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首页> 外文期刊>Molecular medicine reports >Trichosanthes kirilowii extract enhances repair of UVB radiation-induced DNA damage by regulating BMAL1 and miR-142-3p in human keratinocytes
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Trichosanthes kirilowii extract enhances repair of UVB radiation-induced DNA damage by regulating BMAL1 and miR-142-3p in human keratinocytes

机译：Kiricoshers Kirilowii提取物通过调节人类角质形成细胞的Bmal1和miR-142-3p来增强UVB辐射诱导的DNA损伤的修复

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摘要

Ultraviolet B (UVB) radiation induces DNA damage, oxidative stress and inflammation, and suppresses the immune system in the skin, which collectively contribute to skin aging and carcinogenesis. The DNA damage response, including DNA repair, can be regulated by the circadian clock and microRNA (miRNA) expression. The aim of the present study was to evaluate the reparative action of Trichosanthes kirilowii extract (TKE) against UVB irradiation-induced DNA damage in human keratinocytes. TKE demonstrated low cytotoxicity in normal HaCaT keratinocytes at low doses (up to 100 mu g/ml). The results of a comet assay revealed that TKE enhanced the repair of UVB-induced DNA damage. TKE significantly upregulated the expression of the core clock protein, brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein-1 (BMAL1), and downregulated the expression of miRNA (miR)-142-3p, as demonstrated using western blotting and the reverse transcription-quantitative polymerase chain reaction. Furthermore, the suppression of miR-142-3p by a specific inhibitor positively correlated with the repair activity. Overall, the data obtained demonstrated that TKE enhanced the repair of UVB-induced DNA damage by regulating the expression of BMAL1 and miR-142-3p. Consequently, TKE can be considered a potential candidate for the treatment of skin diseases associated with UVB-induced damage.
机译：紫外线B（UVB）辐射诱导DNA损伤，氧化应激和炎症，并抑制皮肤中的免疫系统，其共同促进皮肤衰老和致癌作用。 DNA损伤反应，包括DNA修复，可以由昼夜节点和MicroRNA（miRNA）表达来调节。本研究的目的是评估Trichosantheshirilowi​​i提取物（TKE）对人角质形成细胞中的UVB辐照诱导的DNA损伤的重复作用。 TKE在低剂量（高达100μg/ ml）下正常HACAT角质形成细胞中显示出低细胞毒性。彗星测定的结果表明，TKE增强了UVB诱导的DNA损伤的修复。 TKE显着上调了核心时钟蛋白，脑和肌肉芳烃受体核转移率样蛋白-1（BMA1）的表达，并下调了MiRNA（miR）-142-3p的表达，如使用Western印迹和反向所证明的转录定量聚合酶链反应。此外，通过特异性抑制剂与修复活性呈正相关的特异性抑制剂抑制miR-142-3p。总的来说，所获得的数据证明，TKE通过调节BMA1和miR-142-3p的表达来增强UVB诱导的DNA损伤的修复。因此，TKE可以被认为是治疗与UVB引起的损伤相关的皮肤病的潜在候选者。

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