The protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2023-05-01 DOI:10.4149/gpb_2023006

Chouhui Xuan, Can Jin, Zhengyong Jin, Yongxue Chi

{"title":"The protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway.","authors":"Chouhui Xuan, Can Jin, Zhengyong Jin, Yongxue Chi","doi":"10.4149/gpb_2023006","DOIUrl":null,"url":null,"abstract":"<p><p>Glutamine is proven to have potential therapeutic effects on decreasing hyperoxia-induced acute pulmonary injury. The aim of this study is to investigate the effects and mechanism of glutamine on bronchopulmonary dysplasia (BPD) induced by hyperoxia in rat alveolar type II epithelial cells (AECIIs) RLE-6TN. Following hyperoxia induction and glutamine treatment, ROS levels were detected by DCFH-DA assay and TUNEL staining was performed to detect cell apoptosis. The levels of inflammatory indicators and expression of apoptosis-related proteins were detected through ELISA and Western blot, respectively. Besides, the expression of related proteins in mitogen-activated protein kinase phosphatase-1 (MKP-1)/mitogen-activated protein kinases (MAPK)/cytoplasmic phospholipase A2 (cPLA2) signaling was also detected by Western blot. To further analyze the role of MKP-1/MAPK/cPLA2 signaling, MKP-1 was silenced and anisomycin was used to treat cells, respectively. It was shown that glutamine significantly decreased inflammation, oxidative stress and apoptosis in hyperoxia-induced cells while MKP-1 interference and anisomycin were able to reverse these effects, suggesting that the protective effects of glutamine on BPD induced by hypoxia were related to MKP-1/MAPK/cPLA2 signaling. To sum up, glutamine protected against BPD by decreasing inflammation, oxidative stress and apoptosis via MKP-1/MAPK/cPLA2 signaling.</p>","PeriodicalId":1,"journal":{"name":"Accounts of Chemical Research","volume":null,"pages":null},"PeriodicalIF":16.4000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Accounts of Chemical Research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.4149/gpb_2023006","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}

引用次数: 0

Abstract

Glutamine is proven to have potential therapeutic effects on decreasing hyperoxia-induced acute pulmonary injury. The aim of this study is to investigate the effects and mechanism of glutamine on bronchopulmonary dysplasia (BPD) induced by hyperoxia in rat alveolar type II epithelial cells (AECIIs) RLE-6TN. Following hyperoxia induction and glutamine treatment, ROS levels were detected by DCFH-DA assay and TUNEL staining was performed to detect cell apoptosis. The levels of inflammatory indicators and expression of apoptosis-related proteins were detected through ELISA and Western blot, respectively. Besides, the expression of related proteins in mitogen-activated protein kinase phosphatase-1 (MKP-1)/mitogen-activated protein kinases (MAPK)/cytoplasmic phospholipase A2 (cPLA2) signaling was also detected by Western blot. To further analyze the role of MKP-1/MAPK/cPLA2 signaling, MKP-1 was silenced and anisomycin was used to treat cells, respectively. It was shown that glutamine significantly decreased inflammation, oxidative stress and apoptosis in hyperoxia-induced cells while MKP-1 interference and anisomycin were able to reverse these effects, suggesting that the protective effects of glutamine on BPD induced by hypoxia were related to MKP-1/MAPK/cPLA2 signaling. To sum up, glutamine protected against BPD by decreasing inflammation, oxidative stress and apoptosis via MKP-1/MAPK/cPLA2 signaling.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

谷氨酰胺对支气管肺发育不良的保护作用与MKP-1/MAPK/cPLA2信号介导的NF-kappaB通路有关。

谷氨酰胺对降低高氧性急性肺损伤具有潜在的治疗作用。本研究旨在探讨谷氨酰胺对大鼠肺泡II型上皮细胞(AECIIs) RLE-6TN高氧诱导的支气管肺发育不良(BPD)的影响及其机制。高氧诱导和谷氨酰胺处理后，采用DCFH-DA法检测ROS水平，TUNEL染色检测细胞凋亡。分别通过ELISA和Western blot检测各组炎症指标水平和凋亡相关蛋白表达。Western blot检测丝裂原活化蛋白激酶磷酸酶-1 (MKP-1)/丝裂原活化蛋白激酶(MAPK)/细胞质磷脂酶A2 (cPLA2)信号通路相关蛋白的表达。为了进一步分析MKP-1/MAPK/cPLA2信号通路的作用，我们分别沉默MKP-1和用大霉素处理细胞。结果表明，谷氨酰胺可显著降低高氧诱导的BPD细胞的炎症、氧化应激和凋亡，而MKP-1干扰和大霉素可逆转这些作用，提示谷氨酰胺对缺氧诱导的BPD的保护作用与MKP-1/MAPK/cPLA2信号通路有关。综上所述，谷氨酰胺通过MKP-1/MAPK/cPLA2信号通路减少炎症、氧化应激和细胞凋亡，从而对BPD具有保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.

期刊最新文献

Management of Cholesteatoma: Hearing Rehabilitation. Congenital Cholesteatoma. Evaluation of Cholesteatoma. Management of Cholesteatoma: Extension Beyond Middle Ear/Mastoid. Recidivism and Recurrence.