颗粒酶B在慢性鼓膜穿孔炎症损伤修复中的应用

Role of granzyme B in injury inflammation and repair of the chronic tympanic membrane perforations

鼓膜穿孔延缓愈合可导致声波传递增益减少。文献报道颗粒酶B通过细胞内、外途径介导炎症反应,影响或延缓皮肤等伤口愈合;颗粒酶B基因敲除的小鼠则不发生迟缓愈合。鼓膜结构与皮肤有相似性,但在正常鼓膜与损伤延迟愈合鼓膜中颗粒酶B的表达差异鲜有报道。本文总结了慢性鼓膜穿孔产生和延迟愈合的机制及颗粒酶B可能对其影响的途径,为研究颗粒酶B抑制剂在促进慢性鼓膜穿孔炎症损伤修复中的作用,为临床探索新的治疗手段提供依据。

Delayed healing of tympanic membrane perforations can lead to a decrease of sound transmission gain. It has been reported that granzyme B mediated inflammatory reaction through vivo and vitro pathways, and delayed the healing of skin wounds. There was no delayed healing in granzyme B knock-out mice. Although the structure of tympanic membrane is similar to skin, the different expressions of granzyme B haven＇ t been reported between normal and delayed healing of tympanic membrane perforations. The article reviewed the mechanism of the formation and delayed healing of chronic tympanic membrane perforations, and the possible pathway of granzyme B. It will provide the basis for clinical treatment using inhibitor of granzyme B for delayed healing of tympanic membrane.