School of Pharmacy, Yantai University, Yantai, Shandong 264005, PR China.
Eur J Pharmacol. 2010 Feb 10;627(1-3):235-41. doi: 10.1016/j.ejphar.2009.11.004. Epub 2009 Nov 10.
Asperosaponin VI is a saponin of the medicinal herb Dipsacus asper (Xuduan), and no pharmacological activity has been reported yet. In this study, we investigated the anti-myocardial ischemia effects of Asperosaponin VI (ASA VI) both in vivo and in vitro. An animal model of myocardial ischemia(MI) injury was induced by coronary occlusion, pretreatment with ASA VI (10 and 20mg/kg, i.v.) could protect the heart from ischemia injury by decreasing the levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), glutamic oxalacetic transaminase (GOT) and cardiac troponin T (cTnT) in serum, increasing the levels of catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels in heart, and decreasing that of malondialdehyde (MDA) level in acute MI rats. ASA VI also raised the activities of mitochondrial enzymes (succinate dehydrogenase (SDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH)) and those of adenosine triphosphate (ATP) content, but lowered Ca(2+) level. Electrocardiograph parameters and histopathological observations demonstrated the same protective effects. In vitro experiment, neonatal rat cardiomyocytes were incubated to test the direct cytoprotective effect of ASA VI against H(2)O(2) exposure. Pretreatment with ASA VI (30 and 60 microg/ml) prior to H(2)O(2) exposure increased cell viability and inhibited H(2)O(2)-induced reactive oxygen species increase. ASA VI (15, 30 and 60 microg/ml) also increased the activities of LDH in the cultured supernatant and SOD in cardiomyocytes, but decreased the cardiomyocytes MDA level. Our results suggested that ASA VI could provide significant cardioprotective effects against acute MI in rats. The mechanisms might be attributed to scavenging lipid peroxidation products and reactive oxygen species, increasing antioxidant defense enzymes and preventing mitochondrial damage.
川续断皂苷 VI 是一种来自川续断（续断）的皂苷，目前尚未报道其具有药理学活性。在本研究中，我们分别在体内和体外研究了川续断皂苷 VI（ASA VI）的抗心肌缺血作用。通过冠状动脉阻塞诱导心肌缺血（MI）损伤动物模型，ASA VI（10 和 20mg/kg，静脉注射）预处理可以通过降低血清肌酸激酶同工酶-MB（CK-MB）、乳酸脱氢酶（LDH）、谷草转氨酶（GOT）和心肌肌钙蛋白 T（cTnT）水平，增加心脏中过氧化氢酶、谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）水平，降低丙二醛（MDA）水平，从而保护心脏免受急性 MI 大鼠的缺血损伤。ASA VI 还提高了线粒体酶（琥珀酸脱氢酶（SDH）、异柠檬酸脱氢酶（ICDH）、苹果酸脱氢酶（MDH）和α-酮戊二酸脱氢酶（α-KGDH））和三磷酸腺苷（ATP）的活性，但降低了 Ca(2+)水平。心电图参数和组织病理学观察也显示了相同的保护作用。在体外实验中，孵育新生大鼠心肌细胞以测试 ASA VI 对 H(2)O(2)暴露的直接细胞保护作用。在 H(2)O(2)暴露之前用 ASA VI（30 和 60μg/ml）预处理可增加细胞活力并抑制 H(2)O(2)诱导的活性氧增加。ASA VI（15、30 和 60μg/ml）还增加了培养上清液中的 LDH 活性和心肌细胞中的 SOD，但降低了 MDA 水平。我们的研究结果表明，ASA VI 可显著减轻大鼠急性心肌缺血的影响。其机制可能归因于清除脂质过氧化产物和活性氧、增加抗氧化防御酶和防止线粒体损伤。
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