人参皂苷Rb1与皮瓣缺血再灌注损伤的研究与进展

Research progress of ginsenosides Rb1 in flap ischemia/reperfusion injury

背景:在整形外科中,缺血再灌注损伤是常见的病理生理过程,在随意皮瓣、游离皮瓣及复合组织瓣移植手术中都时有发生,严重者将导致皮瓣部分甚至全部坏死。近年来大量研究报道了人参皂苷Rb1在多种组织器官缺血再灌注损伤中均有良好的保护作用。目的:就皮瓣缺血再灌注损伤机制与人参皂苷Rb1的作用机制研究进展综述。18方法:检索中国期刊全文数据库(CNKI)和PubM ed数据库1996年1月至20年6月相关文献;检索词为"皮瓣,缺血再灌注损伤,人参皂苷Rb1;Ginsenosides,Reperfusion Injury,Flaps"。纳入有关人参皂苷Rb1药理作用、人参皂苷Rb1减轻组织器官缺血再灌注损伤及皮瓣缺血再灌注损伤研究的文献进行分析探讨。结果与结论:皮瓣缺血再灌注损伤是缺血组织器官恢复血供后出现的一种复杂的非特异性损伤级联反应,涉及过量的氧自由基生成、炎症细胞激活浸润及其与内皮相互作用、能量衰竭、细胞内钙超载、一氧化氮生成等方面。人参皂苷Rb1可通过其抗氧化、抑制炎症反应、增加一氧化氮合成、抗凋亡、抑制钙超载等机制在皮瓣缺血再灌注损伤中发挥保护作用。

BACKGROUND: Ischemia/reperfusion injury is a common pathophysiological process in plastic surgery, which happens in random flap, free flap and composite tissue flap transplantation, even will lead to partial or whole flap necrosis. Ginsenosides Rb1 has been shown to exert protection in ischemia/reperfusion injuries of various tissues and organs. OBJECTIVE: To review the mechanism of ischemia/reperfusion injury of flap and action mechanism of ginsenosides Rb1. METHODS: CNKI and PubMed databases were searched for the articles published between January 1996 and June 2018 with the keywords of “ginsenosides, reperfusion injury, flaps” in English and Chinese, respectively. The articles addressing the pharmacological effects of ginsenosides Rb1, ginsenosides Rb1 alleviating tissue ischemia/reperfusion injury and flap ischemia/reperfusion injury were included.RESULTS AND CONCLUSION: Flap ischemia/reperfusion injury is complex non-specific cascade damage after ischemic tissues restoring blood supply, which Involves in excessive production of oxygen free radicals, inflammation infiltration and its interaction with endothelial cells, energy failure, intracellular calcium overload, and nitric oxide production. Ginsenosides Rb1 has the effects of anti-oxidation, anti-inflammation and antiapoptosis. Ginsenosides Rb1 exerts good protection in ischemia/reperfusion injuries of various tissues and organs through anti-oxidation, anti-inflammation, increasing nitric oxide production, antiapoptosis, inhibiting calcium overload.