Autor: |
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 |
Předmět: |
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Zdroj: |
Traditional Medicine Research; Jun2024, Vol. 9 Issue 6, p1-9, 9p |
Abstrakt: |
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] |
Databáze: |
Complementary Index |
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