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香芹酚对紫外线B照射诱导的人外周血淋巴细胞氧化应激和细胞DNA损伤的保护作用。

Protective Effect of Carvacrol on Oxidative Stress and Cellular DNA Damage Induced by UVB Irradiation in Human Peripheral Lymphocytes.

作者信息

Aristatile Balakrishnan, Al-Numair Khalid S, Al-Assaf Abdullah H, Veeramani Chinnadurai, Pugalendi Kodukkur Viswanathan

机构信息

Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, P.O. Box 2460, Riyadh, 11451, Saudi Arabia.

Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh, 11433, Saudi Arabia.

出版信息

J Biochem Mol Toxicol. 2015 Nov;29(11):497-507. doi: 10.1002/jbt.20355. Epub 2010 May 21.

DOI:10.1002/jbt.20355
PMID:26768646
Abstract

Exposure to ultraviolet B (UVB; 280-320 nm) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of carvacrol on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular an-tioxidant status in human lymphocytes. A series of in vitro assays (hydroxyl radical, superoxide, nitric oxide, DPPH (2,2-Diphenyl-1-picryl hydrazyl), and ABTS (2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assays) demonstrate antioxidant property of carvacrol in our study. UVB exposure significantly increased thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHPs), % tail DNA and tail moment; decreased % cell viability and antioxidant status in UVB-irradiated lymphocytes. Treatment with carvacrol 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA, and tail moment and increased % cell viability as carvacrol concentration increased. UVB irradiated lymphocytes with carvacrol alone (at 10 μg/mL) gave no significant change in cell viability, TBARS, LHP, % tail DNA, and tail moment when compared with normal lymphocytes. On the basis of our results, we conclude that carvacrol, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced ROS.

摘要

暴露于紫外线B(UVB;280 - 320纳米)辐射会诱导生物系统中活性氧(ROS)的形成。在本研究中,我们参照人淋巴细胞中细胞抗氧化状态的变化,研究了香芹酚对UVB诱导的脂质过氧化和氧化性DNA损伤的保护作用。一系列体外试验(羟自由基、超氧阴离子、一氧化氮、DPPH(2,2 - 二苯基 - 1 - 苦基肼)和ABTS(2,2 - 联氮 - 双 - 3 - 乙基苯并噻唑啉 - 6 - 磺酸)自由基清除试验)证明了本研究中香芹酚的抗氧化特性。UVB照射显著增加了硫代巴比妥酸反应性物质(TBARS)、脂质氢过氧化物(LHP)、尾DNA百分比和尾矩;降低了UVB照射淋巴细胞的细胞活力百分比和抗氧化状态。在UVB照射前30分钟用香芹酚处理,随着香芹酚浓度增加,TBARS、LHP、尾DNA百分比和尾矩显著下降,细胞活力百分比增加。单独用香芹酚(10μg/mL)处理UVB照射的淋巴细胞,与正常淋巴细胞相比,细胞活力、TBARS、LHP、尾DNA百分比和尾矩没有显著变化。根据我们的结果,我们得出结论,作为一种膳食抗氧化剂,香芹酚通过调节UVB诱导的ROS发挥其保护作用。

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