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首页> 外文期刊>Archives of Toxicology >Metallothionein attenuates carmustine-induced oxidative stress and protects against pulmonary fibrosis in rats
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Metallothionein attenuates carmustine-induced oxidative stress and protects against pulmonary fibrosis in rats

机译：金属硫蛋白可减轻卡莫司汀诱导的氧化应激并防止大鼠肺纤维化

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摘要

The present study was carried out to evaluate the effect of exogenously administered metallothionein (MT) against carmustine (BCNU)-induced lung toxicity in rats. A total of 60 rats were randomly divided into four groups (15/group): control group in which the animals received 0.5 ml physiologic saline containing 10% ethanol (IP) weekly, MT-administered group in which rats received MT (30 μmol/kg, IP) weekly, BCNU-administered group in which rats received BCNU (5 mg/kg, IP) weekly and MT + BCNU group in which rats received weekly doses of BCNU (5 mg/kg, IP) followed 24 h later by MT (30 μmol/kg, IP). At the end of the experiment (after 6 weeks), lung histological changes, collagen staining, the activity of glutathione reductase (GR) and contents of reduced glutathione (GSH) and hydroxyproline (Hpr) in the lung as well as serum level of tumor necrosis factor-alpha (TNF-α) were evaluated. The obtained data revealed that BCNU induced pathological changes and markedly increased lung collagen and level of Hpr but decreased GSH content and GR activity and increased serum TNF-α compared to both control and MT-administered rats. Administration of MT + BCNU markedly improved histological features and decreased staining of collagen along with increased GR activity, GSH content but decreased level of Hpr in lung tissue as well as decreased serum level of TNF-α compared with BCNU-treated rats. Based on our results, it is possible to postulate that exogenous MT can act against BCNU-induced lung toxicity by a mechanism related, at least in part, to its ability to decrease oxidative stress and fibrosis.
机译：本研究旨在评估外源性金属硫蛋白（MT）对卡马汀（BCNU）诱导的大鼠肺毒性的影响。将60只大鼠随机分为四组（每组15只）：对照组（每只动物每周接受0.5 ml含10％乙醇（IP）的生理盐水），MT施用组，每只大鼠接受MT（30μmol/ kg，IP）每周，BCNU给药组，大鼠每周接受BCNU（5 mg / kg，IP），MT + BCNU组，大鼠每周接受BCNU（5 mg / kg，IP），随后24 h MT（30μmol/ kg，IP）。实验结束（6周后），肺组织学变化，胶原蛋白染色，谷胱甘肽还原酶（GR）活性和肺中还原型谷胱甘肽（GSH）和羟脯氨酸（Hpr）含量以及血清肿瘤水平评估坏死因子-α（TNF-α）。获得的数据表明，与对照组和MT组相比，BCNU引起病理变化，肺胶原和Hpr水平显着增加，但GSH含量和GR活性降低，血清TNF-α升高。与BCNU治疗的大鼠相比，MT + BCNU的给药显着改善了组织学特征，减少了胶原蛋白的染色，同时增加了GR活性，GSH含量，但肺组织中的Hpr水平降低，血清TNF-α水平降低。根据我们的结果，可能推测外源性MT可以通过至少部分与其减少氧化应激和纤维化能力有关的机制来对抗BCNU诱导的肺毒性。

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