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铁剂诱发大鼠肝纤维化的组织学变化
目的:探讨饮食中铁过载诱导肝组织纤维化形成的组织学变化.方法:采用♂SD大鼠,在饮食中适量添加铁,共饲喂9wk,然后处死动物,收取肝组织,分别在石蜡切片和透射电镜下观察肝组织损害、肝窦毛细血管化和窦周纤维化形成以及Ⅰ、Ⅳ型胶原和Laminin的分布情况.结果:铁剂组大鼠可见肝细胞凝固坏死,星状细胞活化,肝窦毛细血管化和轻微窦周纤维化,Ⅰ型胶原和laminin含量增多,中央静脉基底膜增厚.结论:饮食中铁过载持续一定时间可损害肝细胞,激活肝星状细胞,减少窦内皮细胞的窗孔,导致肝窦毛细血管化和窦周肝纤维化,故酒精性肝病造模可考虑配合使用.
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Iron overload can lead to cytotoxicity, and it is a risk factor for diabetic peripheral neuropathy. However, the underlying mechanism remains unclear. We conjectured that iron overload-induced neurotoxicity might be associated with oxidative stress and the NF-E2-related factor 2 (Nrf2)/ARE signaling pathway. As an in vitro cellular model of diabetic peripheral neuropathy, PC12 cells ex-posed to high glucose concentration were used in this study. PC12 cells were cultured with ferric ammonium citrate at different concentrations to create iron overload. PC12 cells cultured in ferric ammonium citrate under high glucose concentration had significantly low cellviability, a high rate of apoptosis, and elevated reactive oxygen species and malondialdehyde levels. These changes were dependent on ferric ammonium citrate concentration. Nrf2 mRNA and protein expression in the fer-ric ammonium citrate groups were inhibited markedly in a dose-dependent manner. Al changes could be inhibited by addition of deferoxamine. These results indicate that iron overload aggravates oxidative stress injury in neural cells under high glucose concentration and that the Nrf2/ARE sig-naling pathway might play an important role in this process.
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铁过载诊断与治疗的中国专家共识
定期红细胞输注是重型地中海贫血、骨髓增生异常综合征(MDS)和再生障碍性贫血等贫血性疾病的主要治疗措施,是维持患者生活质量(quality of life,QOL)的重要保证.
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重视骨髓增生异常综合征铁过载的诊断和治疗
骨髓增生异常综合征(MDS)患者主要由于红细胞输注以及骨髓无效造血反馈性刺激肠道铁的吸收增多等原因导致患者体内铁负荷增高,因此部分患者会出现铁过载.
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铁过载与糖尿病关系的研究进展
铁是生物体必不可少的微量元素,铁缺乏或铁过载均会导致铁代谢相关疾病.铁缺乏会导致缺铁性贫血,铁过载主要表现为遗传性血色素沉着症(HH).研究发现HH与二型糖尿病(typeⅡdiabetes meUitus,T2DM)之间存在某种关联.大量的临床、流行病学和基础实验研究均表明组织铁沉积可能与T2DM的发生及其并发症有关.血清铁蛋白(ferritin)已经成为T2DM患者的重要检测指标之一.然而铁在T2DM发病过程中的作用机制研究较少.新研究表明缺氧诱导因子1α(hypoxia-inducible factor 1α,HIF-1α)是连接铁代谢与糖代谢的关键因子.通过减少饮食中血红素铁的摄取、放血以及用铁螯合剂处理可以起到对HH诱导的T2DM的预防和治疗作用.