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. 2021 Oct 1;12(10):898. doi: 10.1038/s41419-021-04180-y

Fig. 7. LncRNA NLRP3/miR-138-5p/NLRP3 functions via the ceRNET during the NLRP3-triggered inflammatory response in vivo.

Fig. 7

Rat lungs were injected with PBS in the control group and LPS-treated rats were further treated with si-r-lncRNA NLRP3, Lv-lncRNA NLRP3, agomiR-138-5p, antagomiR-138-5p, Lv-lncRNA NLRP3 + agomiR-138-5p, and si-r-lncRNA NLRP3 + antagomiR-138-5p. A Lung tissue samples were collected 6 h after establishing LPS-induced ALI to analyse the histopathological changes (×200, ×400). The black arrow indicates neutrophil infiltration, pulmonary oedema, alveolar wall thickening, and alveolar haemorrhage. B The lung injury score was determined via H&E staining, a representative histological analysis (n = 6 animals per group). C ELISA was used to measure the BALF albumin content. D Detection of the lung W/D ratio in rats. E MPO activity in the lung tissues of rats. F, G Immunohistochemical detection of the NLRP3 contents in rat lung tissues (×200, ×400). H The inflammatory response in NR8383 AM cells was suppressed by si-r-lncRNA NLRP3 and miR-138-5p mimics alone or in combination, as shown by the decreased number of cells colabeled with CD68 (green) and NLRP3 (red). LncRNA NLRP3 overexpression, miR-138-5p inhibition, and NLRP3 augmented the inflammatory response in LPS-induced ALI with more NLRP3 and CD68 anchored in the plasma membrane of the AM cells. The data are presented as mean ± SE (n = 6). *P < 0.05; **P < 0.01; ***P < 0.001; NS, no statistically significant difference.