国际儿科学杂志
國際兒科學雜誌
국제인과학잡지
International Journal of Pediatrics
2015年
5期
538-541
,共4页
一氧化碳%抗炎%信号通路%丝裂原激活的蛋白激酶%核转录因子
一氧化碳%抗炎%信號通路%絲裂原激活的蛋白激酶%覈轉錄因子
일양화탄%항염%신호통로%사렬원격활적단백격매%핵전록인자
Carbon monoxide%Anti-inflammation%Signal pathway%MAPK%NF-κB
炎症是临床上常见而又重要的基本病理过程.过度的炎症反应对组织器官有着巨大的损伤作用.一氧化碳是一种小分子气体,在体内主要由血红素氧合酶降解血红素而生成,它的多种生物学活性均与其细胞保护功能有关,如抗炎、抗凋亡、抗增殖及舒张血管.基础研究发现:在多种炎症模型中,一氧化碳均具有良好的抗炎效应,其作用的主要细胞细胞信号通路包括丝裂原活化蛋白激酶信号通路、Toll样受体信号通路、核转录因子-κB信号通路、Janus激酶-信号传导和转录激活子信号通路等.临床研究中,一氧化碳并未取得良好的保护效果.该文探讨一氧化碳的抗炎作用机制,以期为更进一步研究提供理论参考.
炎癥是臨床上常見而又重要的基本病理過程.過度的炎癥反應對組織器官有著巨大的損傷作用.一氧化碳是一種小分子氣體,在體內主要由血紅素氧閤酶降解血紅素而生成,它的多種生物學活性均與其細胞保護功能有關,如抗炎、抗凋亡、抗增殖及舒張血管.基礎研究髮現:在多種炎癥模型中,一氧化碳均具有良好的抗炎效應,其作用的主要細胞細胞信號通路包括絲裂原活化蛋白激酶信號通路、Toll樣受體信號通路、覈轉錄因子-κB信號通路、Janus激酶-信號傳導和轉錄激活子信號通路等.臨床研究中,一氧化碳併未取得良好的保護效果.該文探討一氧化碳的抗炎作用機製,以期為更進一步研究提供理論參攷.
염증시림상상상견이우중요적기본병리과정.과도적염증반응대조직기관유착거대적손상작용.일양화탄시일충소분자기체,재체내주요유혈홍소양합매강해혈홍소이생성,타적다충생물학활성균여기세포보호공능유관,여항염、항조망、항증식급서장혈관.기출연구발현:재다충염증모형중,일양화탄균구유량호적항염효응,기작용적주요세포세포신호통로포괄사렬원활화단백격매신호통로、Toll양수체신호통로、핵전록인자-κB신호통로、Janus격매-신호전도화전록격활자신호통로등.림상연구중,일양화탄병미취득량호적보호효과.해문탐토일양화탄적항염작용궤제,이기위경진일보연구제공이론삼고.
Inflammation is a common and important clinical basic pathological process, and excessive inflammatory response has tremendous damage to tissues and organs.Carbon monoxide is a kind of small-molecular gas, which is generated by degradation of heme in the body.It has been demonstrated that endogenous carbon monoxide has a variety of biological activities involved in its cytoprotective efects, such as anti-inflammation, anti-apoptosis, anti-proliferation and vasodilation.Carbon monoxide has good anti-inflammatory effect in a variety of inflammatory models in basic research, which play roles in following main cell signal pathways include mitogen-activated potein kinase (MAPK) signal pathway, toll-like receptor (TLR) signal pathway, nuclear factor κappaB (NF-κB) signal pathway ,janus kinase-signal transducer and activator of transcription(JAK-STAT) signal pathway.Unfortunately, carbon monoxide did not show good protective effect in clinical research.This review summarizes the anti-inflammatory mechanism of carbon monoxide, so as to provide theoretical reference for further study.