短期应用甲状旁腺激素1-34对大鼠骨髓间充质干细胞氧化应激的保护作用与胰岛素样生长因子- 1和核因子-红系2相关因子2有关

Young-Il Oh, Jong-Hoon Kim, Chang-Won Kang
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引用次数: 8

摘要

骨髓间充质干细胞(MSC)介导的再生是一种很有前途的治疗退行性疾病和创伤性损伤的方法。利用CD105抗体进行磁活化细胞分选,可以从大鼠体内分离出间充质干细胞。我们研究了内源性胰岛素样生长因子-i (IGF-I)和核因子-红细胞2相关因子-2 (Nrf-2)在短期治疗中与甲状旁腺激素(PTH) 1-34诱导的间充质干细胞保护反应之间的关系。PTH 1-34(10−9 M)减少活性氧(ROS)的产生,但增加细胞活力和内源性IGF-I (p <0.01)。使用特异性小干扰RNA (siRNA)抑制IGF-I和Nrf-2可阻断PTH 1-34的作用。此外,用siRNA处理IGF-I和Nr-2可以抑制PTH抗过氧化氢(H2O2)的细胞活力(p <0.05)。外源性IGF-I(10−9 M)也增加了内源性IGF-I、细胞活力和Nrf-2的表达。Nrf-2 siRNA (p <0.05)。外源性IGF-I还能抑制h2o2诱导的ROS生成的增加,抑制IGF-I和Nrf-2 siRNA存在下PTH 1-34诱导的ROS生成的减少。PTH 1-34诱导的Nrf-2表达增加在细胞核中比在细胞质中更为显著(p <0.05)。PTH 1-34抑制h2o2诱导型一氧化氮合酶的表达,增加血红素加氧酶1/2的表达。结果提示PTH 1-34、Nrf-2和IGF-I信号通路参与氧化应激反应。这些因素可能影响igf - 1对间充质干细胞代谢命运和存活的调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective effect of short-term treatment with parathyroid hormone 1-34 on oxidative stress is involved in insulin-like growth factor-I and nuclear factor erythroid 2-related factor 2 in rat bone marrow derived mesenchymal stem cells

Bone marrow-derived mesenchymal stem cell (MSC)-mediated regeneration is a promising treatment for degenerative disease and traumatic injuries. MSCs can be isolated from rats using magnetic-activated cell sorting with CD105 antibody. We investigated the relationships between the expression of endogenous insulin-like growth factor-I (IGF-I) and nuclear factor erythroid 2-related factor 2 (Nrf-2) during short-term treatment with parathyroid hormone (PTH) 1-34-induced protective response in MSCs. PTH 1-34 (10 9 M) decreased reactive oxygen species (ROS) generation but increased cell viability and endogenous IGF-I (p < 0.01). Suppression of IGF-I and Nrf-2 using specific small interfering RNA (siRNA) blocked the effects of PTH 1-34. Furthermore, increasing cell viability of PTH against hydrogen peroxide (H2O2) was suppressed by treatment with siRNA to IGF-I and Nr-2 (p < 0.05). Exogenous IGF-I (10 9 M) also increased endogenous IGF-I, cell viability, and Nrf-2 expression. These incremental increases were lessened by Nrf-2 siRNA (p < 0.05). Exogenous IGF-I also inhibited the increase of H2O2-induced ROS generation, and the decrease of PTH 1-34-induced ROS generation in the presence of IGF-I and Nrf-2 siRNA. The increase of PTH 1-34-induced Nrf-2 expression was more significant in the nucleus than in the cytosol (p < 0.05). PTH 1-34 also inhibited H2O2-induced inducible nitric oxide synthase expression, but increased the expression of heme oxygenase 1/2. The results implicate PTH 1-34, Nrf-2, and IGF-I signaling pathways in the response to oxidative stress. These factors could influence IGF-I regulation of metabolic fate and survival in MSCs.

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来源期刊
Regulatory Peptides
Regulatory Peptides 医学-内分泌学与代谢
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审稿时长
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期刊介绍: Regulatory Peptides provides a medium for the rapid publication of interdisciplinary studies on the physiology and pathology of peptides of the gut, endocrine and nervous systems which regulate cell or tissue function. Articles emphasizing these objectives may be based on either fundamental or clinical observations obtained through the disciplines of morphology, cytochemistry, biochemistry, physiology, pathology, pharmacology or psychology.
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