Karthikeyan K, Sarala Bai B R, Gauthaman K, Niranjali Devaraj S
Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, India.
J Pharm Pharmacol. 2005 Jan;57(1):67-73. doi: 10.1211/0022357055065.
This study was designed to investigate the effect of chronic administration of propyl gallate on myocardial oxidative stress-induced injury. Propyl gallate was administered orally to Wistar albino rats (150-200 g) in three different doses, by gastric gavage (250 mg kg(-1) (P1), 500 mg kg(-1) (P2) and 750 mg kg(-1) (P3)), 6 days a week for 5 weeks. At the end of this period, all the rats, except the normal untreated rats that served as the control group, were administered isoproterenol (ISO), 85 mg kg(-1) subcutaneously, for 2 consecutive days to induce myocardial injury. After 48 h, rats (n = 6 per group) were anaesthetized with anaesthetic ether, sacrificed and the hearts were harvested for the estimation of thiobarbituric acid reactive substances (TBARS), endogenous antioxidants (reduced glutathione (GSH), superoxide dismutase (SOD) and catalase) and for the assessment of histological changes. In the P2 BL group (BL = baseline), there was a significant (P < 0.001) rise in baseline TBARS and SOD when compared with the saline-treated group, while no such changes were observed in the other baseline-treated groups. However, there was a significant (P < 0.001) increase in TBARS and endogenous anti-oxidants (GSH, SOD and catalase) in the P2 ISO and P3 ISO groups, when the hearts were subjected to in-vivo myocardial oxidative stress-induced injury. We observed no such changes in the P1 ISO group. This study showed that propyl gallate modulates the levels of endogenous antioxidants present at the myocardial site. Whether these modifications are a result of direct interference at this site or a remote effect is not immediately clear. In conclusion, from the results it could be stated that chronic administration of 500 mg kg(-1) of propyl gallate offers significant protection against myocardial oxidative stress-induced injury.
本研究旨在探讨长期给予没食子酸丙酯对心肌氧化应激诱导损伤的影响。通过胃管以三种不同剂量（250 mg kg⁻¹（P1）、500 mg kg⁻¹（P2）和750 mg kg⁻¹（P3））对体重150 - 200 g的Wistar白化大鼠口服没食子酸丙酯，每周6天，持续5周。在此期间结束时，除作为对照组的未处理正常大鼠外，所有大鼠皮下注射异丙肾上腺素（ISO）85 mg kg⁻¹，连续2天以诱导心肌损伤。48小时后，用麻醉乙醚麻醉大鼠（每组n = 6），处死后取出心脏，用于评估硫代巴比妥酸反应物质（TBARS）、内源性抗氧化剂（还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）和过氧化氢酶），并评估组织学变化。在P2 BL组（BL = 基线）中，与生理盐水处理组相比，基线TBARS和SOD有显著（P < 0.001）升高，而在其他基线处理组中未观察到此类变化。然而，当心脏受到体内心肌氧化应激诱导损伤时，P2 ISO组和P3 ISO组的TBARS和内源性抗氧化剂（GSH、SOD和过氧化氢酶）有显著（P < 0.001）增加。我们在P1 ISO组中未观察到此类变化。本研究表明，没食子酸丙酯可调节心肌部位存在的内源性抗氧化剂水平。这些修饰是由于在该部位的直接干扰还是远程效应所致，目前尚不清楚。总之，从结果可以看出，长期给予500 mg kg⁻¹的没食子酸丙酯可对心肌氧化应激诱导的损伤提供显著保护。
