
浏览全部资源
扫码关注微信
纸质出版日期:2013
移动端阅览
王兴红, 郑亚萍, 李海霞. 槲皮素对大鼠心肌缺血再灌注损伤的影响[J]. 中国实验方剂学杂志, 2013,19(4):266-270.
WANG Xing-hong, ZHENG Ya-ping, LI Hai-xia. Effects of Quercetin on Myocardial Ischemia Reperfusion Injury in Rats[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(4): 266-270.
目的: 探讨槲皮素(quercetin
Que)对大鼠心肌缺血再灌注损伤(MIRI)的保护机制。 方法: 将大鼠随机分为假手术组、心肌缺血再灌注损伤模型组、阳性对照组(盐酸硫氮卓酮片
0.01 mg·kg-1)和Que低、中、高剂量预处理组(15
30
60 mg·kg-1)
每组10只。冠状动脉前降支根部结扎30 min后剪断结扎线
再灌注60 min建立MIRI大鼠模型;Que预处理组在造模前给予Que各剂量灌胃1周。各组于再灌注60 min后分别取大鼠血清及心肌组织
测定大鼠血清丙二醛(MDA)、白细胞介素6(IL-6)、肿瘤坏死因子(TNF-α)、肌酸激酶同工酶(CK-MB)、肌钙蛋白(cTnI)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性;心肌肌浆网钙泵(SERCA)活性
用TTC染色法确定心肌损伤面积和梗死面积(MIS)。 结果: 模型组血清MDA(17.71±3.24) μmol·L-1
CK-MB(2 010.21±76.31) U·L-1
cTnI(2.25±0.76) μg·L-1
IL-6(5.89±0.34) ng·L-1和TNF-α(114.12±22.13) μg·L-1含量较假手术组显著升高(P<0.01或P<0.05)
SOD(77.58±5.20) U·mL-1
GSH-Px(11.22±4.88) U·mL-1
心肌SERCA(2.76±0.49) μmol·mg-1·prot-1·h-1活性显著降低(P<0.01或P <0.05);Que中、高剂量预处理组血清MDA(11.35±2.68
12.26±2.49)μmol·L-1
CK-MB(1 361.11±33.98
1 350.11±43.02)U·L-1
cTnI(1.75±0.43
1.73±0.33)μg·L-1
IL-6(3.23±0.16
3.12±0.17)ng·L-1和TNF-α(74.01±10.98
73.84±11.87)μg·L-1含量较模型组显著降低(P<0.01或P <0.05)
SOD(96.11±10.63
97.02±12.36)U·mL-1
GSH-Px(14.88±3.89
15.39±3.98)U·mL-1
心肌SERCA(3.98±0.23
3.92±0.31)μmol·mg-1·h-1活性显著升高(P<0.01或P <0.05);且明显缩小梗死面积(P<0.01或P <0.05)。 结论: Que预处理能减轻氧化应激损伤
降低炎症反应和减轻细胞内钙超载
对心肌缺血再灌注损伤有明显的保护作用。
Objective: To investigate the protective mechanism of quercetin(Que) on myocardial ischemia reperfusion injury(MIRI) in rats. Method: The rats were randomly divided control group
MIRI model group
positive control group (diltiazem HCl 0.01 mg·kg-1) and low
medium and high dose Que pretreatment group (15
30
60 mg·kg-1)
10 rats each group. The myocardial ischemia reperfusion model was induced by occulusion of the anterior descending coronary artery for 30 min and reperfusion for 60 min. Each Que dose was proconditioned for a week
and the rats serum and cardiac muscle tissue werecollected seperately 60 minutes after MIRI. The contents of malondialdehyde (MDA)
interleukin 6 (IL-6)
tumor necrosis factor-α(TNF-α)
creative kinase MB(CK-MB) and troponin(cTnI); the acitivity of superoxygen dehydrogenises(SOD)
glutathione peroxidase(GSH-Px) and Sarcoplasmic reticulum Ca2+ pump (SERCA). And by tetrazolium chloride (TTC) staining
the areas of myocardial damage and infraction were observed. Result: In the MIRI group
the contents of MDA (17.71±3.24)μmol·L-1
CK-MB (2 010.21±76.31) U·L-1
cTnI (2.25±0.76) μg·L-1
IL-6 (5.89±0.34) ng·L-1 and TNF-α (114.12±22.13) μg·L-1 in serum were obviously improved(P<0.01 or P<0.05)
and acitivity of SOD (77.58±5.20) U·mL-1
GSH-Px (11.22±4.88) U·mL-1
and myocardial SERCA (2.76±0.49) μmol·mg-1·h-1 were obviously reduced (P<0.01 or P<0.05). The contents of MDA
CK-MB
cTnI
IL-6 and TNF-α in serum in MIRI group were obviously reduced by medium and high dose Que pretreatment (P<0.01 or P<0.05)
and acitivity of SOD
GSH-Px and myocardial SERCA were improved by medium and high dose Que pretreatment (P<0.01 or P<0.05)
and the areas of myocardial damage and infraction were obviously reduced (P<0.01 or P<0.05). Conclusion: Que preconditioning can alleviate the oxidative stress injury
reduce the inflammatory response and calcium overload in cells
and can indicate obvious protective mechanism on myocardial ischemia/reperfusion injury of rats.
0
浏览量
3
下载量
0
CSCD
关联资源
相关文章
相关作者
相关机构
京公网安备11010802024621