MicroRNA-146 protects A549 and H1975 cells from LPS-induced apoptosis and inflammation injury |
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Authors: | Qiang Wang Dagang Li Yuquan Han Xiaoqian Ding Tao Xu Bingjian Tang |
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Affiliation: | 1.Department of Respiratory,The Affiliated Hospital of Qingdao University,Qingdao,China;2.Department of Respiratory, East Medical District,Linyi People’s Hospital,Linyi,China;3.Department of Emergency,Qingdao Huangdao District People’s Hospital,Qingdao,China;4.Department of Respiratory,Linqing People’s Hospital,Linqing,China |
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Abstract: | Pneumonia is an inflammatory condition affecting the lungs, in which pro-inflammatory cytokines are secreted. It has been shown that microRNA-146 (miR-146) is involved in the regulation of immune and inflammatory responses. The present study explored the protective effects of miR-146 overexpression on lipopolysaccharide (LPS)-mediated injury in A549 and H1975 cells. In this study, A549 and H1975 cells were transfected with miR-146 mimic or inhibitor, and then were subjected with LPS. Thereafter, cell viability, colony formation capacity, apoptosis, the release of proinflammatory factors, Sirt1 expression, and the expression of NF-κB and Notch pathway proteins were respectively assessed. As a result, miR-146 overexpression exerted protective functions on LPS-damaged A549 and H1975 cells, as evidenced by the increases in cell viability and colony number, the decrease in apoptotic cell rate, as well as the down-regulations of IL-1, IL-6, and TNF-α. Sirt1 can be positively regulated by miR-146. Furthermore, miR-146 overexpression blocked NF-κB and Notch pathways, while these blocking effects were abolished when Sirt1 was silenced. The findings in the current study indicated that miR-146 protected A549 and H1975 cells from LPS-induced apoptosis and inflammation injury. miR-146 exerted protective functions might be via up-regulation of Sirt1 and thereby blocking NF-κB and Notch pathways. |
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