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阿魏酸通过调节瑞士白化小鼠的炎症和凋亡信号传导来抑制紫外线B辐射诱导的光致癌作用。

Ferulic acid inhibits UVB-radiation induced photocarcinogenesis through modulating inflammatory and apoptotic signaling in Swiss albino mice.

作者信息

Ambothi Kanagalakshmi, Prasad N Rajendra, Balupillai Agilan

机构信息

Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608 002, India.

Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608 002, India.

出版信息

Food Chem Toxicol. 2015 Aug;82:72-8. doi: 10.1016/j.fct.2015.04.031. Epub 2015 May 14.

DOI:10.1016/j.fct.2015.04.031
PMID:25983265
Abstract

The aim of this study was to evaluate the photochemopreventive effects of ferulic acid (FA) against chronic ultraviolet-B (290-320 nm) induced oxidative stress, inflammation and angiogenesis in the skin of Swiss albino mice. Chronic UVB exposure (180 mJ/cm(2) for 30 weeks; thrice in a week) induced tumor formation in the mice skin that showed increased expression of carcinogenic and inflammatory markers when compared with the control animals. The intraperitoneal (FAIP) and topical (FAT) administration of FA significantly reduced the incidence of UVB-induced tumor volume and tumor weight in the mice skin. Histopathological studies revealed that both FAIP and FAT administration prevented the UVB-induced hyperplasia, squamous cell carcinoma (SCC) and dysplastic feature in the mice skin. Further, it has been observed that FA treatment reverted chronic UVB-induced oxidative damage (thiobarbituric acid reactive substances, superoxide dismutase, catalase, glutathione peroxidase) accompanied with modulation of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), TNF-α and IL-6 in the mice skin tumor. FA treatment also modulates mutated p53, Bcl-2 and Bax expressions in the UVB-induced mice skin tumor. Thus, the results of the present study indicate ferulic acid has potential against UVB-induced carcinogenesis in the Swiss albino mice.

摘要

本研究的目的是评估阿魏酸(FA)对慢性紫外线B(290 - 320纳米)诱导的瑞士白化小鼠皮肤氧化应激、炎症和血管生成的光化学预防作用。慢性紫外线B照射(每周三次,每次180毫焦/平方厘米,持续30周)诱导小鼠皮肤肿瘤形成,与对照动物相比,致癌和炎症标志物的表达增加。腹腔注射(FAIP)和局部应用(FAT)阿魏酸显著降低了紫外线B诱导的小鼠皮肤肿瘤体积和肿瘤重量的发生率。组织病理学研究表明,FAIP和FAT给药均能预防紫外线B诱导的小鼠皮肤增生、鳞状细胞癌(SCC)和发育异常特征。此外,观察到FA治疗可逆转慢性紫外线B诱导的氧化损伤(硫代巴比妥酸反应性物质、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶),同时调节小鼠皮肤肿瘤中血管内皮生长因子(VEGF)、诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)。FA治疗还可调节紫外线B诱导的小鼠皮肤肿瘤中突变型p53、Bcl-2和Bax的表达。因此,本研究结果表明阿魏酸对瑞士白化小鼠紫外线B诱导的致癌作用具有潜在的防治作用。

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