Kane K S, Maytin E V
Department of Dermatology, Massachusetts General Hospital, Boston 02114.
J Invest Dermatol. 1995 Jan;104(1):62-7. doi: 10.1111/1523-1747.ep12613497.
Two components of sunlight, ultraviolet (UV) B (290-320 nm) and infrared (greater than 700 nm), each cause damage to the skin. However, we recently identified a protective response in which heat reduces UVB-induced killing of cultured keratinocytes. Here, this investigation is extended to the living epidermis. The effects of hyperthermic preconditioning upon UVB-induced apoptosis were studied morphologically with hematoxylin and eosin staining, and biochemically with TUNEL (terminal deoxynucleotide transferase nick-end labeling) to measure endonucleolytic cleavage of DNA in situ. Anesthetized SKH-1 hairless mice were exposed to UVB light (0 to 120 mJ/cm2), after which their skin was biopsied at 24 h and paraffin sections were stained with hematoxylin and eosin or with TUNEL. Apoptotic keratinocytes were found to increase after UVB in a dose-related manner. In contrast, if one flank of the mouse was pretreated at 40 degrees C for 1 h and both flanks subsequently were UVB-irradiated at 6 h, the resulting formation of apoptotic cells was reduced twofold or more in the heated flank. Protection appeared by 3 h, reached a maximum at 6 h, and disappeared by 12 h. In summary, heat induces a transient protective effect that reduces UVB-mediated death of keratinocytes in skin at physiologically attainable doses of heat and UVB.
阳光中的两个成分,紫外线(UV)B(290 - 320纳米)和红外线(大于700纳米),均可对皮肤造成损伤。然而,我们最近发现了一种保护性反应,即热能够减少UVB诱导的培养角质形成细胞的死亡。在此,本研究扩展至活体表皮。采用苏木精和伊红染色进行形态学研究,并使用TUNEL(末端脱氧核苷酸转移酶介导的缺口末端标记法)进行生化研究,以原位测量DNA的核酸内切酶切割,从而研究热预处理对UVB诱导的细胞凋亡的影响。将麻醉后的SKH - 1无毛小鼠暴露于UVB光(0至120 mJ/cm²)下,24小时后取其皮肤进行活检,将石蜡切片用苏木精和伊红或TUNEL染色。发现UVB照射后凋亡角质形成细胞呈剂量相关增加。相反,如果在40摄氏度下对小鼠的一侧腹进行1小时预处理,随后两侧腹均在6小时接受UVB照射,则受热一侧腹凋亡细胞的形成减少两倍或更多。保护作用在3小时出现,6小时达到最大,12小时消失。总之,在生理上可达到的热剂量和UVB剂量下,热可诱导一种短暂的保护作用,减少UVB介导的皮肤角质形成细胞死亡。