Neuroprotective effect of progesterone on focal cerebral ischemia/reperfusion injury in rats and its mechanism.
- Author:
Xin-juan LI
;
Lin-yu WEI
;
Chao-kun LI
;
Dong-liang LI
- Publication Type:Journal Article
- MeSH: Animals; Brain; drug effects; pathology; Brain Ischemia; drug therapy; Infarction, Middle Cerebral Artery; Male; Neuroprotective Agents; pharmacology; Potassium Channels, Tandem Pore Domain; metabolism; Progesterone; pharmacology; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Reperfusion Injury; drug therapy
- From: Chinese Journal of Applied Physiology 2015;31(3):231-234
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the neurological protective effects of progesterone (PROG) on focal cerebral ischemia/reperfusion injury in rats and to explore its possible mechanism.
METHODSOne handred and twenty male SD rats were divided into three groups randomly: sham-operated group, middle cerebral artery occlusion ( MCAO ) group and PROG + MCAO group( n = 40). The right temporary MCAO model was established by the line-embolism method. The PROG + MCAO group rats were according to 8 mg/kg intraperitoneal injection PROG, after that 30 min, the rats were suffered ischemia/reperfusion. After rats were suffered ischemia for 2 h and reperfusion 0, 24, 48, 72 h stress, the nervous functional defect degree were evaluated by longe scoring, and the expression of two-pore domain K channel 3 (TASK3) mRNA in brain tissue were detected by the real-time PCR.
RESULTSPROG (8 mg/kg) could significantly reduced the nervous functional defect degree in rats after ischemia/reperfusion 24, 48, 72 h (P < 0.05). The results of real-time PCR showed that the TASK3 mRNA expression in the brain tissue at all time points significantly decreased in MCAO group compared with sham-operated group (P < 0.05). However, compared with MCAO group, the expression of TASK3 mRNA in brain tissue at all time points dramatically increased in PROG + MCAO group (P < 0.05).
CONCLUSIONPROG can improve the nervous functional defect degree after focal cerebral ischemia/reperfusion injury in rats, and the mechanism might be associated with up-regulating the expression of TASK3 mRNA in brain tissue.