Open AccessRetracted: Micro RNA ‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway
Author(s) -
Han XinRui,
Wen Xin,
Wang YongJian,
Wang Shan,
Shen Min,
Zhang ZiFeng,
Fan ShaoHua,
Shan Qun,
Wang Liang,
Li MengQiu,
Hu Bin,
Sun ChunHui,
Wu DongMei,
Lu Jun,
Zheng YuanLin
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13597
Subject(s) - dexmedetomidine , wnt signaling pathway , apoptosis , brain damage , hypoxia (environmental) , medicine , ischemia , hippocampus , endocrinology , pharmacology , anesthesia , biology , chemistry , signal transduction , microbiology and biotechnology , biochemistry , organic chemistry , sedation , oxygen
Hypoxia–ischaemia ( HI ) remains a major cause of foetal brain damage presented a scarcity of effective therapeutic approaches. Dexmedetomidine ( DEX ) and micro RNA ‐140‐5p (miR‐140‐5p) have been highlighted due to its potentially significant role in the treatment of cerebral ischaemia. This study was to investigate the role by which miR‐140‐5p provides cerebral protection using DEX to treat hypoxic–ischaemic brain damage ( HIBD ) in neonatal rats via the Wnt/β‐catenin signalling pathway. The HIBD rat models were established and allocated into various groups with different treatment plans, and eight SD rats into sham group. The learning and memory ability of the rats was assessed. Apoptosis and pathological changes in the hippocampus CA 1 region and expressions of the related genes of the Wnt/β‐catenin signalling pathway as well as the genes responsible of apoptosis were detected. Compared with the sham group, the parameters of weight, length growth, weight ratio between hemispheres, the rate of reaching standard, as well as Bcl‐2 expressions, were all increased. Furthermore, observations of increased levels of cerebral infarction volume, total mortality rate, response times, total response duration, expressions of Wnt1, β‐catenin, TCF ‐4, E‐cadherin, apoptosis rate of neurons, and Bax expression were elevated. Following DEX treatment, the symptoms exhibited by HIBD rats were ameliorated. miR‐140‐5p and si‐Wnt1 were noted to attenuate the progression of HIBD . Our study demonstrates that miR‐140‐5p promotes the cerebral protective effects of DEX against HIBD in neonatal rats by targeting the Wnt1 gene through via the negative regulation of the Wnt/β‐catenin signalling pathway.