活性氧对缺血再灌注损伤皮瓣的影响及中药干预研究进展

Research progress of the effect of reactive oxygen species on ischemia-reperfusion injury skin flaps and traditional Chinese medicine intervention

缺血再灌注损伤(ischemia-reperfusion injury,IRI)是机体组织、器官灌注不足引发组织、器官出现缺血样改变,当组织、器官再次获得充分血流灌注时,其损伤状态未能得到改善,反而损伤持续加重,最终导致坏死的疾病,常见于移植后皮瓣及肝、肾、脑等器官。目前IRI的发病机制尚未充分阐明,既往研究发现,活性氧(reactive oxygen species,ROS)是IRI的发病因素之一,ROS可刺激IRI组织释放磷脂酶A2、肿瘤坏死因子-α(tumour necrosis factorα,TNF-α)、白介素-1β(interleukin-1β,IL-1β)、干扰素-γ(interferon-γ,IFN-γ)、血管紧张素II等促炎物质,诱导黄嘌呤氧化酶(xantheine oxidase,XO)和烟酰胺腺嘌呤二核苷酸磷酸(nicotinamide adenine dinucleotide phosphate,NADPH)氧化酶系统,加重局部氧化应激和炎症反应,同时ROS参与细胞凋亡、自噬、坏死,进而对IRI组织造成继发性损伤。本文综述了ROS对IRI皮瓣的影响及中药干预研究进展,以为开发新的治疗干预手段提供参考。

Ischemia-reperfusion injury(IRI)is a disease in which ischemia-like changes occurrs in tissues and organs triggered by inadequate perfusion of tissues and organs,and when the tissues and organs received adequate blood perfusion again,the damage state of the tissues and organs fails to improve, and on the contrary, the damage continues to aggravate, ultimately resulting in necrosis, which is commonly seen in post-transplantation flaps, and multiple organs, such as the liver, kidneys, and brain. The detailed mechanisms of IRI have yet to be fully elucidated, previous studies found that reactive oxygen species (ROS) was an important pathogenetic factor in IRI, and ROS could stimulate the release of pro-inflammatory substances, such as phospholipase A2, tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon-γ (IFN-γ), and angiotensin II from IRI tissues, and induce xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase systems, exacerbating local oxidative stress and inflammatory responses, while ROS was involved in apoptosis, autophagy, and necrosis, causing secondary damage to IRI tissues. This paper reviewed the effect of ROS in IRI skin flaps and the progress of traditional Chinese medicine intervention research, in order to provide reference for the development of new therapeutic interventions.