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作 者:陈亮[1] 颜王鑫[1] 唐兰兰[2] 郝卯林[2] 谢克俭[3] 王万铁[2]
机构地区:[1]温州市第三人民医院外科,浙江温州325000 [2]温州医学院病理生理学教研室,浙江温州325035 [3]温州医学院检验医学院分析中心,浙江温州325035
出 处:《肝胆胰外科杂志》2010年第3期200-202,共3页Journal of Hepatopancreatobiliary Surgery
基 金:浙江省卫生厅科研基金资助项目(98A087)
摘 要:目的探讨L-精氨酸(L-Arg)对肝缺血再灌注损伤(HIRI)时肝细胞能量代谢的影响及其机制。方法实验兔30只,随机分为对照组(C组),模型组(HIRI组)和L-Arg干预组(L-Arg组)。在再灌注45min时,分别检测肝组织内三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量,总腺苷酸量(TAN),能荷(EC),丙二醛浓度(MDA),超氧化物歧化酶活性(SOD),一氧化氮代谢产物(NO_2-/NO_3-)水平,血栓素B_2(TXB_2)和6-酮基-前列腺素F_1α(6-keto-PGF_1α)含量以及TXB_2/6-keto-PGF_1α(T/K)值。结果 L-Arg组与HIRI组比较,肝组织内ATP、NO_2-/NO_3-、6-keto-PGF_1α含量,EC和SOD活性均明显增高(P<0.05或P<0.01),AMP含量及T/K值显著降低(P<0.05或P<0.01)。结论 L-精氨酸可通过降低体内氧自由基水平,提高一氧化氮水平,纠正TXA_2与PGI_2的平衡,从而改善缺血再灌注损伤肝脏的能量代谢。Objective To explore the positive effects of L-arginine (L-Arg) on hepatocellular energymetabolism against the reperfusion injury after hepatic ischemia in rabbits. Methods Thirty rabbits were randomly divided into three groups: control group (C group), model group (HIRI group) and L-Arg interventiongroup (L-Arg group), the contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosinemonophosphate (AMP), total adenylic acid number (TAN), energy charge (EC), malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide products (NO2-/NO3-), thromboxane B2(TXB2), 6-keto-prostaglandin F1α(6-keto-PGF1α) and TXB2/6-keto-PGF1α (T/K) in the liver tissue were analyzed at 45 min after reperfusion. Re-sults Compared with the HIRI group, L-Arg group showed a significant increase in contents of ATP, NO,6-keto-PGF1α, EC and SOD activity (P0.05 or P0.01), decrease in AMP content and a reduction of T/K (P0.05 or P0.01). Conclusion These data suggest that L-Arg can improve hepatocellular energy metabolismagainst the reperfusion injury after liver ischemia by decreasing oxygen free radical level, raising NO leveland correcting the imbalance of TXA2/PGI2.
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