Wedelolactone mitigates UVB induced oxidative stress, inflammation and early tumor promotion events in murine skin: plausible role of NFkB pathway
Wedelolactone mitigates UVB induced oxidative stress, inflammation and early tumor promotion events in murine skin: plausible role of NFkB pathway
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DOI：
10.1016/j.ejphar.2016.05.008
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发表时间：
2016-09-05
影响因子：
5
通讯作者：
Sultana, Sarwat
中科院分区：
文献类型：
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作者：
Ali, Farrah;Khan, Bilal Azhar;Sultana, Sarwat
UVB（紫外线B）辐射是各种皮肤病理学的主要病因之一。皮炎、光化性毛囊炎、日光性荨麻疹、牛皮癣和癌症等。 UVB 通过引发炎症和肿瘤促进事件而在组织中引起毒性表现。我们设计这项研究是为了评估一种特定的 IKK 抑制剂蟛蜞菊内酯 (WDL) 的抗炎和抗肿瘤促进作用。结果表明，WDL 治疗后抗氧化酶显着恢复。我们还发现，WDL 可有效减轻炎症标志物，包括 MPO（髓过氧化物酶）、肥大细胞运输、朗格汉斯细胞抑制和 UVB 暴露导致的 COX 2 表达上调。 ODC（鸟氨酸脱羧酶）、胸苷测定、波形蛋白和 VEGF（血管内皮生长因子）表达结果表明，WDL 在减弱 UVB 暴露引起的早期肿瘤促进事件方面具有良好的干预作用。这项研究能够为蜈蚣内酯对抗小鼠皮肤炎症和肿瘤促进事件的治疗能力提供重要线索，描绘了 NFkB 通路的合理作用。 (C) 2016 Elsevier B.V. 保留所有权利。
UVB (Ultra-violet B) radiation is one of the major etiological factors in various dermal pathology viz. dermatitis, actinic folliculitis, solar urticaria, psoriasis and cancer among many others. UVB causes toxic manifestation in tissues by inciting inflammatory and tumor promoting events. We have designed this study to assess the anti-inflammatory and anti-tumor promotion effect of Wedelolactone (WDL) a specific IKK inhibitor. Results indicate significant restoration of anti-oxidative enzymes due to WDL treatments. We also found that WDL was effective in mitigating inflammatory markers consisting of MPO (myeloperoxidase), Mast cells trafficking, Langerhans cells suppression and COX 2 expression up regulation due to UVB exposure. We also deduce that WDL presented a promising intervention in attenuating early tumor promotion events caused by UVB exposure as indicated by the results of ODC (Ornithine Decarboxylase), Thymidine assay, Vimentin and VEGF (Vascular-endothelial growth factor) expression. This study was able to provide substantial cues for the therapeutic ability of Wedelolactone against inflammatory and tumor promoting events in murine skin depicting plausible role of NFkB pathway. (C) 2016 Elsevier B.V. All rights reserved.