About: Effects of Xinjiaxiangruyin on the TLR7 pathway in influenza virus-infected lungs of mice housed in a hygrothermal environment

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About: Effects of Xinjiaxiangruyin on the TLR7 pathway in influenza virus-infected lungs of mice housed in a hygrothermal environment Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Effects of Xinjiaxiangruyin on the TLR7 pathway in influenza virus-infected lungs of mice housed in a hygrothermal environment
Creator	Jiang, Zhen-You Zheng, Xiao Fu, Ying-Jie Shi, Shan-Shan Wu, Sha Yan, Yu-Qi
source	Medline; PMC
abstract	BACKGROUND: To investigate the effects and immunological mechanisms of the traditional Chinese medicine Xinjiaxiangruyin on controlling influenza virus (FM1 strain) infection in mice housed in a hygrothermal environment. METHODS: Mice were housed in normal and hygrothermal environments, and intranasally infected with influenza virus (FM1). A high-performance liquid chromatography fingerprint of Xinjiaxiangruyin was used to provide an analytical method for quality control. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to measure messenger RNA expression of Toll-like receptor 7 (TLR7), myeloid differentiation primary response 88 (MyD88), and nuclear factor-kappa B (NF-κB) p65 in the TLR7 signaling pathway and virus replication in the lungs. Western blotting was used to measure the expression levels of TLR7, MyD88, and NF-κB p65 proteins. Flow cytometry was used to detect the proportion of Th17/T-regulatory cells. RESULTS: Xinjiaxiangruyin effectively alleviated lung inflammation in C57BL/6 mice in hot and humid environments. Guizhimahuanggebantang significantly reduced lung inflammation in C57BL/6 mice. The expression of TLR7, MyD88, and NF-κB p65 mRNA in lung tissue of WT mice in the normal environment, GZMHGBT group was significantly lower than that in the model group (P < 0.05). In WT mice exposed to the hot and humid environment, the expression levels of TLR7, MyD88, and NF-κB p65 mRNA in the XJXRY group were significantly different from those in the virus group. The expression levels of TLR7, MyD88, and NF-κB p65 protein in lung tissue of WT mice exposed to the normal environment, GZMHGBT group was significantly lower than those in the model group. In WT mice exposed to hot and humid environments, the expression levels of TLR7, MyD88, and NF-κB p65 protein in XJXRY group were significantly different from those in the virus group. CONCLUSION: Guizhimahuanggebantang demonstrated a satisfactory therapeutic effect on mice infected with the influenza A virus (FM1 strain) in a normal environment, and Xinjiaxiangruyin demonstrated a clear therapeutic effect in damp and hot environments and may play a protective role against influenza through downregulation of the TLR7 signal pathway.
has issue date	2019-09-27(xsd:dateTime)
bibo:doi	10.1186/s13020-019-0256-7
bibo:pmid	31572491
has license	cc-by
sha1sum (hex)	f3f9545f7a7fee9a2b6d72c0cd36ca66687809be
schema:url	https://doi.org/10.1186/s13020-019-0256-7
resource representing a document's title	Effects of Xinjiaxiangruyin on the TLR7 pathway in influenza virus-infected lungs of mice housed in a hygrothermal environment
has PubMed Central identifier	PMC6764144
has PubMed identifier	31572491
schema:publication	Chin Med
resource representing a document's body	covid:f3f9545f7a7fee9a2b6d72c0cd36ca66687809be#body_text
is schema:about of	named entity 'MICE' named entity 'PATHWAY' named entity 'EFFECTS' named entity 'infection' named entity 'INFECTED' named entity 'BACKGROUND' named entity 'TRADITIONAL CHINESE MEDICINE' named entity 'TO INVESTIGATE' named entity 'INFLUENZA VIRUS' named entity 'HOUSED' named entity 'EFFECTS' named entity 'HOUSED' named entity 'LUNGS' named entity 'ENVIRONMENT' named entity 'TLR7' named entity 'INFLUENZA VIRUS' named entity 'MICE' named entity 'IMMUNOLOGICAL' named entity 'INFECTION' named entity 'STRAIN' named entity 'ENVIRONMENT' named entity 'MECHANISMS' named entity 'CONTROLLING' covid:arg/f3f9545f7a7fee9a2b6d72c0cd36ca66687809be named entity 'effects' named entity 'controlling' named entity 'FlowJo' named entity 'cytokine' named entity 'upper respiratory tract infections' named entity 'mice' named entity 'immunological' named entity 'lungs' named entity 'microbial' named entity 'PVDF' named entity 'weight loss' named entity 'gene' named entity 'Bonferroni correction' named entity 'forsythia' named entity 'left lung' named entity 'spleen' named entity 'autoimmune' named entity 'treatment groups' named entity 'virus' named entity 'influenza' named entity 'anti-viral' named entity 'humidity' named entity 'alveolar' named entity 'TLR7' named entity 'influenza virus' named entity 'pathogens' named entity 'clinical treatment' named entity 'MyD88' named entity 'lung tissue' named entity 'protein' named entity 'TLR7' named entity 'organism' named entity 'virus' named entity 'Tregs' named entity 'Endogenous' named entity 'volumetric flask' named entity 'morphology' named entity 'mice' named entity 'BSA' named entity 'flow cytometer' named entity 'influenza' named entity 'MyD88' named entity 'anti-allergy' named entity 'TLR7' named entity 'oseltamivir' named entity 'transcription factors' named entity 'chloral hydrate' named entity 'traditional Chinese medicines' named entity 'pharmacology' named entity 'TLR7' named entity 'plague' named entity 'influenza A virus'

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