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Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3β signaling
Hung, Shih-Ya Chung, Hsin-Yi Luo, Sih-Ting Chu, Yu-Ting Chen, Yu-Hsin MacDonald, Iona J. Chien, Szu-Yu Kotha, Peddanna Yang, Liang-Yo Hwang, Ling-Ling
Hung, Shih-Ya
Chung, Hsin-Yi
Luo, Sih-Ting
Chu, Yu-Ting
Chen, Yu-Hsin
MacDonald, Iona J.
Chien, Szu-Yu
Kotha, Peddanna
Yang, Liang-Yo
Hwang, Ling-Ling
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Journal article
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2022-08-09
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Medicine
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http://dx.doi.org/10.3389/fncel.2022.880267
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.
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Hung S-Y, Chung H-Y, Luo S-T, Chu Y-T, Chen Y-H, MacDonald IJ, Chien S-Y, Kotha P, Yang L-Y, Hwang L-L, Dun NJ, Chuang D-M and Chen Y-H (2022) Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3β signaling. Front. Cell. Neurosci. 16:880267. doi: 10.3389/fncel.2022.880267
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Frontiers in Cellular Neuroscience, Vol. 16
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