Devi Sampath Pandima, Vijayaraghavan Kannan
Centre for Advanced Studies in Botany, University of Madras, Guindy Campus, Chennai, India.
J Biochem Mol Toxicol. 2007;21(6):336-9. doi: 10.1002/jbt.20199.
Increased oxidative stress and antioxidant deficit have been suggested to play a major role in isoproterenol-induced myocardial infarction. The present study was designed to evaluate the effect of alpha-mangostin on the antioxidant defense system and lipid peroxidation against isoproterenol-induced myocardial infarction in rats. Induction of rats with ISO (150 mg/kg body weight, ip) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT) and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GST, and GSH). Pre-treatment with alpha-mangostin (200 mg/kg of body weight per day) orally for 6 days prior to the ISO administration and 2 days along with ISO administration significantly attenuated these changes when compared to the individual treatment groups. These findings indicate the protective effect of alpha-mangostin on lipid peroxidation and antioxidant tissue defense system during ISO-induced myocardial infarction in rats.
氧化应激增加和抗氧化剂缺乏被认为在异丙肾上腺素诱导的心肌梗死中起主要作用。本研究旨在评估α-山竹黄酮对异丙肾上腺素诱导的大鼠心肌梗死的抗氧化防御系统和脂质过氧化的影响。用ISO（150mg/kg体重，腹腔注射）诱导大鼠2天导致脂质过氧化、血清标志物酶（LDH、CPK、GOT和GPT）显著升高，内源性抗氧化剂（SOD、CAT、GPx、GST和GSH）活性显著降低。在给予ISO前6天和给予ISO的同时口服α-山竹黄酮（每天200mg/kg体重）2天进行预处理，与单独治疗组相比，显著减轻了这些变化。这些发现表明α-山竹黄酮对异丙肾上腺素诱导的大鼠心肌梗死期间的脂质过氧化和抗氧化组织防御系统具有保护作用。
