论文部分内容阅读
目的探讨二巯基丙磺酸钠(Na-DMPS)、N-乙酰-L-半胱氨酸(NAC)对溴苯腈急性中毒小鼠脑组织能量代谢影响。方法ICR小鼠40只,每组8只,随机分为对照(CG)组、急性中毒(AI)组、Na-DMPS组、NAC组与NAC联用Na-DMPS(NN)组;反相高效液相色谱(RP-HPLC)法检测各组小鼠脑组织三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺甙(AMP)含量,并计算细胞能荷(EC)值;分光光度法测定脑组织钠钾腺甙三磷酸酶(Na+-K+-ATPase)、钙镁腺苷三磷酸酶(Ca2+-Mg2+-ATPase)活性。结果AI组脑组织ATP含量、EC水平和Na+-K+-ATPase、Ca2+-Mg2+-AT-Pase活性比CG组明显降低(P<0.05);Na-DMPS组、NAC组与NN组ATP含量分别为(1.53±0.38),(1.81±0.41),(2.04±0.38)μmol/g;EC水平分别为(0.64±0.05),(0.71±0.03),(0.76±0.02);Na+-K+-ATPase活性分别为(4.27±0.53),(4.56±0.66),(4.82±0.62)U/(mg.prot);Ca2+-Mg2+-ATPase活性分别为(3.67±0.37),(3.85±0.65),(4.17±0.59)U/(mg.prot),均明显高于AI组(P<0.05)。结论Na-DMPS、NAC单用及联用均可改善小鼠溴苯腈急性中毒脑组织能量代射障碍,有效保护神经细胞生物膜上的泵功能,以两者联用效果最佳。
Objective To investigate the effects of sodium dimercaptopropanesulfonate (Na-DMPS) and N-acetyl-L-cysteine (NAC) on energy metabolism in brain of bromoxynil acute poisoning mice. Methods 40 ICR mice were randomly divided into control group (CG), acute poisoning (AI) group, Na-DMPS group, NAC group and NAC combined with N-DMPS (NN) The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in brain tissue of each group were detected by liquid chromatography (RP-HPLC) method and the cell energy load (EC) Method to determine the activity of Na + -K + -ATPase and Ca2 + -Mg2 + -ATPase in brain tissue. Results The ATP content, EC level and the activities of Na + -K + -ATPase and Ca2 + -Mg2 + -AT-Pase in AI group were significantly lower than those in CG group (P <0.05). The ATP content in Na-DMPS group, NAC group and NN group were (1.53 ± 0.38), (1.81 ± 0.41) and (2.04 ± 0.38) μmol / g, respectively; the levels of EC were (0.64 ± 0.05), (0.71 ± 0.03) and (4.27 ± 0.53), (4.56 ± 0.66) and (4.82 ± 0.62) U / (mg.prot) respectively. The activities of Ca2 + -Mg2 + -ATPase were (3.67 ± 0.37), (3.85 ± 0.65) and (4.17 ± 0.59 ) U / (mg.prot) were significantly higher than AI group (P <0.05). Conclusion Both Na-DMPS and NAC alone or in combination can improve brain injury induced by bromoxynil in mice and effectively protect the pump function of nerve cell biofilm.