Vileikyte Loretta
Department of Medicine, University of Manchester, Manchester, UK.
Clin Dermatol. 2007 Jan-Feb;25(1):49-55. doi: 10.1016/j.clindermatol.2006.09.005.
There are substantial data to suggest that stress-induced disruption of neuroendocrine immune equilibrium is detrimental to health, with the strongest evidence to date in wound healing. Murine and human studies demonstrated that the down-regulation of the early inflammatory response by an increase in cortisol levels results in delayed wound repair and identified several potential cellular mechanisms linking stress and wound healing. The impact of stress on wound healing has been studied almost exclusively in acute experimentally induced wounds. Because chronic wounds are different entities from acute wounds, the cellular/molecular mechanisms by which stress affects acute wound healing may not necessarily be applied to chronic wounds, hence, the need for studies in stress and chronic wound (eg, diabetic foot ulcer) healing.
有大量数据表明,应激诱导的神经内分泌免疫平衡紊乱对健康有害,迄今为止在伤口愈合方面有最有力的证据。小鼠和人类研究表明,皮质醇水平升高导致早期炎症反应下调,从而导致伤口修复延迟,并确定了几种将应激与伤口愈合联系起来的潜在细胞机制。应激对伤口愈合的影响几乎完全是在急性实验性诱导伤口中进行研究的。由于慢性伤口与急性伤口不同,应激影响急性伤口愈合的细胞/分子机制不一定适用于慢性伤口,因此,需要开展关于应激与慢性伤口(如糖尿病足溃疡)愈合的研究。