Objective: To explore the effect of lncRNA A_30_P01029806 on acute lung injury in sepsis and its mechanism. Methods: Endotoxin(LPS) was used to treat mouse lung epithelial cells(MLE-12) cultured in vitro. The experiment was divided into control group(Ctrl group), LPS treatment group(LPS group), and knockdown A_30_P01029806 group(LPS+si-A30P group) and transfection control group(LPS+si-NC group). Real-time fluorescence quantitative polymerase chain reaction(PCR)(qPCR) was used to detect the expression of A_30_P01029806 in each group of cells. Thiazole blue(MTT) test was used to detect cell viability. Flow cytometry was used to detect apoptosis. Enzyme-linked immunosorbent assay(ELISA) was used to detect the levels of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6). Western blot was used to detect the expression of key proteins in the NF-κB signaling pathway. The NF-κB signaling pathway specific inhibitor BAY11-7082 was added to the LPS+si-A30P cells, and the same method was used to analyze the effects of BAY11-7082 on cell viability, apoptosis, and the expression of TNF-α and IL-6.24 male C57BL/6 mice were randomly divided into sham operation group(Sham group), sepsis group(CLP group), knockdown A_30_P01029806 group(si-A30P group) and siRNA control group(si-NC Group), lung tissues were taken from each group 24 h after modeling, and lung injury semi-quantitative scoring(IQA) was performed to calculate lung wet/dry weight ratio(W/D) content. Results In vitro experiments:Compared with the control group, the cell viability of the LPS group was significantly reduced, the expression level of A_30_P01029806, the apoptosis rate, the phosphorylation level of IκBα and p65 in the cells were significantly increased, and the content of TNF-α and IL-6 was significantly increased, the differences were statistically significant(P<0.05). Compared with the LPS group, the above indicators in the LPS+si-A30P group were significantly reversed, and the differences were statistically significant(P<0.05). There was no statistically significant difference of the above indicators between LPS group and LPS+si-NC group(P>0.05). BAY11-7082 partially reversed the inhibitory effects of knocking down A_30_P01029806 on cell viability, apoptosis and secretion of inflammatory factors.Compared with the Sham group, the lung injury score, W/D ratio and the content of TNF-α and IL-6 in the lung tissue of the CLP group were significantly increased, and the differences were statistically significant(P<0.05). Compared with the CLP group, the lung injury score, W/D ratio, TNF-α and IL-6 content of the si-A30P group were significantly reduced, and the differences were statistically significant(P<0.05).There was no statistically significant difference of the indicators between the CLP group and the si-NC group(P>0.05). Conclusion: Knocking down A_30_P01029806 can reduce acute lung injury in sepsis, and its mechanism may be related to blocking the NF-κB signaling pathway and inhibiting the inflammatory response.
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