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N-乙酰半胱氨酸通过抑制炎症、氧化和凋亡对脓毒症大鼠急性肺损伤的保护作用。

Protective effect of N-acetylcysteine on acute lung injury in septic rats by inhibiting inflammation, oxidation, and apoptosis.

作者信息

Le Jian-Wei, Sun Min, Zhu Jian-Hua, Fan Heng

机构信息

Department of Intensive Care Unit, Ningbo First Hospital, Ningbo, Zhejiang Province, P.R China.

出版信息

Iran J Basic Med Sci. 2022 Jul;25(7):859-864. doi: 10.22038/IJBMS.2022.65350.14384.

DOI:10.22038/IJBMS.2022.65350.14384
PMID:36033949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9392567/
Abstract

OBJECTIVES

Acute lung injury (ALI) is a common comorbidity in patients with sepsis, and finding drugs that can effectively reduce its mortality is a hot spot in current research. The purpose of this study is to explore the protective mechanism of N-acetylcysteine (NAC) on ALI in septic rats.

MATERIALS AND METHODS

We used NAC to intervene in septic rats to evaluate the plasma inflammatory factors and lung tissue pathological damage. Biochemical methods were used to determine the levels of oxidases in lung tissue, the expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) proteins, and observed lung tissue cell apoptosis.

RESULTS

NAC pretreatment decreased the mortality of septic rats, improved lung tissue pathological damage, reduced the levels of tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-8, and malondialdehyde, and increased activity of superoxide dismutase, glutathione peroxidase, and catalase. Moreover, NAC pretreatment significantly decreased iNOS protein expression and increased eNOS protein expression in lung tissue. Meanwhile, NAC significantly decreased the number of apoptosis and the levels of Bax and Caspase-3 mRNA and increased the level of Bcl-2 mRNA in the lung tissue of septic rats.

CONCLUSION

NAC protects ALI in septic rats by inhibiting inflammation, oxidative stress, and apoptosis.

摘要

目的

急性肺损伤(ALI)是脓毒症患者常见的合并症,寻找能有效降低其死亡率的药物是当前研究的热点。本研究旨在探讨N-乙酰半胱氨酸(NAC)对脓毒症大鼠ALI的保护机制。

材料与方法

我们用NAC干预脓毒症大鼠,以评估血浆炎症因子和肺组织病理损伤。采用生化方法测定肺组织中氧化酶水平、诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)蛋白的表达,并观察肺组织细胞凋亡情况。

结果

NAC预处理降低了脓毒症大鼠的死亡率,改善了肺组织病理损伤,降低了肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、白细胞介素-8和丙二醛水平,并提高了超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性。此外,NAC预处理显著降低了肺组织中iNOS蛋白的表达,增加了eNOS蛋白的表达。同时,NAC显著降低了脓毒症大鼠肺组织中的凋亡细胞数量以及Bax和Caspase-3 mRNA水平,并增加了Bcl-2 mRNA水平。

结论

NAC通过抑制炎症、氧化应激和凋亡来保护脓毒症大鼠的ALI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/a1416de6a44c/IJBMS-25-859-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/05d0870a7e40/IJBMS-25-859-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/1d29dffdaf68/IJBMS-25-859-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/1569b241ae79/IJBMS-25-859-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/f27d0e399a7e/IJBMS-25-859-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/a1416de6a44c/IJBMS-25-859-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/05d0870a7e40/IJBMS-25-859-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/1d29dffdaf68/IJBMS-25-859-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/1569b241ae79/IJBMS-25-859-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/f27d0e399a7e/IJBMS-25-859-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a8/9392567/a1416de6a44c/IJBMS-25-859-g005.jpg

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