title: microRNA-33A expression is reduced in cerebral cortex in a rat model of ischemic tolerance.
abstract: This study examined the microRNA&mdash;33a (miR&mdash;33a) expression levels in cerebral cortex in rat model of cerebral ischemic tolerance (IT), with 3&mdash;nitropropionic acid (3&mdash;NPA) preconditioning. Rat model of cerebral IT was established as follows: 14 male Sprague&mdash;Dawley rats were randomly divided into two groups, the 3&mdash;NPA treated group and the control group. Intraperitoneal injection of 3&mdash;NPA or normal saline was performed in 3&mdash;NPA treated group and control group, respectively. Middle cerebral artery occlusion (MCAO) was performed in all the rats 3 days after injection and the infarct volume was measured on postoperative day&mdash;2. To study miR&mdash;33a expression levels in this model, male Sprague&mdash;Dawley rats (n = 31) were randomly divided into 4 groups, 3&mdash;NPA treatment group (n = 8), 3&mdash;NPA treatment + MCAO group (n = 9), MCAO group (n = 9), and control group (n = 5). Surviving rats were sacrificed 4 days after injection and cerebral cortex samples were obtained for total RNA isolation. MiR&mdash;33a expression levels were determined by real&mdash;time quantitative PCR (qRT&mdash;PCR). Infarct volume in 3&mdash;NPA treated group decreased significantly in comparison to the control group (P &lt; 0.05). Expression analysis by qRT&mdash;PCR revealed that miR&mdash;33a expression levels in 3&mdash;NPA treated group were significantly higher than that in control group (P &lt; 0.05). However, no statistically significant difference in miR&mdash;33a expression levels were observed in 3&mdash;NPA + MCAO and MCAO groups (both P > 0.05). Our results present convincing evidence that miR&mdash;33a expression levels are significantly reduced in the cerebral cortex in rat model of cerebral IT, which may have significantly impacted the infarct volume.
authors.affiliation: Henan Provincial People&apos;s Hospital Department of Neurology Zhengzhou China fengyanfy1028&commat;163.com.
authors.forename: Y
authors.initials: Y
authors.lastname: Feng
authors.affiliation: Henan Provincial People&apos;s Hospital Department of Neurology Zhengzhou China.
authors.forename: W
authors.initials: W
authors.lastname: Li
authors.affiliation: Henan Provincial People&apos;s Hospital Department of Neurology Zhengzhou China.
authors.forename: J Q
authors.initials: JQ
authors.lastname: Wang
mesh_terms: D000818:Animals; D001285:Atropine; D002540:Cerebral Cortex / Q000098:blood supply / Q000378:metabolism*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D020244:Infarction, Middle Cerebral Artery / Q000235:genetics / Q000401:mortality / Q000473:pathology*; D019194:Ischemic Preconditioning; D008297:Male; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D009574:Nitro Compounds / Q000008:administration & dosage; D011422:Propionates / Q000008:administration & dosage; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D012720:Severity of Illness Index
chemical_list: C580642:MIRN33 microRNA, rat; D035683:MicroRNAs; D009574:Nitro Compounds; D011422:Propionates; D001285:Atropine; C015392:3-nitropropionic acid