Department of Histology-Embryology, Medicine Faculty of Erciyes University, Kayseri, 38280, Turkey.
Department of Cardiovascular Surgery, Medicine Faculty of Erciyes University, Kayseri, 38280, Turkey.
Chem Biol Interact. 2022 Sep 25;365:110090. doi: 10.1016/j.cbi.2022.110090. Epub 2022 Aug 5.
This study aims to investigate the protective effects of thymoquinone (THQ) in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Thirty-two rats were divided into four equal groups. Control, THQ; Intragastric(ig) by dissolved 20 mg/kg in 500 μl olive oil at 24-h intervals for 7 days, ISO; On the 6th and 7th days of the experiment, it was dissolved in 1 ml distilled water, 100 mg/kg, subcutaneously(sb), THQ + ISO; THQ was given 20 mg/kg at 24-h intervals for 7 days, 100 mg/kg was given on days 6 and 7 of the ISO experiment. At the end of the experiment, blood and heart tissues were taken and histological, Western blot and biochemical analyzes were performed. In the ISO group, cardiomyocyte damage and large necrotic areas were observed. While neuronal nitric oxide synthase (nNOS) decreased, inducible NOS (iNOS) and endothelial NOS (eNOS) expression increased. Receptor-interacting serine-threonine kinase (RIP/RIPK) RIP1 and RIP3 protein levels were increased. Lactate dehydrogenase (LDH), creatin-kinase (CK-MB) and cardiac troponin I (cTn-I) levels were increased. Atrial natriuretic peptide (ANP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were decreased. THQ caused the reduction of necrotic areas caused by ISO. NOS regulated enzyme levels. Increased ISO-induced decreased RIP1 and RIP3 expressions. THQ regulated the biochemical parameter levels. ISO triggers MI-induced necrosis through NOS enzymes by causing severe histological changes in heart tissue. THQ, on the other hand, reveals that it can be an important antinecrotic agent in the prevention of MI-induced damage by regulating both NOS enzyme levels and necrosis markers.
本研究旨在探讨百里醌（THQ）对异丙肾上腺素（ISO）诱导的大鼠心肌梗死（MI）的保护作用。将 32 只大鼠分为四组，每组 8 只。对照组、THQ 组；连续 7 天，24 小时间隔通过溶解在 500μl 橄榄油中的 20mg/kg 进行胃内给药；ISO 组；在实验的第 6 和第 7 天，将其溶解在 1ml 蒸馏水中，皮下给予 100mg/kg；THQ+ISO 组；THQ 连续 7 天，24 小时间隔给予 20mg/kg，ISO 实验第 6 和第 7 天给予 100mg/kg。实验结束时，采集血液和心脏组织，进行组织学、Western blot 和生化分析。在 ISO 组中，观察到心肌细胞损伤和大的坏死区。神经元型一氧化氮合酶（nNOS）减少，诱导型一氧化氮合酶（iNOS）和内皮型一氧化氮合酶（eNOS）表达增加。受体相互作用丝氨酸-苏氨酸激酶（RIP/RIPK）RIP1 和 RIP3 蛋白水平增加。乳酸脱氢酶（LDH）、肌酸激酶（CK-MB）和心肌肌钙蛋白 I（cTn-I）水平增加。心钠肽（ANP）和氨基末端脑钠肽前体（NT-proBNP）水平降低。THQ 导致 ISO 引起的坏死区减少。NOS 调节酶水平。增加的 ISO 诱导的 RIP1 和 RIP3 表达减少。THQ 调节生化参数水平。ISO 通过在心脏组织中引起严重的组织学变化，通过 NOS 酶触发 MI 诱导的坏死。另一方面，THQ 通过调节 NOS 酶水平和坏死标志物，表明它可以成为预防 MI 诱导损伤的重要抗坏死剂。
