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本文旨在研究低氧暴露对骨骼肌细胞铁代谢的影响。培养大鼠骨骼肌L6细胞,随机分成3组,分别低氧(1%O2)暴露0、12和24h。采用同位素55Fe示踪法测定细胞铁摄取和铁释放能力的变化;用流式细胞仪检测细胞内可变铁池(labile ironpool,LIP);应用蛋白免疫印迹检测转铁蛋白受体1(transferrin receptor1,TfR1)、二价金属离子转运体(divalent metal transport-er1,DMT1)、膜铁转运蛋白1(ferroportin1,FPN1)和低氧诱导因子1(hypoxia-inducible transcription factor-1,HIF-1)的变化。结果显示,与0h低氧暴露组相比,12h低氧暴露组细胞的铁摄取能力明显升高(P<0.05),铁释放能力显著降低(P<0.01),LIP明显升高(P<0.05)。24h低氧暴露组肌细胞铁摄取、铁释放能力及LIP均明显低于0h和12h低氧暴露组(P<0.05或P<0.01)。与0h低氧暴露组比较,12h低氧暴露组HIF-1、DMT1(IRE)、DMT1(non-IRE)和TfR1表达显著升高(P<0.05或P<0.01),而FPN1表达则显著降低(P<0.01);24h低氧暴露组DMT1(IRE)、DMT1(non-IRE)和FPN1表达均低于0和12h低氧暴露组(P<0.01),但TfR1表达却显著增加(P<0.05或P<0.01)。以上结果提示,低氧对骨骼肌铁代谢的影响与暴露时间密切相关,一定时间的低氧暴露可以提高肌细胞的铁摄取能力,降低铁释放,增加细胞内的铁含量,而长时间的低氧暴露会引起细胞铁代谢紊乱。
This article aims to study the effects of hypoxic exposure on iron metabolism in skeletal muscle cells. Rat skeletal muscle L6 cells were cultured and randomly divided into 3 groups: hypoxia (1% O2) exposure for 0, 12 and 24 h, respectively. The changes of iron uptake and iron release were measured by isotope 55Fe tracer method. The intracellular soluble iron pool (LIP) was detected by flow cytometry. The expression of transferrin receptor 1 , TfR1), divalent metal transporter1 (DMT1), ferroportin1 (FPN1) and hypoxia-inducible transcription factor-1 (HIF-1) Variety. The results showed that compared with 0h hypoxia exposure group, the iron uptake capacity of 12h hypoxia exposure group was significantly increased (P <0.05), iron release ability was significantly reduced (P <0.01), LIP was significantly increased (P <0.05 ). The iron uptake, iron release ability and LIP in 24h hypoxia exposure group were significantly lower than those in 0h and 12h hypoxia exposure group (P <0.05 or P <0.01). Compared with 0h hypoxia exposure group, the expressions of HIF-1, DMT1 (IRE), DMT1 (non-IRE) and TfR1 in hypoxic exposure group were significantly increased (P <0.05 or P <0.01) (P <0.01). The expressions of DMT1 (IRE), DMT1 (non-IRE) and FPN1 in hypoxia exposure group were lower than those in 0 and 12h hypoxia exposure group (P <0.01), but the expression of TfR1 increased significantly 0.05 or P <0.01). The above results suggest that hypoxia is closely related to the iron metabolism of skeletal muscle and exposure time. Hypoxia exposure can increase the iron uptake ability of muscle cells, decrease the release of iron, and increase the intracellular iron content, while prolonged low Oxygen exposure can cause cellular iron metabolism disorders.