Kupffer细胞在内毒素诱导肝损伤发病机制中的作用

Role of Kupffer cells in the pathogenesis of endotoxininduced liver injury

内毒素脂多糖(lipopolysaccharide,LPS)诱导的肝损伤参与了多种肝脏疾病发生发展的进程,肝脏巨噬细胞(即Kupffer细胞)在LPS诱导肝损伤的过程中发挥着重要作用.一方面,Kupffer细胞通过LPS信号转导系统被激活而释放促炎因子,并在肝脏内其他细胞的相互作用下介导肝脏损害;另一方面,Kupffer细胞的活性又被LPS耐受和其他生理调控机制所抑制,避免Kupffer细胞活化而诱导肝脏损害.因此,Kupffer细胞同时受到激活和抑制性因素的共同作用并维持在相对平衡状态,一旦这种平衡机制被病理因素打破,就可能招致肝脏损伤;而Kupffer细胞活性的抑制性干预就成为保护内毒素诱导肝损伤的重要策略.

Endotoxin （lipopolysaccharide, LPS）-induced liver injury was involved in the initiation and development of various liver diseases, and liver macrophages （Kupffer cells） were demonstrated to play important roles in these processes. On one hand, Kupffer cells were activated to release pro-inflammatory factors via the system of LPS-induced signal transduction, and this responsibility was also cooperated by the interaction of other liver cells to mediate liver injury. On the other hand, the activation of Kupffer cells were also inhibited by LPS tolerance and other physiological regulatory mechanisms, which prevented the liver injury mediated by Kupffer cells. Thus, Kupffer cells were simultaneously co-stimulated by factors of activation and inhibition to keep a relative balance. LPS-induced liver injury may occur once the balance is pathologically broken,whereas inhibitory intervention of Kupffer cells＇ activation is a key strategy＇to protect the LPS- induced injury.