Experimental Autoimmune Encephalomyelitis Inhibited by Huangqi Guizhi Wuwu Decoction via Th2 Cytokine Enhancement
  
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DOI:10.4103/2311-8571.328617
KeyWord:CD8‑Positive T‑lymphocytes, experimental autoimmune encephalomyelitis, multiple sclerosis, myelin‑oligodendrocyte glycoprotein, Th2 cytokine, traditional Chinese medicine
                             
AuthorInstitution
Yong Penga a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Fei‑Zhou Zhub b.Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, Hunan, China
Xiang Denga a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Jian‑Xiong Zhoua a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Shuai Gaob b.Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, Hunan, China
Zhi‑Xing Chena a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Shan‑Shan Yanga a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Lu Gana a.Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou
Zhuo‑Lin Lib b.Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, Hunan, China
Qian‑Qian Liub b.Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, Hunan, China
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Abstract:
      Background: Huangqi Guizhi Wuwu decoction (HQGZWW) exhibits good effects when administered to treat multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Understanding the precise mechanism of this decoction is thus important. Based on the findings of our previous study, the aim of the present study was to understand the role of antigen‑specific CD8+ T-cells on the pathogenesis of MS/EAE when HQGZWW is administered as treatment. Methods: Myelin oligodendrocyte glycoprotein (MOG) 35-55-induced mice were administered distilled water, prednisone, and high dose or low dose HQGZWW.After purified CD4+ and CD8+ T-cells were stimulated with the MOG35-55 peptide, proliferation and cytokine secretion assays were performed. To establish the adoptive transfer EAE model, naïve mice were injected with MOG35-55 -CD8+ or CD4+ T-cells. Results: Significant improvements in EAE score and pathology were observed in the high dose HQGZWW and prednisone groups. Compared to the low dose HQGZWW and distilled water groups, lower antigen‑specific responses, lower levels of interferon-gamma, and higher levels of interleukin (IL)-4 and IL-10 from CD8+ and CD4+ T cells were observed in the high dose HQGZWW and prednisone groups. Finally, the EAE score was observed to be similar between the high dose HQGZWW group and prednisone group; however, this finding was not observed in the low dose HQGZWW group. Conclusion: Our findings suggest that high dose HQGZWW has similar effects on cell proliferation, cytokine secretion, and EAE score to prednisone, while low dose HQGZWW does not have such effect. The protective role of HQGZWW against EAE might thus depend on the Th2 cytokine secretion profile induced by either MOG35-55 specific CD8+ or CD4+ T-cells.
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