Berberine Alleviates Acute Lung Injury in Septic Mice by Modulating Treg/Th17 Homeostasis and Downregulating NF-KB Signaling

doi:10.2147/DDDT.S401293

科研成果详情

题名	Berberine Alleviates Acute Lung Injury in Septic Mice by Modulating Treg/Th17 Homeostasis and Downregulating NF-KB Signaling
作者	Chen, Longwang 1; Liu, Xinyong 2; Wang, Xuetao 3; Lu, Zhongqiu1; Ye, Yumei4
发表日期	2023
发表期刊	DRUG DESIGN DEVELOPMENT AND THERAPY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	berberine sepsis inflammation cell differentiation immunodeficiency T lymphocyte
其他关键词	SEPSIS ; CELLS ; INFLAMMATION ; DYSFUNCTION ; INHIBITION ; EXPRESSION ; MORTALITY ; IMBALANCE ; PATHWAY
摘要	Purpose: A common complication of sepsis is acute lung injury (ALI), which is associated with an acute onset, rapid disease changes, and high mortality. Regulatory T (Treg) and T helper 17 (Th17) cells comprise CD4+ T cell subsets, which strongly influence inflammation during ALI. In this study, we investigated the effect of berberine (BBR), an antioxidant, anti-inflammatory, and immunomodulatory drug, on the inflammatory response and immune state in mice with sepsis.Methods: A mouse model of cecal ligation and puncture (CLP) was established. The mice were intragastrically administered 50 mg/ kg BBR. We used histological techniques to evaluate inflammatory tissue injury and flow cytometry for analyzing Treg/Th17 levels. We also assessed NF-KB signaling pathways by Western blotting assays and immunofluorescence staining. Enzyme-linked immuno-sorbent assay (ELISA) was performed to measure the content of cytokines. Results: Treatment with BBR considerably mitigated lung injury while improving survival, post-cecal ligation, and puncture (CLP). Treatment with BBR ameliorated pulmonary edema and hypoxemia in septic mice and inhibited the NF-KB signaling pathway. BBR also increased Treg cells and decreased Th17 proportions in the spleen and lung tissue of CLP-treated mice. Blocking Treg cells weakened the protective effect of BBR on sepsis-associated lung injury. Conclusion: Overall, these results suggested that BBR is a potential therapeutic agent for sepsis.
资助项目	Wenzhou Municipal Science and Technology Project [Y2020094]; Natural Science Foundation of Zhejiang Province [LQ22H150003]; National Key R&D Program of China [2018YFC2000305]
出版者	DOVE MEDICAL PRESS LTD
ISSN	1177-8881
卷号	17 页码:1139-1151
DOI	10.2147/DDDT.S401293
页数	13
WOS类目	Chemistry, Medicinal ; Pharmacology & Pharmacy
WOS研究方向	Pharmacology & Pharmacy
WOS记录号	WOS:000970762600001
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	37077411
SCOPUSEID	2-s2.0-85152978290
通讯作者地址	[Ye, Yumei]Department of Ultrasound Imaging,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China
Scopus学科分类	Pharmacology;Pharmaceutical Science;Drug Discovery
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/174844
专题	附属第一医院附属第一医院_超声影像科
通讯作者	Ye, Yumei
作者单位	1.Department of Emergency,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China; 2.Department of Critical Care Medicine,Affiliated Jinhua Hospital,Zhejiang University School of Medicine,Zhejiang,Jinhua,China; 3.Department of Intensive Care Unit,Wenzhou Longwan District First People’s Hospital,Zhejiang,Wenzhou,China; 4.Department of Ultrasound Imaging,the First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China
第一作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
通讯作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
第一作者的第一单位	附属第一医院
推荐引用方式 GB/T 7714	Chen, Longwang,Liu, Xinyong,Wang, Xuetao,et al. Berberine Alleviates Acute Lung Injury in Septic Mice by Modulating Treg/Th17 Homeostasis and Downregulating NF-KB Signaling[J]. DRUG DESIGN DEVELOPMENT AND THERAPY,2023,17:1139-1151.
APA	Chen, Longwang, Liu, Xinyong, Wang, Xuetao, Lu, Zhongqiu, & Ye, Yumei. (2023). Berberine Alleviates Acute Lung Injury in Septic Mice by Modulating Treg/Th17 Homeostasis and Downregulating NF-KB Signaling. DRUG DESIGN DEVELOPMENT AND THERAPY, 17, 1139-1151.
MLA	Chen, Longwang,et al."Berberine Alleviates Acute Lung Injury in Septic Mice by Modulating Treg/Th17 Homeostasis and Downregulating NF-KB Signaling".DRUG DESIGN DEVELOPMENT AND THERAPY 17(2023):1139-1151.