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4-香豆酸对兔角膜衍生细胞(SIRC)中紫外线B诱导的氧化性DNA损伤的保护作用。

Protection against ultraviolet B-induced oxidative DNA damage in rabbit corneal-derived cells (SIRC) by 4-coumaric acid.

作者信息

Lodovici Maura, Raimondi Laura, Guglielmi Francesco, Gemignani Samanta, Dolara Piero

机构信息

Department of Pharmacology, University of Florence, Florence, Italy.

出版信息

Toxicology. 2003 Mar 3;184(2-3):141-7. doi: 10.1016/s0300-483x(02)00572-3.

Abstract

The exposure of cells to ultraviolet B radiation (UV-B) can induce the production of reactive oxygen species (ROS) which damage cellular components. Free radical scavengers and antioxidants can interfere with the production of ROS. We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, a marker of oxidative DNA damage in rabbit corneal-derived cells (SIRC) exposed to UV-B in the presence of 4-coumaric acid, a natural polyphenol. The levels of 8-OHdG were increased significantly (P<0.01) following irradiation (from 12+/-1.2x10(-6) to 29+/-6.2x10(-6) dG, means+/-SE). When 10 microM 4-coumaric acid was added to the medium, 8-OHdG levels were similar to those of unexposed cells (16.8+/-0.8x10(-6) dG). UV-B irradiation decreased superoxide dismutase (SOD) activity in SIRC cells from 0.29+/-0.6 to 0.15+/-0.04 mU/mg (means+/-SE). The presence of 10 microM 4-coumaric acid prevented the decrease in SOD activity (0.20+/-0.05 mU/mg, P<0.05). On the contrary, SIRC cells exposed to UV-B had higher levels of xanthine oxidase (XO) activity compared with control ones (0.40+/-0.07 and 0.24+/-0.08 mU/mg, means+/-SE, respectively). In the presence of 10 microM 4-coumaric acid, the increase in XO activity was prevented (0.16+/-0.03 mU/mg; mean+/-SE). In conclusion, UV-B-induced oxidative DNA damage in SIRC cells is inhibited by 4-coumaric acid, which, probably through its free radical scavenging activity, stabilizes SOD activity and blocks the increase of XO activity following UV-B irradiation. Thus, the topical use of 4-coumaric acid may prevent free radical damage in the cornea.

摘要

细胞暴露于紫外线B辐射(UV-B)可诱导活性氧(ROS)的产生,而ROS会损害细胞成分。自由基清除剂和抗氧化剂可干扰ROS的产生。我们测定了在天然多酚4-香豆酸存在下,暴露于UV-B的兔角膜衍生细胞(SIRC)中氧化DNA损伤的标志物8-羟基-2'-脱氧鸟苷(8-OHdG)的水平。照射后,8-OHdG水平显著升高(P<0.01)(从12±1.2×10(-6) 至29±6.2×10(-6) dG,平均值±标准误)。当向培养基中添加10μM 4-香豆酸时,8-OHdG水平与未暴露细胞相似(16.8±0.8×10(-6) dG)。UV-B照射使SIRC细胞中的超氧化物歧化酶(SOD)活性从0.29±0.6降至0.15±0.04 mU/mg(平均值±标准误)。10μM 4-香豆酸的存在可防止SOD活性降低(0.20±0.05 mU/mg,P<0.05)。相反,与对照细胞相比,暴露于UV-B的SIRC细胞具有更高水平的黄嘌呤氧化酶(XO)活性(分别为0.40±0.07和0.24±0.08 mU/mg,平均值±标准误)。在10μM 4-香豆酸存在下,XO活性的增加受到抑制(0.16±0.03 mU/mg;平均值±标准误)。总之,4-香豆酸可抑制UV-B诱导的SIRC细胞中的氧化DNA损伤,其可能通过自由基清除活性稳定SOD活性并阻止UV-B照射后XO活性的增加。因此,局部使用4-香豆酸可能预防角膜中的自由基损伤。

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