| 黄潇潇,黄连军.丁香酚对异丙肾上腺素诱导的大鼠心肌梗死的保护作用[J].浙江中西医结合杂志,2023,33(5): |
| 丁香酚对异丙肾上腺素诱导的大鼠心肌梗死的保护作用 |
| Protective effect of eugenol on myocardial infarction induced by isoproterenol in rats |
| 投稿时间：2022-08-02 修订日期：2023-03-17 |
| DOI： |
| 中文关键词: 丁香酚 异丙肾上腺素 急性心肌梗死 iNOS 氧化应激 |
| 英文关键词:Eugenol Isoproterenol Acute myocardial infarction iNOS Oxidative stress |
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| 中文摘要: |
| 目的 探讨丁香酚对异丙肾上腺素（ISO）诱导的急性心肌梗死（AMI）大鼠的保护作用及其机制。方法 40只Wistar大鼠按随机数字表法分成对照组、模型组和丁香酚低、中、高剂量组，每组8只。连续2 d注射ISO建立大鼠AMI模型，不同剂量（1、10和100 mg/kg）丁香酚处理后，酶联免疫吸附试验（ELISA）测定肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）、心肌肌钙蛋白T（cTnT）、肿瘤坏死因子-α（TNF-α）、白介素6（IL-6）丙二醛（MDA）和超氧化物歧化酶（SOD）水平，2,3,5-氯化三苯基四氮唑（TTC）染色计算大鼠心脏梗死面积，流式细胞仪检测心肌细胞凋亡水平，Western blot分析iNOS 和Cleaved Caspase 3蛋白表达。结果 与对照组比较，模型组大鼠CK [（0.93±0.06）U/mL比（0.22±0.04）U/mL，P<0.01]、CK-MB [（210.06±11.96）IU/L比（81.61±3.36）IU/L，P<0.01]、LDH [（5870.87±681.37）U/L比（1699.72±250.51）U/L，P<0.01]、cTnT [（0.63±0.09）U/mL比（0.07±0.03）U/mL，P<0.01]、iNOS蛋白表达[（1.15±0.02）比（0.42±0.03），P<0.01]、TNF-α[（318.61±28.27）pg/mg比（86.68±6.24）pg/mg，P<0.01]、IL-6[（5.33±0.98）pg/mg比（1.76±0.30）pg/mg，P<0.01]、MDA[（7.38±0.54）nmol/mg比（2.14±0.43）nmol/mg，P<0.01]和Cleaved Caspase 3蛋白表达[（1.13±0.07）比（0.64±0.03），P<0.01]升高，SOD含量[（82.46±14.77）U/mg比（188.19±19.34）U/mg，P<0.01]下降，梗死面积[（45.95±3.35）%比（0.00±0.00）%，P<0.01]和心肌细胞凋亡[（41.74±5.02）%比（9.05±0.71）%，P<0.01]增加。丁香酚给药后，AMI大鼠CK [中高剂量（0.64±0.02）U/mL、（0.45±0.06）U/mL比（0.93±0.06）U/mL，P<0.01]、CK-MB[（181.75±9.09）IU/L、（144.11±8.28）IU/L、（121.10±7.88）IU/L比（210.06±11.96）IU/L，P<0.01]、LDH [（4841.55±265.25）U/L、（4076.81±465.13）U/L、（3438.28±361.19）U/L比（5870.87±681.37）U/L，P<0.05]、cTnT [中高剂量（0.40±0.03）U/mL、（0.26±0.04）U/mL比（0.63±0.09）U/mL，P<0.01]、iNOS[（0.88±0.02）、（0.62±0.03）、（0.41±0.07）比（1.15±0.02），P<0.05]、TNF-α[中高剂量（252.79±26.56）pg/mg、（222.29±18.4）pg/mg比（318.61±28.27）pg/mg，P<0.01]、IL-6[中高剂量（3.33±0.47）pg/mg、（2.91±0.52）pg/mg比（5.33±0.98）pg/mg，P<0.01]、MDA[中高剂量（4.47±0.45）nmol/mg、（3.97±0.49）nmol/mgg比（7.38±0.54）nmol/mg，P<0.01]和Cleaved Caspase 3蛋白表达[（0.95±0.04）、（0.73±0.07）、（0.65±0.09）比（1.13±0.07），P<0.05]显著降低，SOD含量[（108.3±10.21）U/mg、（138.62±13.76）U/mg、（159.67±15.32）U/mg比（82.46±14.77）U/mg，P<0.05]显著升高。同时，丁香酚可有效减少AMI大鼠的梗死面积[（35.57±2.62）%、（26.23±4.02）%、（15.49±3.13）%比（45.95±3.35）%，P<0.05]，抑制心肌细胞凋亡[中高剂量（23.34±2.73）%、（18.44±2.03）%比（41.74±5.02）%，P<0.01]。结论 丁香酚能够改善ISO诱导的大鼠AMI，其机制可能与调节iNOS、炎症和氧化应激有关。 |
| 英文摘要: |
| Aim To investigate the protective effect and mechanism of eugenol on acute myocardial infarction (AMI) caused by isoproterenol (ISO) in rats. Methods Forty Wistar rats were randomly divided into control group, model group, eugenol low, middle and high dose groups, 8 rats in each group. The rat AMI model was established by continuous 2 d injection of ISO, and creatine kinase (CK), CK-MB Isoenzyme (CK-MB), lactate dehydrogenase (LDH), cardiac troponin T (cTnT), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by enzyme linked immunosorbent assay (ELISA) method. 2,3,5-Triphenyltetrazolium chloride (TTC) staining was used to calculate rat heart infarct area, and flow cytometry was used to detect cardiomyocyte apoptosis. Besides, the protein expression levels of iNOS and Cleaved Caspase 3 were determined using Western blot. Results Compared with the control group, in the model group, CK (0.93±0.06 U/mL vs. 0.22±0.04 U/mL, P<0.01), CK-MB (210.06±11.96 IU/L vs. 81.61±3.36 IU/L, P<0.01), LDH (5870.87±681.37 U/L vs. 1699.72±250.51 U/L, P<0.01), cTnT (0.63±0.09 U/mL vs. 0.07±0.03 U/mL, P<0.01), iNOS protein expression (1.15±0.02 vs. 0.42±0.03, P<0.01), TNF-α (318.61±28.27 pg/mg vs. 86.68±6.24 pg/mg, P<0.01), IL-6 (5.33±0.98 pg/mg vs. 1.76±0.30 pg/mg, P<0.01), MDA (7.38±0.54 nmol/mg vs. 2.14±0.43 nmol/mg, P<0.01), and Cleaved Caspase 3 protein expression (1.13±0.07 vs. 0.64±0.03, P<0.01] were increased, while SOD content (82.46±14.77 U/mg vs. 188.19±19.34 U/mg, P<0.01] decreased, the infarct area (45.95±3.35 % vs. 0.00±0.00 %, P<0.01], and myocardial cell apoptosis (41.74±5.02 % vs. 9.05±0.71 %, P<0.01] were increased. After administration of eugenol, the levels of CK (0.64±0.02 U/mL, 0.45±0.06 U/mL vs. 0.93±0.06 U/mL, P<0.01), CK-MB (181.75±9.09 IU/L, 144.11±8.28 IU/L, 121.10±7.88 IU/L vs. 210.06±11.96 IU/L, P<0.01), LDH (4841.55±265.25 U/L, 4076.81±465.13 U/L, 3438.28±361.19 U/L vs. 5870.87±681.37 U/L, P<0.05), cTnT (0.40±0.03 U/mL, 0.26±0.04 U/mL vs. 0.63±0.09 U/mL, P<0.01), iNOS (0.88±0.02, 0.62±0.03, 0.41±0.07 vs. 1.15±0.02, P<0.05), TNF-α (252.79±26.56 pg/mg, 222.29±18.4 pg/mg vs. 318.61±28.27 pg/mg, P<0.01), IL-6 (3.33±0.47 pg/mg, 2.91±0.52 pg/mg vs. 5.33±0.98 pg/mg, P<0.01), MDA (4.47±0.45 nmol/mg, 3.97±0.49 nmol/mg vs. 7.38±0.54 nmol/mg, P<0.01), and cleaved caspase 3 protein expression (0.95±0.04, 0.73±0.07, 0.65±0.09 vs. 1.13±0.07, P<0.05) in AMI rats were significantly reduced, while SOD content (108.3±10.21 U/mg, 138.62±13.76 U/mg, 159.67±15.32 U/mg vs. 82.46±14.77 U/mg, P<0.05) was significantly increased. At the same time, eugenol could effectively reduce the infarct area of AMI rats (35.57±2.62%, 26.23±4.02%, 15.49±3.13% vs. 45.95±3.35%, P<0.05) and inhibit myocardial cell apoptosis (23.34±2.73%, 18.44±2.03% vs. 41.74±5.02%, P<0.01). Conclusion Eugenol can improve the AMI induced by ISO in rats, and its mechanism may be related to the regulation of iNOS, inflammation and oxidative stress. |
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