Sogut Ibrahim, Paltun Sıla Ozlem, Tuncdemir Matem, Ersoz Melike, Hurdag Canan
a Vocational School of Health Services, Istanbul Bilim University, Istanbul, Turkey.
b Department of Histology and Embryology, Faculty of Medicine, Istanbul Bilim University, Istanbul, Turkey.
Can J Physiol Pharmacol. 2018 Apr;96(4):404-411. doi: 10.1139/cjpp-2017-0487. Epub 2017 Sep 12.
The harmful use of alcohol is a worldwide problem involving all ages. This study aims to investigate chronic alcohol exposure related hepatotoxicity on the rat liver and possible hepatoprotective effects of boric acid. Rats were separated into 4 different groups: control, ethanol, ethanol+boric acid, and boric acid. We measured (i) malondialdehyde (MDA), total sialic acid (TSA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels, which are known to be the markers of alcohol damage; and also (ii) caspase-3, tumor necrosis factor-alpha (TNF-α), and the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) as the markers of apoptosis. In the ethanol group, MDA, TSA, and TNF-α levels increased whereas SOD and CAT levels decreased compared with the control group. Ethanol+boric acid group MDA, TSA, caspase-3, and TNF-α levels decreased whereas SOD and CAT levels increased compared with the ethanol group. Using histopathological evaluation of light microscope images, immunohistochemical caspase-3 and TNF-α activity in the ethanol+boric acid group were shown to be decreased compared with that in the ethanol group. Our results revealed that ethanol is capable of triggering oxidative stress and apoptosis in the rat liver. We propose that boric acid is an effective compound in protecting the rat liver against ethanol.
酒精的有害使用是一个涉及所有年龄段的全球性问题。本研究旨在调查慢性酒精暴露对大鼠肝脏的肝毒性以及硼酸可能的肝保护作用。将大鼠分为4个不同组：对照组、乙醇组、乙醇+硼酸组和硼酸组。我们测量了：（i）丙二醛（MDA）、总唾液酸（TSA）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）水平，这些都是已知的酒精损伤标志物；以及（ii）半胱天冬酶-3、肿瘤坏死因子-α（TNF-α）和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）作为细胞凋亡标志物。与对照组相比，乙醇组的MDA、TSA和TNF-α水平升高，而SOD和CAT水平降低。与乙醇组相比，乙醇+硼酸组的MDA、TSA、半胱天冬酶-3和TNF-α水平降低，而SOD和CAT水平升高。通过光学显微镜图像的组织病理学评估，显示乙醇+硼酸组的免疫组化半胱天冬酶-3和TNF-α活性与乙醇组相比降低。我们的结果表明，乙醇能够在大鼠肝脏中引发氧化应激和细胞凋亡。我们提出，硼酸是一种保护大鼠肝脏免受乙醇损伤的有效化合物。
