Kowal-Vern A, Goral J, Gamelli R L, McGill V, Clancy J
Department of Pathology, Loyola University Medical Center, Maywood, Ill 60153, USA.
J Burn Care Rehabil. 2000 May-Jun;21(3):213-9. doi: 10.1067/mbc.2000.105085.
An acquired deficiency of antithrombin (AT), an anti-inflammatory protein, develops in patients with thermal injuries. Skin thermotolerance is regulated by heat shock protein (hsp) genes. hsp70, hsp32, hsp27, and glucose-regulated protein78 (grp78) were studied in burned and unburned human skin to determine whether correction of the AT deficiency modulated the intensity of expression of these proteins. Fifty-four human skin samples were prepared by Western blot analysis: 11 unburned and 22 burned control skin samples and 7 unburned and 14 burned skin samples from patients treated with AT(Human), or AT(H). The intensity of hsp32 expression in burned AT(H)-treated skin (P < .001) and in burned control skin (P < .01) was significantly increased compared with unburned control skin. The intensity of expression of hsp70 was statistically significant in burned AT(H)-treated skin compared with unburned control skin (P < .02), as was that of grp78 (P < .01). Thermally injured skin with or without AT(H) treatment had an increased expression of hsp70, hsp32, and grp78 compared with unburned control skin.
抗凝血酶（AT）是一种抗炎蛋白，热损伤患者会出现获得性抗凝血酶缺乏。皮肤耐热性由热休克蛋白（hsp）基因调节。对烧伤和未烧伤的人体皮肤中的hsp70、hsp32、hsp27和葡萄糖调节蛋白78（grp78）进行了研究，以确定抗凝血酶缺乏的纠正是否会调节这些蛋白的表达强度。通过蛋白质印迹分析制备了54份人体皮肤样本：11份未烧伤和22份烧伤的对照皮肤样本，以及7份未烧伤和14份接受抗凝血酶（人）或抗凝血酶（AT）治疗患者的烧伤皮肤样本。与未烧伤的对照皮肤相比，烧伤后接受抗凝血酶（AT）治疗的皮肤（P < 0.001）和烧伤对照皮肤（P < 0.01）中hsp32的表达强度显著增加。与未烧伤的对照皮肤相比，烧伤后接受抗凝血酶（AT）治疗的皮肤中hsp70的表达强度具有统计学意义（P < 0.02），葡萄糖调节蛋白78（grp78）的表达强度也是如此（P < 0.01）。与未烧伤的对照皮肤相比，无论是否接受抗凝血酶（AT）治疗，热损伤皮肤中hsp70、hsp32和grp78的表达均增加。
