Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3b signaling

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

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题名:	Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3b signaling
作者:	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
贡献者:	資訊電機學院光電與通訊學系
关键词:	Akt/GSK-3β;BDNF;electroacupuncture;histone deacetylases;motor function tests;preclinical traumatic brain injury.
日期:	2022-08-01
上传时间:	2023-03-28 02:04:38 (UTC+0)
出版者:	亞洲大學
摘要:	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.
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