摘要
肝脏缺血再灌注损伤(hepatic ischemia reperfusion injury,HIRI)的分子机制迄今尚未完全清楚。血红素加氧酶-1(heme oxygenase-1,HO-1)是体内血红素降解的起始酶和限速酶,在体内分解血红素生成一氧化碳(CO)、胆绿素和自由铁。HO-1系统具有抗炎、抗氧化、抗凋亡和促进细胞存活、循环稳定和免疫调节的作用,在HIRI中发挥着至关重要的作用。通过药物或基因工程的方法诱导产生HO-1,能减轻HIRI,目前这一方向已经成为该领域的研究热点。
The molecular mechanisms involved in hepatic ischemia reperfusion injury (HIRI) are still largely incomplete.Heme oxygenase-1 (HO-1) is the key enzyme that catalyzes the rate-limiting step in the degradation of the prooxidant heme to yield biliverdin,iron and CO.HO-1 system exerts anti-inflammatory,antioxidant,antiapoptosis,immune regulation effects and promotes cell survival,cycle stability,so it plays a vital role in HIRI.HO-1 is the inducible form of HO.Administration of HO-1 inducers or HO-1 gene transfer has showed a significant therapeutic effect today.
出处
《胃肠病学和肝病学杂志》
CAS
2014年第10期1121-1123,共3页
Chinese Journal of Gastroenterology and Hepatology
基金
黑龙江省自然基金面上项目(D200944)