| 兰惠琴,朱光旭,王志远,等.花旗松素调节 AMPK/mTOR信号通路对急性心肌梗死大鼠心肌损伤的影响[J].安徽医药,2024,28(12):2339-2344. |
| 花旗松素调节 AMPK/mTOR信号通路对急性心肌梗死大鼠心肌损伤的影响 |
| Impact of taxifolin on myocardial injury in rats with acute myocardial infarction by regulating AMPK/mTOR signal pathway |
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| DOI：10.3969/j.issn.1009-6469.2024.12.002 |
| 中文关键词: 黄杉属 花旗松素 心肌梗死 AMP活化的蛋白质激酶 /哺乳动物雷帕霉素靶蛋白信号通路 心肌损伤 炎症 |
| 英文关键词: Pseudotsuga Taxifolin Myocardial infarction AMP-activated protein kinase/mammalian target of rapamycin signal pathway Myocardial injury Inflammation |
| 基金项目:四川省卫生健康科研课题普及项目( 19PJ190) |
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| 中文摘要: |
| 目的探讨花旗松素( TAX)调节 AMP活化的蛋白质激酶( AMPK)/哺乳动物雷帕霉素靶蛋白( mTOR)信号通路对急性心肌梗死( AMI)大鼠心肌损伤的影响。方法 2022年 2—11月，从 90只雄性 SD大鼠中按随机数字表法选择 18只大鼠作为空白对照( CON)组，其他大鼠构建 AMI模型，将造模成功的 AMI大鼠按随机数字表法分为 AMI组、 TAX组( 50 mg/kg)、 DOR组(0.01 mol/L的 AMPK/mTOR抑制剂 DOR)、 TAX+DOR组( 50 mg/kg TAX+0.01 mol/L的 AMPK/mTOR抑制剂 DOR)，每组 18只大鼠。观察超声心动图评估舒张期室间隔厚度( IVSd)、舒张期左室内径( LVIDd)、收缩期左室内径( LVIDs)、左心室舒张期后壁厚度( LVPWd)、左室射血分数( EF)和缩短分数( FS)；酶联免疫吸附测定( ELISA)检测心肌损伤标志物肌酸激酶( CK)、肌酸激酶同工酶( CK-MB)、乳酸脱氢酶( LDH)以及炎症因子白细胞介素( IL)-1β水平；苏木精 -伊红( HE)染色检测心脏组织病理变化； 2，3，5-氯化三苯基四氮唑( TTC)染色检测心肌梗死面积； TUNEL染色检测细胞凋亡；蛋白质印迹法检测 AMPK/mTOR信号通路蛋白水平。结果 CON组心脏组织结构完整，细胞排列整齐有序，染色清晰； AMI组出现炎症细胞浸润现象； TAX组炎症细胞浸润现象减轻，而 DOR组炎症细胞浸润现象加重； TAX+DOR组与 AMI组结构相似。与 CON组相比， AMI组 LVIDd、 LVIDs、CK、CK-MB、LDH、IL-1β含量、细胞凋亡率、梗死面积［(17.82±2.31)%比(3.91±0.15)%］mTOR(1.26±0.14比 0.54±0.04)、核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体 3(NLRP3)(0.76±0.08比 0.26、±0.02)蛋白水平显著升高( P<0.05)IVSd、LVPWd、EF、FS以及 p-AMPK/AMPK(0.49±0.05比 0.93±0.07)蛋白水平显著下降( P<0.05)；与 AMI组相比， TAX组 LVIDdVIDs、CK、CK-MB、LDH、IL-1β含量、细胞凋亡率、梗死面积［( 12.36±1.76)%比( 17.82±2.31)%］、 mTOR(0.69±0.07比、L，1.26±0.14)、 NLRP3(0.39±0.04比 0.76±0.08)蛋白水平显著降低( P<0.05)，IVSd、LVPWd、EF、FS以及 p-AMPK/AMPK(0.85±0.09比 0.49±0.05)蛋白水平显著升高( P<0.05)，而 DOR组趋势相反( P<0.05)； TAX+DOR组减弱了 TAX对 AMI大鼠心肌损伤的改善作用。结论 TAX可通过调控 AMPK/mTOR信号通路减轻 AMI大鼠心肌损伤。 |
| 英文摘要: |
| Objective To investigate the impact of taxifolin (TAX) on myocardial injury in rats with acute myocardial infarction(AMI) by regulating AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signal pathway.Methods From February 2022 to November 2022, 18 male SD rats were selected from 90 ones as blank control group (CON group) according to randomnumber table method, and AMI models were constructed for other rats. AMI rats successfully modeled were assigned into AMI group,TAX group (50 mg/kg), DOR group (0.01 mol/L AMPK/mTOR inhibitor DOR), TAX+DOR group (50 mg/kg TAX+0.01 mol/L AMPK/mTOR inhibitor DOR) by random number table method, with 18 rats in each group. Diastolic inlet ventricular septal thickness (IVSd),diastolic left ventricular internal diameter (LVIDd), systolic left ventricular internal diameter (LVIDs), left ventricular posterior diastol-ic wall thickness (LVPWd), left ventricular ejection fraction (EF) and fractional shortening (FS) were evaluated by echocardiography.The levels of myocardial injury markers creatine kinase (CK), creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH) and in-flammatory factors interleukin1β (IL-1β) were detected by enzyme-linked immunosorbent assay (ELISA). Hematoxylin eosin (HE) stain-ing was used to detect the pathological changes of heart tissue, and myocardial infarction area was measured by 2, 3, 5, triphenyl-2H-tetrazolium chloride (TTC) staining. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining wasused to detect apoptosis, and Western blotting was used to detect the protein level of AMPK/mTOR signal pathway.Results In CON group, the heart tissue structure was complete, the cells were orderly arranged, and the staining was clear; inflammatory cell infiltrationoccurred in AMI group; inflammatory cell infiltration was reduced in TAX group, but increased in DOR group; the structure of TAX+DOR group was similar to that of AMI group. Compared with CON group, the levels of LVIDd, LVIDs, CK, CK-MB, LDH, IL-1β, apop-tosis rate, infarct size [(17.82±2.31)% vs. (3.91±0.15)%], levels of mTOR (1.26±0.14 vs. 0.54±0.04) and nucleotide-binding domain leu.cine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) (0.76±0.08 vs. 0.26±0.02) in AMI group were significantly increased (P<0.05), while the IVSd, LVPWd, EF, FS and the level of p-AMPK/AMPK protein (0.49±0.05 vs. 0.93±0.07) were significantly de-creased (P<0.05); compared with AMI group, levels of LVIDd, LVIDs, CK, CK-MB, LDH, IL-1β, apoptosis rate, infarct size [(12.36± 1.76)% vs. (17.82±2.31)%], levels of mTOR (0.69±0.07 vs. 1.26±0.14) and NLRP3 (0.39±0.04 vs. 0.76±0.08) in TAX group were signifi-cantly decreased (P<0.05), while the levels of IVSd, LVPWd, EF, FS and the level of p-AMPK/AMPK (0.85±0.09 vs. 0.49±0.05) were significantly increased (P<0.05); the trend in DOR group was opposite (P<0.05). TAX+DOR group attenuated the improvement effect of TAX on myocardial injury in AMI rats.Conclusion TAX can alleviate myocardial injury in AMI rats by regulating AMPK/mTOR sig-nal pathway. |
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