased in experimental stroke, and whether they play a role or just a secondary change is awaiting further research.

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Acknowledgments

This study is funded by the Role of New Th9 Cells on the Mechanism of Malignant MCA Infarction and the Change of TH9 after MSCs Implanting Ischemic Stroke Mice (No. 81271328), National Natural Science Foundation.

Conflict of interest

The authors declare that there are no conflicts of interest.

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    Authors and Affiliations

    1. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou, Guangdong, China

      Yinyao Lin, Yongqiang Dai, Haiyan Li, Yanqiang Wang, Bingjun Zhang & Zhengqi Lu

    2. Department of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, No. 52 Meihuadong Road, Zhuhai, Guangdong, China

      Lei Zhang

    3. Department of Neurology, Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-sen University, No. 186 Zhongxingbei Road, Huizhou, Guangdong, China

      Suqin Chen

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    1. Yinyao Lin
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    Correspondence to Zhengqi Lu.

    Additional information

    Y. Lin, L. Zhang and Y. Dai contributed equally to this work.

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    Lin, Y., Zhang, L., Dai, Y. et al. Expression of interleukin-9 and its upstream stimulating factors in rats with ischemic stroke. Neurol Sci 36, 913–920 (2015). https://doi.org/10.1007/s10072-015-2096-2

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    • DOI: https://doi.org/10.1007/s10072-015-2096-2

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