EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response

Abstract Acute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer prop...

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Autores principales: Mian Wang, Hua Zhong, Xian Zhang, Xin Huang, Jing Wang, Zihao Li, Mengshi Chen, Zhenghui Xiao
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/ebbaa7305f0741cfa6ad2a7d9ac81215
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spelling oai:doaj.org-article:ebbaa7305f0741cfa6ad2a7d9ac812152021-12-02T15:49:31ZEGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response10.1038/s41598-021-90398-x2045-2322https://doaj.org/article/ebbaa7305f0741cfa6ad2a7d9ac812152021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90398-xhttps://doaj.org/toc/2045-2322Abstract Acute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer properties, including epigallocatechin-3-gallate (EGCG). In the present study, protein kinase C alpha (PRKCA) is involved in EGCG protection against LPS-induced inflammation and ALI. EGCG treatment attenuated LPS-stimulated ALI in mice as manifested as improved lung injury scores, decreased total cell amounts, neutrophil amounts and macrophage amounts, inhibited the activity of MPO, decreased wet-to-dry weight ratio of lung tissues, and inhibited release of inflammatory cytokines TNF-α, IL-1β, and IL-6. PRKCA mRNA and protein expression showed to be dramatically decreased by LPS treatment while reversed by EGCG treatment. Within LPS-stimulated ALI mice, PRKCA silencing further aggravated, while PRKCA overexpression attenuated LPS-stimulated inflammation and ALI through MAPK signaling pathway. PRKCA silencing attenuated EGCG protection. Within LPS-induced RAW 264.7 macrophages, EGCG could induce PRKCA expression. Single EGCG treatment or Lv-PRKCA infection attenuated LPS-induced increases in inflammatory factors; PRKCA silencing could reverse the suppressive effects of EGCG upon LPS-stimulated inflammatory factor release. In conclusion, EGCG pretreatment inhibits LPS-induced ALI in mice. The protective mechanism might be associated with the inhibitory effects of PRKCA on proinflammatory cytokine release via macrophages and MAPK signaling pathway.Mian WangHua ZhongXian ZhangXin HuangJing WangZihao LiMengshi ChenZhenghui XiaoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Mian Wang
Hua Zhong
Xian Zhang
Xin Huang
Jing Wang
Zihao Li
Mengshi Chen
Zhenghui Xiao
EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
description Abstract Acute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer properties, including epigallocatechin-3-gallate (EGCG). In the present study, protein kinase C alpha (PRKCA) is involved in EGCG protection against LPS-induced inflammation and ALI. EGCG treatment attenuated LPS-stimulated ALI in mice as manifested as improved lung injury scores, decreased total cell amounts, neutrophil amounts and macrophage amounts, inhibited the activity of MPO, decreased wet-to-dry weight ratio of lung tissues, and inhibited release of inflammatory cytokines TNF-α, IL-1β, and IL-6. PRKCA mRNA and protein expression showed to be dramatically decreased by LPS treatment while reversed by EGCG treatment. Within LPS-stimulated ALI mice, PRKCA silencing further aggravated, while PRKCA overexpression attenuated LPS-stimulated inflammation and ALI through MAPK signaling pathway. PRKCA silencing attenuated EGCG protection. Within LPS-induced RAW 264.7 macrophages, EGCG could induce PRKCA expression. Single EGCG treatment or Lv-PRKCA infection attenuated LPS-induced increases in inflammatory factors; PRKCA silencing could reverse the suppressive effects of EGCG upon LPS-stimulated inflammatory factor release. In conclusion, EGCG pretreatment inhibits LPS-induced ALI in mice. The protective mechanism might be associated with the inhibitory effects of PRKCA on proinflammatory cytokine release via macrophages and MAPK signaling pathway.
format article
author Mian Wang
Hua Zhong
Xian Zhang
Xin Huang
Jing Wang
Zihao Li
Mengshi Chen
Zhenghui Xiao
author_facet Mian Wang
Hua Zhong
Xian Zhang
Xin Huang
Jing Wang
Zihao Li
Mengshi Chen
Zhenghui Xiao
author_sort Mian Wang
title EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
title_short EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
title_full EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
title_fullStr EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
title_full_unstemmed EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response
title_sort egcg promotes prkca expression to alleviate lps-induced acute lung injury and inflammatory response
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/ebbaa7305f0741cfa6ad2a7d9ac81215
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