摘要
目的探究冬凌草甲素对心肌缺血再灌注损伤的影响及其作用机制。方法将108只大鼠随机分为假手术组,I/R组,冬凌草甲素低、中、高剂量治疗组(2.5、5、10 mg/kg术前连续干预7 d)和阳性对照组(前列地尔造模后静注),每组18只,检测大鼠血流动力学指标、心肌病理损伤、血清氧化应激指标、内质网应激和细胞凋亡相关mRNA、蛋白表达、心肌细胞凋亡情况。结果与I/R组比较,冬凌草甲素高剂量治疗组和阳性对照组治疗组氧化应激指标和血流动力学显著改善,心肌梗死范围、心肌细胞凋亡率降低(P<0.05),内质网应激相关mRNA表达水平下调(P<0.05),凋亡相关蛋白表达水平降低(P<0.05)。结论冬凌草甲素可减轻I/R大鼠心肌损伤,可能与减轻氧化应激损伤和减弱内质网应激诱导的细胞凋亡相关。
Objective To explore the effect of oridonin on myocardial ischemia-reperfusion injury.Methods A total of 108 rats were randomly divided into 6 groups:sham operation group,I/R group,low-dose,middle-dose and high-dose oridonin treatment groups(2.5,5 and 10 mg/kg,continuous intervention for 7 days before surgery)and positive control group(intravenous injection of alprostadil after modeling),with 18 rats in each group.The hemodynamic indicators,myocardial pathological injury,serum oxidative stress indicators,endoplasmic reticulum stress and apoptosisrelated mRNA and protein expression levels and the apoptosis of myocardial cells were detected.Results The oxidative stress indicator and hemodynamics were significantly improved in the high-dose oridonin treatment group and positive control group when compared with those in the I/R group,and the myocardial infarction range and myocardial cell apoptosis rate were decreased(P<0.05).The mRNA expression levels of endoplasmic reticulum stress-related genes were down-regulated(P<0.05),and the expression levels of apoptosis-related proteins were declined(P<0.05).Conclusion Oridonin can alleviate the myocardial injury in I/R rats,which may be related to alleviating oxidative stress injury and attenuating endoplasmic reticulum stress-induced apoptosis.
作者
袁芳
宋海平
王聪聪
侯彬彬
侯爱军
赵威瑾
YUAN Fang;SONG Haiping;WANG Congcong;HOU Binbin;HOU Aijun;ZHAO Weijin(Department of Cardiology,Handan Central Hospital,Handan,Hebei,056000,China;Catheter Room,Handan Central Hospital,Handan,Hebei,056000,China)
出处
《医学分子生物学杂志》
2025年第2期180-186,共7页
Journal of Medical Molecular Biology
基金
河北省医学科学研究课题计划(No.20220526)。
关键词
冬凌草甲素
心肌缺血再灌注损伤
内质网应激
细胞凋亡
氧化应激
oridonin
myocardial ischemia-reperfusion injury
endoplasmic reticulum stress
apoptosis
oxidative stress
