Gendimenico G J, Kochevar I E
Wellman Laboratories, Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston.
Photodermatol Photoimmunol Photomed. 1990 Apr;7(2):51-5.
The purpose of this study was to further characterize acridine-photosensitized inhibition of mast cell degranulation. Acridine plus UVA radiation (320-400 nm) inhibited degranulation in response to antigen in IgE-sensitized rat serosal mast cells and in response to concanavalin A, which acts by a mechanism similar to antigen-IgE challenge. Removing oxygen from the incubation medium prevented the acridine-photosensitized inhibition of mast cell degranulation in response to 48/80. Acridine plus UVA radiation did not decrease mast cell ATP content, thus excluding inhibition of ATP production as a mechanism for photosensitized inhibition of mast cell degranulation. Although the viability of mast cells, as determined by uptake of trypan blue, was not affected 3 h after treatment with acridine plus UVA radiation, viability decreased by 6 h, and by 22 h 44% of the cells were nonviable. These results indicate that degranulation of mast cells by a variety of agents is inhibited by UVA plus acridine treatment, and that photosensitization requires oxygen and occurs before cytotoxicity.
本研究的目的是进一步描述吖啶光致敏对肥大细胞脱颗粒的抑制作用。吖啶加UVA辐射（320 - 400 nm）可抑制IgE致敏大鼠浆膜肥大细胞对抗原的脱颗粒反应，以及对刀豆球蛋白A的脱颗粒反应，刀豆球蛋白A的作用机制与抗原-IgE刺激相似。从孵育培养基中去除氧气可防止吖啶光致敏对肥大细胞因48/80刺激而产生的脱颗粒抑制作用。吖啶加UVA辐射并未降低肥大细胞的ATP含量，因此排除了抑制ATP生成作为光致敏抑制肥大细胞脱颗粒的机制。虽然用吖啶加UVA辐射处理3小时后，通过台盼蓝摄取测定的肥大细胞活力未受影响，但6小时后活力下降，到22小时，44%的细胞失去活力。这些结果表明，UVA加吖啶处理可抑制多种试剂诱导的肥大细胞脱颗粒，且光致敏需要氧气，并且发生在细胞毒性之前。
