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目的 研究 1,6 二磷酸果糖 (FDP)对阿霉素 (ADM )导致大鼠心肌酪氨酸硝基化的影响。方法 给大鼠腹腔注射ADM(2 5 0mg·kg-1,隔日 1次 ,共 6次 )处理大鼠 ;给ADM处理的大鼠腹腔注射不同剂量的FDP(隔日 1次 ,共2 1次 )进行干预。分别用TBA法、硝酸还原酶法、邻苯三酚自氧化法测定心肌的脂质过氧化物 (LPO)含量、一氧化氮(NO)含量、超氧化物歧化酶 (SOD)活性 ;分别用原位杂交法、免疫组织化学法检测心肌的诱导型一氧化氮合酶 (iN OS)mRNA表达、硝基酪氨酸 (NT) ,半定量分析心肌的iNOSmRNA表达水平、NT水平。结果 FDP(30 0 ,6 0 0 ,12 0 0mg·kg-1)干预ADM处理的大鼠后 ,均可显著降低心肌的LPO及NO含量、显著降低心肌的iNOSmRNA表达水平、显著降低心肌的NT水平、显著增加心肌的SOD活性 (P <0 0 1)。结论 FDP抑制ADM导致心肌酪氨酸硝基化而减轻ADM对心肌的毒性损伤。其机制可能与FDP抑制ADM引起心肌的iNOSmRNA表达而使心肌产生NO减少 ,以及FDP保护心肌的SOD活性而增强心肌清除超氧阴离子的能力 ,从而减少心肌生成过氧亚硝基阴离子有关
Objective To investigate the effects of fructose 1,6 diphosphate (FDP) on the tyrosine nitration in rats induced by adriamycin (ADM). Methods Rats were intraperitoneally injected with ADM (250 mg · kg -1, once every other day for 6 times). Rats in ADM group were injected intraperitoneally with different doses of FDP (once every other day for 21 times) Intervene. The lipid peroxidation (LPO) content, nitric oxide (NO) content and superoxide dismutase (SOD) activity were measured by TBA method, nitrate reductase method and pyrogallol autoxidation method. In situ hybridization was used to detect the expression of inducible nitric oxide synthase (iNOS) mRNA and nitrotyrosine (NT) in myocardium. The levels of iNOS mRNA and NT were determined by semi-quantitative analysis. Results FDP (30, 60, 120 mg · kg-1) significantly decreased the levels of LPO and NO in myocardium and significantly decreased the expression of iNOS mRNA in myocardium and decreased the NT in myocardium Level, significantly increased myocardial SOD activity (P <0 01). Conclusions FDP can inhibit the tyrosine nitration of ADM and reduce the damage of ADM to myocardium. The mechanism may be related to FDP inhibiting ADM-induced iNOS mRNA expression in myocardium and reducing myocardial NO production, and FDP protects cardiac SOD activity and enhances myocardial scavenging ability of superoxide anion, thereby reducing myocardial production of peroxynitrite anion