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Pudilan Xiaoyan oral liquid regulates tissue inflammation and apoptosis in mice with influenza virus pneumonia.

Authors :
Shan Cao
Shuang-Rong Gao
Chen Ni
Zi-Han Geng
Ying-Li Xu
Bo Pang
Meng-Ping Chen
Yu Zhang
Shan-Shan Guo
Yu-Jing Shi
Li-Qi Ni
Kun Wang
Rong-Hua Zhao
Xiao-Lan Cui
Yan-Yan Bao
Source :
Traditional Medicine Research; Jun2024, Vol. 9 Issue 6, p1-9, 9p
Publication Year :
2024

Abstract

Background: The influenza A virus is the primary cause of respiratory infections and poses a global health risk. Pudilan Xiaoyan oral liquid (PDL) exhibits anti-inflammatory and immunomodulatory properties. PDL is commonly employed in clinical practice to manage upper respiratory tract infections. However, there is still much to uncover regarding its potential therapeutic mechanism. Methods: Institute of cancer research mice were infected with influenza A virus via nasal drip. The general state of the mice, lung index, and lung index inhibition rate were used to evaluate the efficacy of PDL. Enzyme-linked immunosorbent assay, western blotting, and immunohistochemistry were used to observe the presence of proteins and cytokines in the lung tissue. Apoptosis was evaluated using the TUNEL assay. Results: PDL improved the mental state of influenza A virus-infected mice, reduced the lung index, and inhibited viral replication. The expression of interleukin-1β and tumor necrosis factor-α were decreased, whereas the expression of interleukin-10 in the lung tissue was increased due to PDL treatment. In addition, PDL treatment modulated Toll-like receptor 4 and MyD88 expressions in the lung tissues. PDL significantly reduced apoptosis and decreased cleaved caspase-3 and PARP levels, whereas increased B-cell lymphoma-2 expression in the lung tissue. Notably, the moderate-dose group of PDL exhibited a more pronounced effect. These findings indicate that PDL exerts a protective effect against pneumonia injury in influenza A virus-infected mice. Conclusion: PDL inhibited the inflammatory response and regulated apoptosis by regulating Toll-like receptor 4 and MyD88 protein expressions, thereby protecting the lung tissue from viral infection-induced lung tissue injury. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
24133973
Volume :
9
Issue :
6
Database :
Complementary Index
Journal :
Traditional Medicine Research
Publication Type :
Academic Journal
Accession number :
177074704
Full Text :
https://doi.org/10.53388/TMR20231010001