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作 者:刘培党[1]
机构地区:[1]东南大学医学院人体解剖学与组织胚胎学系,江苏南京210009
出 处:《东南大学学报(医学版)》2010年第2期123-126,共4页Journal of Southeast University(Medical Science Edition)
基 金:江苏省自然科学基金资助项目(BK2003059)
摘 要:目的:研究成纤维细胞生长因子(FGF)-23过表达对小鼠肾、肝和海马组织中氧化及抗氧化系统的影响,探讨FGF-23过表达致衰老的可能机制。方法:采用8周龄过表达人FGF-23转基因小鼠模型,检测转基因和野生型小鼠血清磷水平,测定肾、肝和海马组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)的活力以及丙二醛(MDA)的含量。结果:与野生型小鼠相比,FGF-23转基因小鼠血清磷水平显著降低(P<0.001);肾组织中SOD和GSH-PX的活力均显著降低(P<0.001),MDA的含量显著升高(P<0.001);海马组织中SOD和GSH-PX的活力明显降低(P<0.05或P<0.01),MDA的含量明显升高(P<0.01)。肝组织中SOD、GSH-PX的活力和MDA的含量与野生型小鼠相比差异不显著(P>0.05)。结论:FGF-23过表达能够导致肾和海马组织氧化损伤,FGF-23过表达致衰老与这些组织中氧化与抗氧化系统的失衡有一定的关系。Objective: To investigate the effects of fibroblast growth factor(FGF)-23 overexpression on oxidant and antioxidant systems in mouse renal,hepatic and hippocampal tissues in order to elucidate the mechanism of aging caused by FGF-23 overexpression.Methods: The serum phosphate levels,superoxide dismutase(SOD) and glutathione peroxidase(GSH-PX) activity and malondialdehyde(MDA) contents were measured and analyzed by the comparison of eight-week-old transgenic mice overexpressing human FGF-23 to their age-matched wild-type littermates.Results: Compared with the wild-type littermates,serum phosphate level of FGF-23 transgenic mice was decreased significantly(P0.001);SOD and GSH-PX activity were reduced significantly(P0.001),MDA content was increased significantly(P0.001) in renal tissue;SOD and GSH-PX activity were decreased significantly(P0.05 or P0.01) while MDA content was increased significantly(P0.01) in hippocampal tissue.However,there were no significant differences in SOD and GSH-PX activity and MDA contents in hepatic tissues between these two groups(P0.05).Conclusion: FGF-23 overexpression can result in oxidant injury in renal and hippocampal tissues which may be contributed to the aging caused by FGF-23 overexpression.
关 键 词:成纤维细胞生长因子-23 超氧化物歧化酶 谷胱甘肽过氧化物酶 丙二醛 衰老
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