Mohammadi Mohammad Taghi, Amini Reza, Jahanbakhsh Zahra, Shekarforoush Shahnaz
Dept. of Physiology and Biophysics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Dept. of Physiology, Islamic Azad University, Arsanjan Branch, Fars, Iran.
Iran Biomed J. 2013;17(3):152-7. doi: 10.6091/ibj.1189.2013.
It is well known that the development of brain oxidative stress is one of the most serious complications of arterial hypertension that evokes brain tissue damage. The aim of this study was to examine the effects of atorvastatin treatment (20 mg/kg/day), as an antioxidant, to prevent the brain tissue oxidative stress in the hypertensive (HTN) rats.
Experiments were performed in four groups of rats (n = 5 each group): sham, sham-treated, HTN and HTN treated. Rats were made HTN by aortic constriction above the renal arteries. After 30 days, rats were slaughtered under deep anesthesia to remove brain hemispheres. After tissue homogenization, enzyme activities of superoxide dismutase (SOD) and catalase (CAT), as well as glutathione (GSH) content and malondialdehyde (MDA) level were determined by biochemical methods.
In HTN rats, arterial blood pressure was increased about 40% and brain enzyme activities of SOD and CAT were significantly decreased compared with sham group. Induction of hypertension significantly decreased GSH content and increased MDA level of brain tissue. Treatment with atorvastatin enhanced the activity of SOD and prevented from GSH decrement during hypertension.
Based on the findings of this study, treatment with atorvastatin might have saved the brain tissue of HTN rats from hypertension-induced oxidative stress.
众所周知,脑氧化应激的发展是动脉高血压最严重的并发症之一,可引发脑组织损伤。本研究的目的是研究阿托伐他汀治疗(20毫克/千克/天)作为一种抗氧化剂,对预防高血压(HTN)大鼠脑组织氧化应激的作用。
实验在四组大鼠中进行(每组n = 5):假手术组、假手术治疗组、高血压组和高血压治疗组。通过肾动脉上方的主动脉缩窄使大鼠患高血压。30天后,在深度麻醉下宰杀大鼠以取出脑半球。组织匀浆后,采用生化方法测定超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的酶活性,以及谷胱甘肽(GSH)含量和丙二醛(MDA)水平。
与假手术组相比,高血压大鼠的动脉血压升高约40%,脑SOD和CAT酶活性显著降低。高血压的诱导显著降低了脑组织的GSH含量并增加了MDA水平。阿托伐他汀治疗增强了SOD的活性,并在高血压期间防止了GSH的减少。
基于本研究的结果,阿托伐他汀治疗可能使高血压大鼠的脑组织免受高血压诱导的氧化应激。