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大蒜素预处理对急性心肌梗死后心肌病理改变的影响
引用本文:方燕,郑旭旭,李丽燕.大蒜素预处理对急性心肌梗死后心肌病理改变的影响[J].浙江中西医结合杂志,2020,30(12).
作者姓名:方燕  郑旭旭  李丽燕
作者单位:温州市中医院,,
基金项目:温州市科技局科研基金资助项目(2019Y0874)
摘    要:目的 研究大蒜素(Allicin)预处理对急性心肌梗死(AMI)模型大 鼠心肌组织病理改变的影响。方法 180只实验用SD大鼠随机分为假手术组(生理盐水预处理)、AMI组(生理盐水预处理)、维拉帕米2.5mg/(kg?d)预处理组和大蒜素5、10、20mg/(kg?d)预处理组,每组30只;采用结扎左冠状动脉前降支的方法复制AMI大鼠模型,造模手术前7d开始1次/d腹腔注射给药预处置。造模24h后,通过超声影像检测各组大鼠左心室舒张末期内径(LVIDd)和收缩末期左室内径(LVIDs)、射血分数(EF)和每搏输出量(SV),计算心脏指数,硝基蓝四氮唑(NBT)染色法计算心肌梗死体积百分比,苏木精-尹红(Hematoxylin-Eosin,HE)染色法行心肌组织病理学检查并进行损伤评分,原位末端转移酶标记(TUNEL)法观察细胞凋亡状况并计算凋亡指数(AI),透射电子显微镜观察心肌细胞超微结构变化。结果 与AMI组比较,经大蒜素10、20mg/(kg?d)或维拉帕米2.5mg/(kg?d)预处理7d能够明显抑制AMI大鼠LVIDd (6.93±0.46)mm、(6.84±0.42)mm、(6.87±0.45)mm比(7.42±0.50)mm,P均<0.05]、LVIDs(5.47±0.48)mm、(4.62±0.41)mm、(5.13±0.45)mm比(6.09±0.57)mm,P<0.05或P<0.01]升高和EF(39.76±8.14)%、(47.08±8.65)%、(43.91±8.40)%比(31.12±5.64) %,P<0.05或P<0.01]、SV(102.63±21.58)ul、(129.19±23.17)ul、(107.05±22.83)ul比(83.74±18.59)ul,P<0.05或P<0.01]降低,抑制心脏指数(2.63±0.28)×10-3、(2.44±0.25)×10-3、(2.64±0.27)×10-3比(2.91±0.30)×10-3,P<0.05或P<0.01]和心肌梗死体积(12.54±2.03)%、(5.18±1.02)%、(11.62±1.84)%比(22.75±3.16)%,P均<0.01]升高,抑制心肌组织缺血性病变及损伤评分(5.94±1.01)分、(3.76±0.85)分、(4.82±0.93)分比(7.24±1.18)分,P<0.05或P<0.01]升高,抑制心肌细胞凋亡及AI(23.50±3.79)%、(13.07±1.82)%、(21.63±2.47)%比(43.83±4.75)%,P均<0.01]升高,抑制心肌细胞超微结构病变。与维拉帕米2.5mg/(kg?d)预处理比较,大蒜素20mg/(kg?d)预处理对AMI大鼠LVIDs升高(4.62±0.41)mm比(5.13±0.45)mm,P<0.05]和SV降低(129.19±23.17)ul比(107.05±22.83)ul,P<0.05]、梗死体积升高(5.18±1.02)%比(11.62±1.84)%,P<0.01]、心肌组织损伤评分(3.76±0.85)分比(4.82±0.93)分,P<0.05]和AI升高(13.07±1.82)%比(21.63±2.47)%,P <0.01]的抑制作用较优。结论 较大剂量大蒜素预处理对AMI大鼠心肌组织病理改变、心肌细胞超微结构病理改变和心功能具有保护作用。

关 键 词:大蒜素  急性心肌梗死  病理  细胞凋亡  超微结构
收稿时间:2020/5/29 0:00:00
修稿时间:2020/10/22 0:00:00

Effect of Allicin Pretreatment on Myocardial Pathological Changes After Acute Myocardial Infarction.
Abstract:Objective To study the effect of Allicin pretreatment on myocardial pathological changes of the model rats with acute myocardial infarction(AMI). Methods 180 experimental Sprague-Dawley (SD) rats were randomly divided into sham operation group (Saline pretreatment), AMI group (Saline pretreatment), Verapami 2.5 mg/(kg?d) pretreatment group and Allicin 5, 10, 20 mg/(kg?d) pretreatment group, n=30. The AMI rat model was established by ligating the left anterior descending coronary artery, the drugs were given by Intraperitoneal injection for 7d before modeling. 24h after modeling surgery; the left ventricular end-diastolic diameter (LVIDd), left ventricular diameter at the end of systole (LVIDs), ejection fraction (EF), stroke volume (SV) were detected by ultrasound imaging system; the cardiac index and infarct volume percentage was detected by nitroblue tetrazolium (NBT); the histopathological changes were observed by Hematoxylin-Eosin (HE) staining and the injury score was calculated; the cardiomyocytes apoptosis was observed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining and the Apoptosis Index (AI) were calculated; the ultrastructure of cardiomyocytes was observed by transmission electron microscope(TEM). Results Compared with AMI group, pretreatment with Allicin 10, 20 mg/(kg?d) or Verapami 2.5 mg/(kg?d) for 7d could significantly inhibit the increase of LVIDd(6.93±0.46)mm, (6.84±0.42)mm, (6.87±0.45)mm vs (7.42±0.50)mm; P<0.05], LVIDs (5.47±0.48)mm, (4.62±0.41)mm, (5.13±0.45)mm vs (6.09±0.57)mm; P<0.05 or P<0.01] and the decrease of EF (39.76±8.14)%, (47.08±8.65)%, (43.91±8.40)% vs (31.12±5.64)%; P<0.05 or P<0.01], SV(102.63±21.58)ul, (129.19±23.17)ul, (107.05±22.83)ul vs (83.74±18.59)ul; P<0.05 or P<0.01]; inhibit the increase of cardiac index (2.63±0.28)×10-3, (2.44±0.25)×10-3, (2.64±0.27)×10-3 vs (2.91±0.30)×10-3; P<0.05 or P<0.01] and myocardial infarction volume percentage (12.54±2.03)%, (5.18±1.02)%, (11.62±1.84)% vs (22.75±3.16)%, P<0.01], inhibite the myocardial ischemic lesions and injury score (5.94±1.01) score, (3.76±0.85) score, (4.82±0.93) score vs (7.24±1.18) score; P<0.05 or P<0.01], inhibit cardiomyocyte apoptosis and the increase of AI(23.50±3.79)%, (13.07±1.82)%, (21.63±2.47)% vs (43.83±4.75)%; P<0.01], inhibit the ultrastructural lesions of myocardial cell. Compared with Verapami 2.5 mg/(kg?d) pretreatment group, pretreatment with Allicin 20 mg/(kg?d) had better inhibitory effects on LVIDs(4.62±0.41)mm vs (5.13±0.45)mm; P<0.05] and SV (129.19±23.17) ul vs (107.05±22.83)ul; P<0.05], myocardial infarction volume percentage (5.18±1.02)% vs (11.62±1.84)%; P<0.01], myocardial tissue injury score (3.76±0.85) score vs (4.82±0.93) score; P<0.05] and AI (13.07±1.82)% vs (21.63±2.47)%; P<0.01] in AMI rats. Conclusion Pretreatment with large dose of Allicin has protective effects on myocardial tissue pathological changes and myocardial cell ultrastructural pathological changes in AMI rats.
Keywords:Allicin  Acute Myocardial Infarction(AMI)  Pathology  Apoptosis  Ultrastructure
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