Abstract：
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.
摘要：
本研究评估了虾青素（ASX）通过线粒体生物发生途径作为虾青素的可能分子靶标对异丙肾上腺素（ISO）诱导的大鼠心肌梗死的心脏保护作用。对照组皮下注射生理盐水2天。第二组以85mg/kgbwt的剂量皮下注射ISO2天。第三，第四和第五组以10、20、30mg/kgbwt的剂量补充ASX，分别每天口服灌胃21天，然后连续2天皮下注射85mg/kgbwt的ISO剂量。大鼠服用异丙肾上腺素可提高肌酸激酶-MB（CK-MB）的活性，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），核因子-κB(NF-KB),虽然它降低了过氧化物酶体增殖物激活受体-γ共激活剂（PGC-1α），核因子-2相关因子2（Nfe212），线粒体转录因子A（mtTFA），线粒体DNA拷贝数和谷胱甘肽系统参数。然而,虾青素降低血清AST的活性，LDH,CK-MB,和肌钙蛋白I被ISO提升。此外,它增加了谷胱甘肽过氧化物酶和还原酶的活性，总谷胱甘肽和减少的GSH含量，和GSH/GSSG比率，mtDNA拷贝数,PGC-1α表达和Tfam表达改善了线粒体生物发生，同时降低了心脏组织中的GSSG和MDA含量以及NF-KB水平。本研究表明虾青素通过清除自由基，减轻心肌组织的氧化损伤和凋亡，减轻异丙肾上腺素引起的心肌梗死。
