Enomoto D N, Schellekens P T, Yong S L, ten Berge I J, Mekkes J R, Bos J D
Department of Dermatology, University of Amsterdam, The Netherlands.
Photochem Photobiol. 1997 Jan;65(1):177-80. doi: 10.1111/j.1751-1097.1997.tb01895.x.
The mechanism of action of psoralen plus UVA (PUVA) and photopheresis is not entirely understood. These therapies are assumed to be immunomodulating partly by gradually decreasing leukocyte viability. We investigated whether this delayed form of cell death was due to apoptosis. Untreated and treated (PUVA exposed) leukocytes obtained from six patients with systemic sclerosis and (untreated) leukocytes from healthy control individuals were studied. Qualitative gel electrophoresis and quantitative in situ nick translation analysis of DNA fragmentation was performed. Apoptosis of the treated cells did occur (gel electrophoresis) after 24 h. At t = 0 h, immediately after exposure to PUVA, there was no evidence of DNA fragmentation in the treated cells. The percentage of treated cells undergoing apoptosis was 20-55% at t = 24 h (in situ nick translation). The untreated leukocytes of the patients and the healthy individuals showed no distinctive rise in apoptotic cells. Apoptosis of the leukocytes after PUVA or photopheresis treatment might be a mechanism of action and might explain the therapeutic response.
补骨脂素加紫外线A（PUVA）和光分离置换法的作用机制尚未完全明确。这些疗法被认为部分通过逐渐降低白细胞活力来调节免疫。我们研究了这种延迟性细胞死亡是否是由于凋亡所致。研究了从6例系统性硬化症患者获取的未经处理和经处理（暴露于PUVA）的白细胞以及健康对照个体的（未经处理）白细胞。进行了DNA片段化的定性凝胶电泳和定量原位缺口平移分析。经处理的细胞在24小时后确实发生了凋亡（凝胶电泳）。在t = 0小时，即暴露于PUVA后立即，未发现经处理细胞中有DNA片段化的证据。在t = 24小时时，经处理发生凋亡的细胞百分比为20 - 55%（原位缺口平移）。患者和健康个体的未经处理的白细胞未显示出凋亡细胞有明显增加。PUVA或光分离置换法治疗后白细胞的凋亡可能是一种作用机制，并且可能解释治疗反应。
