BACKGROUND: Pneumonia is a respiratory disease, which is triggered by pathogenic microorganisms or physical/chemical factors. Increasing evidence confirmed the vital impacts of long noncoding RNAs on various inflammatory diseases. Nonetheless, the influence of taurine-upregulated 1 (TUG1) in pneumonia remains vague. The research tried to disclose the protective impacts of TUG1 against lipopolysaccharide (LPS)-evoked injury in MRC-5 cells. METHODS: MRC-5 cells were disposed with LPS to construct pulmonary injury model. Then, pc-TUG1 vector was transfected into MRC-5 cells and the influence of overexpressed TUG1 in cell viability, apoptosis, and pro-inflammatory cytokines in LPS-disposed cells were evaluated. The correlation between TUG1 and microRNA (miR)-127 was estimated via utilizing real-time quantitative polymerase chain reaction (RT-qPCR), meanwhile whether miR-127 affected the impacts of TUG1 on LPS-injured MRC-5 cells was explored. Besides, NF-κB and p38MAPK pathways were evaluated to understand the dormant mechanisms. RESULTS: LPS administration apparently evoked inflammatory injury in MRC-5 cells by restraining cell viability, accelerating apoptosis, and enhancing TNF-α and IL-6 productions. But, TUG1 lightened LPS-evoked pro-inflammatory response in MRC-5 cells. In addition, miR-127 was repressed by overexpressed TUG1, meanwhile the protective impacts of TUG1 against LPS-evoked inflammatory injury in MRC-5 cells were overturned by overexpressed miR-127. Finally, we disclosed that TUG1 hindered the activation of NF-κB and p38MAPK pathways via restraining miR-127. CONCLUSIONS: These explorations testified that taurine-upregulated 1 (TUG1) protected MRC-5 cells against lipopolysaccharide (LPS)-evoked inflammatory injury via hindering miR-127/NF-κB/p38MAPK axis.
BACKGROUND:Pneumonia is a respiratory disease, which is triggered by pathogenic microorganisms or physical/chemical factors. Increasing evidence confirmed the vital impacts of long noncoding RNAs on various inflammatory diseases. Nonetheless, the influence of taurine-upregulated 1 (TUG1) in pneumonia remains vague. The research tried to disclose the protective impacts of TUG1 against lipopolysaccharide (LPS)-evoked injury in MRC-5 cells. METHODS: MRC-5 cells were disposed with LPS to construct pulmonary injury model. Then, pc-TUG1 vector was transfected into MRC-5 cells and the influence of overexpressed TUG1 in cell viability, apoptosis, and pro-inflammatory cytokines in LPS-disposed cells were evaluated. The correlation between TUG1 and microRNA (miR)-127 was estimated via utilizing real-time quantitative polymerase chain reaction (RT-qPCR), meanwhile whether miR-127 affected the impacts of TUG1 on LPS-injured MRC-5 cells was explored. Besides, NF-κB and p38MAPK pathways were evaluated to understand the dormant mechanisms. RESULTS:LPS administration apparently evoked inflammatory injury in MRC-5 cells by restraining cell viability, accelerating apoptosis, and enhancing TNF-α and IL-6 productions. But, TUG1 lightened LPS-evoked pro-inflammatory response in MRC-5 cells. In addition, miR-127 was repressed by overexpressed TUG1, meanwhile the protective impacts of TUG1 against LPS-evoked inflammatory injury in MRC-5 cells were overturned by overexpressed miR-127. Finally, we disclosed that TUG1 hindered the activation of NF-κB and p38MAPK pathways via restraining miR-127. CONCLUSIONS: These explorations testified that taurine-upregulated 1 (TUG1) protected MRC-5 cells against lipopolysaccharide (LPS)-evoked inflammatory injury via hindering miR-127/NF-κB/p38MAPK axis.