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    ASIA unversity > 資訊學院 > 光電與通訊學系 > 期刊論文 >  Item 310904400/115039


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/115039


    Title: Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3b signaling
    Authors: 洪詩雅;Hung, Shih-Ya;鍾欣怡;Chung, Hsin-Yi;羅思庭;Luo, Sih?Ting;朱鈺婷;Chu, Yu-Ting;陳禹心;Chen, Yu-Hsin;MacD, Iona J.;MacDonald, Iona J.;錢思佑;Chien, Szu?Yu;Kot, Peddanna;Kotha, Peddanna;楊良友;Yang, Liang-Yo;黃玲玲;Hwang, Ling-Ling;陳易宏;Chen, Yi-Hung
    Contributors: 資訊電機學院光電與通訊學系
    Keywords: Akt/GSK-3β;BDNF;electroacupuncture;histone deacetylases;motor function tests;preclinical traumatic brain injury.
    Date: 2022-08-01
    Issue Date: 2023-03-28 02:04:38 (UTC+0)
    Publisher: 亞洲大學
    Abstract: Background: Acupuncture or electroacupuncture (EA) appears to be a potential treatment in acute clinical traumatic brain injury (TBI); however, it remains uncertain whether acupuncture affects post-TBI histone deacetylase (HDAC) expression or impacts other biochemical/neurobiological events.

    Materials and methods: We used behavioral testing, Western blot, and immunohistochemistry analysis to evaluate the cellular and molecular effects of EA at LI4 and LI11 in both weight drop-impact acceleration (WD)- and controlled cortical impact (CCI)-induced TBI models.

    Results: Both WD- and CCI-induced TBI caused behavioral dysfunction, increased cortical levels of HDAC1 and HDAC3 isoforms, activated microglia and astrocytes, and decreased cortical levels of BDNF as well as its downstream mediators phosphorylated-Akt and phosphorylated-GSK-3β. Application of EA reversed motor, sensorimotor, and learning/memory deficits. EA also restored overexpression of HDAC1 and HDAC3, and recovered downregulation of BDNF-associated signaling in the cortex of TBI mice.

    Conclusion: The results strongly suggest that acupuncture has multiple benefits against TBI-associated adverse behavioral and biochemical effects and that the underlying mechanisms are likely mediated by targeting HDAC overexpression and aberrant BDNF-associated Akt/GSK-3 signaling.
    Appears in Collections:[光電與通訊學系] 期刊論文

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