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Epigenetic modulation of the MAPK pathway prevents isoflurane‑induced neuronal apoptosis and cognitive decline in aged rats

Isoflurane is a broadly used inhalation anesthetic that causes cognitive impairment in rodent models as well as humans. Although previous studies suggested an association between isoflurane exposure and neuro-inflammation, apoptosis and mitochondrial dysfunction, the pathogenesis of isoflurane-induc...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2020-11, Vol.20 (5), p.1-1
Main Authors: Huang, Lei, Fang, Hai-Bin, Cheng, Hui-Hui, Mei, Sheng-Lan, Cheng, Yun-Ping, Lv, Yao, Meng, Qing-Tao, Xia, Zhong-Yuan
Format: Article
Language:English
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Summary:Isoflurane is a broadly used inhalation anesthetic that causes cognitive impairment in rodent models as well as humans. Although previous studies suggested an association between isoflurane exposure and neuro-inflammation, apoptosis and mitochondrial dysfunction, the pathogenesis of isoflurane-induced cognitive decline remains elusive. In the present study, 22-month-old male Sprague-Dawley male rats (n=96) were divided into three groups: Control (Cont), isoflurane (ISO) and MS-275 pre-treated groups. The rats were sacrificed following exposure to isoflurane and a cognitive test. The hippocampus of each animal was harvested for quantitative PCR, TUNEL staining and western blot analysis. Histone deacetylases (HDAC)-1, -2 and -3 exhibited a significant increase at the gene and protein expression levels, whereas negligible mRNA expressions were observed for genes HDAC 4-11 (P >0.05; compared with Cont). Pre-treatment with the HDAC inhibitor MS-275 significantly inhibited the increase in TUNEL-positive cells induced by isoflurane exposure (70.72% decrease; P
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2020.9162