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目的:黄嘌呤氧化还原酶(xanthine oxidoreductase, XOR)可催化亚硝酸盐(nitrite,NO2-)还原生成一氧化氮(nitric oxide,NO·).研究XOR催化NO2-生成的NO·能否保护肝脏对抗缺血再灌注(ischemia- reperfusion,I/R)损伤. 方法:Wistar鼠分别予以生理盐水、一氧化氮合酶(nitric oxide synthase,NOS)抑制剂Nω-硝基-L-精氨酸甲基酯(Nω-nitro-L-arginine-methyl ester,L- NAME),XOR抑制剂别嘌呤醇(allopurinol)、L- NAME+allopurinol以及NO·清除剂carboxy-PTIO 预处理(每组动物12只),然后行全肝缺血40 min接着再灌注.再灌注3 h后取血液标本及肝组织用作分析,并作生存研究. 结果:Allopurinol预处理动物与生理盐水预处理动物相比,I/R后血清ALT水平及肝脏髓过氧化物酶(myeloperoxidase,MPO)活性进一步升高,而肝脏ATP 含量进一步降低(13 845±1 805 vs 8 432±3 071 nkat/L, 942±184 vs 692±170 nkat/g 及1.93±0.47 vs 3.05±0.55 μmol/g; t= -3.722,-2.443及3.802;P<0.01,0.05及0.01),肝细胞损伤进一步加剧而整体生存率显著降低(t=-2.474, Log Rank=4.15;P<0.05).L-NAME和allopurinol联合预处理动物比L-NAME或allopurinol单独预处理动物表现出更严重的肝脏损伤(t=2.488和-4.194或t=2.883 和-3.68;P<0.05和0.01)及进一步降低的整体生存率(Log Rank=5.23或4.26;P<0.05),但与carboxy-PTIO 预处理动物无明显差异. 结论:XOR催化NO2-生成的NO·能保护肝脏对抗I/ R损伤.
OBJECTIVE: Xanthine oxidoreductase (XOR) can catalyze the reduction of nitrite (NO2-) to form nitric oxide (NO ·). The purpose of this study was to investigate whether XOR-catalyzed NO2- Against ischemia / reperfusion injury.Methods: Wistar rats were treated with normal saline and Nω-nitro-L-arginine A inhibitor of nitric oxide synthase (NOS) (Nω-nitro-L-arginine-methyl ester, L-NAME), XOR inhibitor allopurinol, L-NAME + allopurinol and NO · scavenger carboxy-PTIO ), And then subjected to whole liver ischemia for 40 min followed by reperfusion. Blood samples and liver tissues were taken for analysis after 3 h of reperfusion, and were used for survival study.Results: Allopurinol pretreatment animals compared with saline pretreatment animals, I Serum ALT levels and liver myeloperoxidase (MPO) activity were further increased after R / R administration, while the content of hepatic ATP was further decreased (13 845 ± 1 805 vs 8 432 ± 3 071 nkat / L, 942 ± 184 vs 692 ± 170 nkat / g and 1.93 ± 0.47 vs 3.05 ± 0.55 μmol / g; t = -3.722, -2.443 and 3.802; P <0.01, 0.05 and 0.01) L-NAME and allopurinol pretreated animals were more severe than L-NAME or allopurinol pretreated animals alone (t = -2.474, Log Rank = 4.15; P <0.05) (T = 2.488 and -4.194 or t = 2.883 and -3.68; P <0.05 and 0.01) and further decreased overall survival (Log Rank = 5.23 or 4.26, P <0.05) No significant difference was observed in animals treated with XOR.Conclusion: NO X-catalyzed NO · can protect liver against I / R injury.