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Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway

Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) am...

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Detalles Bibliográficos
Autores principales: Deng, Guiming, He, Hai, Chen, Zheng, OuYang, Linqi, Xiao, Xiaoqin, Ge, Jinwen, Xiang, Biao, Jiang, Sichen, Cheng, Shaowu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Masson SAS. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678351/
https://www.ncbi.nlm.nih.gov/pubmed/28972887
http://dx.doi.org/10.1016/j.biopha.2017.09.094
Descripción
Sumario:Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) ameliorates lipopolysaccharide(LPS)-induced acute lung injury in rats and aimed to determine the anti-inflammatory effects of LQJD. Rat model with ALI induced by intraperitoneal injection of LPS was treated by oral administration of LQJD. The recruitment of body temperature and the histopathology of lung tissue from all groups were evaluated to grade the severity of the inflammation. The inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α)and interleukin-6 (IL-6), were examined by ELISA assay, and the TLR4 and NF-κBp65 expression levels were evaluated by Real time-PCR and western blotting. It was observed that LQJD reduced the LPS-induced body temperature, inflammatory cytokines level, and lung injuries, and blocked the activation of TLR4/NF-κBp65 signaling in lung tissue. This study demonstrates that LQJD has a protective effect on LPS-induced inflammatory rats through the signaling pathway of TLR4 and NF-κBp65.