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目的:观察和探讨心房钠尿肽(atria1 natriuretic peptide,ANP)对小鼠的抗疲劳作用及其机制。方法:观察ANP13.10,6.55 ng.kg-1 iv对小鼠负重游泳时间及对游泳力竭小鼠腓肠肌MDA含量的影响;离体试验观察ANP高质量浓度13.10ng.kg-1对H2 O2(0.2mol.L-1)诱导小鼠腓肠肌MDA含量的影响。结果:ANP 13.10 ng.kg-1能够明显延长小鼠的游泳力竭时间(P<0.01);并能使小鼠腓肠肌MDA含量显著降低(P<0.05);ANP 13.10μg.L-1对H2O2致小鼠腓肠肌组织损伤有保护作用(P<0.001),而蛋白激酶G的阻断剂LY83583可阻止这种保护作用(P<0.01)。结论:ANP具有抗运动性疲劳的作用,其作用与ANP-环磷酸鸟苷-蛋白激酶G(ANP-cGMP-PKG)信号转导途径有关。
Objective: To observe and explore the anti-fatigue effect of atrial natriuretic peptide (ANP) on mice and its mechanism. Methods: The effects of ANP13.10 and 6.55 ng.kg-1 iv on the weight-bearing swimming time and the MDA content in the gastrocnemius muscle of swimming exhausted mice were observed. The effects of ANP13.10, (0.2mol.L-1) induced gastrocnemius MDA content in mice. Results: ANP 13.10 ng.kg-1 significantly prolonged swimming time (P <0.01) and decreased MDA content in gastrocnemius muscle of ANP group (P <0.05) (P <0.001), whereas LY83583, a blocker of protein kinase G, prevented this protective effect (P <0.01). CONCLUSION: ANP has the effect of anti-exercise fatigue and its effect is related to ANP-ANP-cGMP-PKG signal transduction pathway.