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褪黑素治疗通过减轻组织抗氧化能力和炎症反应来预防四氯化碳诱导的大鼠急性肺损伤。

Melatonin treatment prevents carbon tetrachloride-induced acute lung injury in rats by mitigating tissue antioxidant capacity and inflammatory response.

作者信息

Radovic M, Ristic L, Krtinic D, Rancic M, Nickovic V, Vujnovic Zivkovic Z N, Zivkovic J B, Mirkovic M V, Toskic D R, Sokolovic D

出版信息

Bratisl Lek Listy. 2019;120(7):527-531. doi: 10.4149/BLL_2019_085.

DOI:10.4149/BLL_2019_085
PMID:31602989
Abstract

AIM

Carbon tetrachloride (CCl4) is an organic chemical that produces different tissue‑damaging effects when ingested or inhaled. Present study aims to determine whether the application of exogenous melatonin, a neurohormone with numerous biological properties, can prevent disturbances in lung tissue antioxidative capacities and arginine metabolism, tissue inflammation and oxidative damage induced by exposure to CCl4 in rats.

METHODS

The effects of melatonin on the changes occurring in rat lung tissue after an acute exposure to CCl4 were studied by monitoring alterations in antioxidant capacities, inflammatory parameters, parameters of arginine metabolism, and lipid and protein oxidative damage.

RESULTS

The results indicated that melatonin prevents CCl4-induced lung damage by mitigating tissue antioxidant capacity and preventing nitric oxide production through a shift from nitric oxide synthase to arginase. Also, melatonin partially prevented tissue inflammation and molecules' oxidative modification seen after exposure to CCl4.

CONCLUSIONS

The protective activity of melatonin can be attributed to its ability to scavenge both free radicals, as well as to its potential to increase tissue antioxidant capacity. The modulation of inflammatory response through both decrease in tissue inflammatory parameters and influence on arginine-nitric oxide metabolism might be an additional mechanism of action (Tab. 1, Fig. 2, Ref. 33).

摘要

目的

四氯化碳(CCl4)是一种有机化学物质,摄入或吸入后会产生不同的组织损伤效应。本研究旨在确定外源性褪黑素(一种具有多种生物学特性的神经激素)的应用是否能预防大鼠因接触CCl4而引起的肺组织抗氧化能力和精氨酸代谢紊乱、组织炎症和氧化损伤。

方法

通过监测抗氧化能力、炎症参数、精氨酸代谢参数以及脂质和蛋白质氧化损伤的变化,研究褪黑素对大鼠急性接触CCl4后肺组织发生的变化的影响。

结果

结果表明,褪黑素通过减轻组织抗氧化能力以及通过从一氧化氮合酶向精氨酸酶的转变来阻止一氧化氮的产生,从而预防CCl4诱导的肺损伤。此外,褪黑素部分预防了接触CCl4后出现的组织炎症和分子的氧化修饰。

结论

褪黑素的保护活性可归因于其清除自由基的能力以及增加组织抗氧化能力的潜力。通过降低组织炎症参数和影响精氨酸-一氧化氮代谢来调节炎症反应可能是另一种作用机制(表1,图2,参考文献33)。

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