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5-aminolaevulinic acid-based photodynamic therapy inhibits ultraviolet B-induced skin photodamage

机译:基于5-氨基松油酸的光动力疗法可抑制紫外线B诱导的皮肤光损伤

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摘要

To evaluate the photoprotective effect of 5-aminolaevulinic acid-based photodynamic therapy (ALA-PDT) on ultraviolet B (UVB)-induced skin photodamage. In vivo experiments, the dorsal skin of hairless mice were treated with ALA-PDT or saline-PDT, and then exposed to 180 mJ/m2 UVB. Results showed that the number of sunburn cells and apoptotic cells in the epidermis of ALA-PDT-treated groups at 24 h after UVB irradiation were significantly decreased compared with those in the UVB groups. And the removal rate of CPDs was obviously higher in ALA-PDT-treated groups. At 48 h, the number of Ki67 positive nuclei in ALA-PDT-UVB group was significantly fewer than that in UVB group. Further in vitro experiments, human keratinocyte cell line (HaCaT) cells of two groups (one treated with ALA-PDT, the other untreated), were exposed to 60 mJ/m2 UVB irradiation. We found 0.5 mmol/L of ALA and 3 J/cm2 of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53. Thus, our data demonstrate that ALA-PDT pretreatment can induce a protective DNA damage response that protects skin cells from UVB-induced photodamages.
机译:若要评估基于5-氨基壬酸的光动力疗法(ALA-PDT)对紫外线B(UVB)诱导的皮肤光损伤的光保护作用。在体内实验中,用ALA-PDT或生理盐水-PDT处理无毛小鼠的背部皮肤,然后暴露于180 mJ / m 2 UVB。结果显示,与UVB组相比,在UVB照射后24小时,ALA-PDT处理组的表皮中晒伤细胞和凋亡细胞的数量明显减少。在ALA-PDT治疗组中,CPDs的去除率明显更高。 48h时,ALA-PDT-UVB组的Ki67阳性核数明显少于UVB组。进一步的体外实验中,将两组的人角质形成细胞系(HaCaT)细胞(一组用ALA-PDT处理,另一组未处理)暴露于60 mJ / m 2 UVB照射下。我们发现0.5 mmol / L的ALA和3 J / cm 2 的红光不会影响细胞的活力,并能减少UVB诱导的细胞凋亡,加速CPD清除,抑制增殖并激活p53 。因此,我们的数据表明,ALA-PDT预处理可以诱导保护性DNA损伤反应,从而保护皮肤细胞免受UVB诱导的光损伤。

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