Effect of selective brain hypothermia on long noncoding RNA AK009271 of cerebral cortex following cerebral ischemia-reperfusion in rats
10.3969/j.issn.1672-5921.2019.12.007
- Author:
Ya'nan TANG
1
Author Information
1. Department of Anesthesiology, Qingdao Municipal Hospital, Affiliated to Qingdao University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Brain ischemia;
Long non-coding RNA;
Reperfusion injury;
Selective brain hypothermia
- From:
Chinese Journal of Cerebrovascular Diseases
2019;16(12):647-652
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the expression of long noncoding RNA (LncRNA) AK009271 in the cortex of rats with cerebral ischemia-reperfusion,and to evaluate the effect of selective brain hypothermia on the its expression. Methods: All 75 healthy male Sprague-Dawley (SD) rats of SPF grade, weighing 200-250 g,were randomly divided into the sham operation group (group S), the ischemia-reperfusion group (group I/R) and the hypothermia group (group HT) by random digital scale method,with 25 rats in each group. Focal cerebral ischemia-reperfusion model was induced by string Longa's thread thrombus method of the middle cerebral artery for 2 hours. The group HT was infused with 4°C cold isotonic saline for 15 min (20 ml/kg) through internal carotid artery immediately after reperfusion. During the procedure, brain and rectal temperatures were monitored to ensure successful construction of selective brain hypothermia model. The group S only separated the carotid artery without performing middle cerebral artery embolization. At 6,24,and 48 h after reperfusion, the neurological deficit scores were measured and the expression of LncRNA AK009271 was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). At 24 h after reperfusion, the expression of Fisl was determined by Western Blot, and mitochondrial morphology was observed by electron microscopy. The apoptosis rate of cells was detected by TUNEL staining. Results: (1) Compared with the group I/R, the group HT had decreased brain temperature after perfusion of 4 °C isotonic saline for 15 min (32. 27 ± 0. 15 vs. 34. 52 ± 0. 22,t = 1. 603, P < 0. 05), but without significant changes in rectal temperature (P > 0. 05). (2) Compared with the group S,the neurological deficit scores were increased in the other two groups;the neurological deficit score in the group HT was lower than the group I/R; all P < 0. 05. (3) Compared with the group S, the expression of LncRNA AK009271 in the group I/R all decreased at 6,24 and 48 h after reperfusion,and reached the lowest at 24 h after reperfusion (all P <0. 05);however,the expression of LncRNA AK009271 in the group HT increased at 6,24 and 48h after reperfusion compared with the group I/R (both P<0.05). (4) Compared with the group S, up-regulated expression of Fisl, mitochondrial ultrastructure damage and increased apoptosis rate were observed in the other two groups at 24 h after reperfusion (all P < 0. 05); However, compared with group I/R, down-regulated expression of Fisl (P <0. 05), less damaged mitochondrial ultrastructure and decreased apoptosis rate were observed in the HT group (P < 0. 05). Conclusions The expression of LncRNA AK009271 in the cortex of rats with cerebral ischemia-reperfusion is decreased. Selective brain hypothermia could ameliorate focal cerebral I/R injury in rats through up-regulating LncRNA AK009271 expression, inhibiting Fisl expression and lightening cell apoptosis.
