Effect of betulinic acid preconditioning on oxidative stress response during cerebral ischemia-reperfusion in mice
10.3760/cma.j.issn.0254-1416.2014.07.023
- VernacularTitle:白桦脂酸预处理对小鼠脑缺血再灌注时氧化应激反应的影响
- Author:
Chenchen ZHANG
;
Pei LU
;
Yuke TIAN
;
Hui XU
- Publication Type:Journal Article
- Keywords:
Pentacyclic triterpenes;
Ischemic preconditioning;
Brain;
Reperfusion injury;
Oxidative stress
- From:
Chinese Journal of Anesthesiology
2014;34(7):859-862
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of betulinic acid preconditioning on oxidative stress response during cerebral ischemia-reperfusion (I/R) in mice.Methods Seventy-two male Kunming mice,aged 3 months,weighing 25-35 g,were randomly divided into 3 groups (n =24 each) using a random number table:sham operation group (group S),I/R group,and betulinic acid preconditioning group (group BP).Cerebral I/R was induced by middle cerebral artery occlusion in mice anesthetized with 10％ chloral hydrate 40 ml/kg.In group BP,betulinic acid 50 mg/kg was administered by intragastric gavage everyday for 7 days before ischemia,while the equal volume of solvent dimethyl sulfoxide was given in S and I/R groups.At 22 h of reperfusion,neurological function was assessed and scored.The mice were then sacrificed and brains were removed for determination of infarct size,expression of NADPH oxidase (Nox1,Nox2 and Nox4) and p22phox mRNA,activity of ROS and apoptosis rate in the infarcted zone.Results Compared with S group,neurological score,cerebral infarct size,activity of ROS and apoptosis rate in the infarcted zone were significantly increased,and the expression of Nox1,Nox2,Nox4 and p22phox mRNA was up-regulated in group I/R.Compared with group I/R,neurological score,cerebral infarct size,activity of ROS and apoptosis rate in the infarcted zone were significantly decreased,and the expression of Nox1,Nox2,Nox4 and p22phox mRNA was down-regulated in group BP.Conclusion Betulinic acid preconditioning mitigates cerebral I/R injury through inhibiting oxidative stress response in mice.
