Doaa Salah Eddin Mahmoud, Maher A. Kamel, Ibrahim El-Tantawy El-Sayed, Reem Binsuwaidan, Elshaymaa I. Elmongy, Mohand Kareem Razzaq, Mabrouk Attia Abd Eldaim, El S. Abdel Megeed Ahmed, Sara A. Shaker
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Isoproterenol administration in rats elevated the activities of Creatine kinase-MB (CK-MB), aspartate transaminase (AST), lactate dehydrogenase (LDH), and other serum cardiac biomarkers Troponin-I activities, oxidative stress biomarkers, malondialdehyde(MDA), Nuclear factor-kappa B (NF-KB), while it decreased Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α), Nuclear factor erythroid-2-related factor 2 (Nfe212), mitochondrial transcriptional factor A (mt TFA), mitochondrial DNA copy number and glutathione system parameters. However, Astaxanthin decreased the activities of serum AST, LDH, CK-MB, and Troponin I that elevated by ISO. In addition, it increased glutathione peroxidase and reductase activities, total glutathione and reduced GSH content, and GSH/GSSG ratio, mtDNA copy number, PGC-1α expression and Tfam expression that improved mitochondrial biogenesis while it decreased GSSG and MDA contents and NF-KB level in the cardiac tissues. 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引用次数: 0
摘要
本研究评估了虾青素(ASX)通过线粒体生物生成途径(虾青素可能的分子靶点)对异丙肾上腺素(ISO)诱导的大鼠心肌梗死的心脏保护作用。对照组皮下注射正常生理盐水 2 天。第二组皮下注射 ISO,剂量为 85 毫克/千克体重,连续 2 天。第三组、第四组和第五组每天分别口服 10、20 和 30 毫克/千克体重的 ASX,连续 21 天,然后皮下注射剂量为 85 毫克/千克体重的 ISO,连续 2 天。大鼠服用异丙肾上腺素后,肌酸激酶-MB(CK-MB)、天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)和其他血清心脏生物标志物肌钙蛋白-I 活性、氧化应激生物标志物、丙二醛(MDA)活性升高、核因子卡巴 B (NF-KB),同时降低过氧化物酶体增殖激活受体-γ 辅激活因子 (PGC-1α)、核因子红细胞-2 相关因子 2 (Nfe212)、线粒体转录因子 A (mt TFA)、线粒体 DNA 拷贝数和谷胱甘肽系统参数。然而,虾青素降低了因 ISO 而升高的血清 AST、LDH、CK-MB 和肌钙蛋白 I 的活性。此外,虾青素还能提高谷胱甘肽过氧化物酶和还原酶活性、总谷胱甘肽和还原型GSH含量、GSH/GSSG比率、mtDNA拷贝数、PGC-1α表达和Tfam表达,从而改善线粒体生物生成,同时降低心脏组织中GSSG和MDA含量以及NF-KB水平。这项研究表明,虾青素通过清除自由基、减少氧化损伤和心肌组织凋亡,缓解了异丙肾上腺素诱发的心肌梗死。
Astaxanthin ameliorated isoproterenol induced myocardial infarction via improving the mitochondrial function and antioxidant activity in rats
The present study evaluated the cardioprotective effect of astaxanthin (ASX) against isoproterenol (ISO) induced myocardial infarction in rats via the pathway of mitochondrial biogenesis as the possible molecular target of astaxanthin. The control group was injected with normal physiological saline subcutaneously for 2 days. The second group was injected with ISO at a dose of 85 mg/kg bwt subcutaneously for 2 days. The third, fourth and fifth groups were supplemented with ASX at doses of 10, 20, 30 mg/kg bwt, respectively daily by oral gavage for 21 days then injected with ISO dose of 85 mg/kg bwt subcutaneously for 2 successive days. Isoproterenol administration in rats elevated the activities of Creatine kinase-MB (CK-MB), aspartate transaminase (AST), lactate dehydrogenase (LDH), and other serum cardiac biomarkers Troponin-I activities, oxidative stress biomarkers, malondialdehyde(MDA), Nuclear factor-kappa B (NF-KB), while it decreased Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α), Nuclear factor erythroid-2-related factor 2 (Nfe212), mitochondrial transcriptional factor A (mt TFA), mitochondrial DNA copy number and glutathione system parameters. However, Astaxanthin decreased the activities of serum AST, LDH, CK-MB, and Troponin I that elevated by ISO. In addition, it increased glutathione peroxidase and reductase activities, total glutathione and reduced GSH content, and GSH/GSSG ratio, mtDNA copy number, PGC-1α expression and Tfam expression that improved mitochondrial biogenesis while it decreased GSSG and MDA contents and NF-KB level in the cardiac tissues. This study indicated that astaxanthin relieved isoproterenol induced myocardial infarction via scavenging free radicals and reducing oxidative damage and apoptosis in cardiac tissue.
期刊介绍:
The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.