[The expression changes in microRNA-132 in the lipopolysaccharide-induced inflammation of rat alveolar macrophages].

Objective To observe the kinetic changes in microRNA-132 (miR-132) expression in rat alveolar macrophages after lipopolysaccharide (LPS)-induced inflammation,and to investigate initially on the role of miR-132 in alveolar macrophages inflammatory response.Methods The rat alveolar macrophages NR8383 cultured without pyrogen in vitro were divided into blank control group and LPS (1 mg/L) stimulated 3,6,12,24 hours groups.Culture supernatants and cell pellets were collected at each time point respectively.Enzyme-linked immunosorbent assay (ELISA) was used to assay the production changes in tumor necrosis factor-α (TNF-α),interleukins (IL-1β and IL-6) in the supernatant.Real-time quantitative polymerase chain reaction (PCR) was used to detect the expression of miR-132 in the cells.Results After stimulating rat alveolar macrophages with LPS,the production of TNF-α (ng/L:364.83 ± 46.29 vs.34.07 ± 8.62,P＜0.01),IL-1 β (ng/L:153.83 ± 43.67 vs.32.33 ± 10.62,P＜0.05) and IL-6 (ng/L:183.85 ± 43.52 vs.42.62 ± 1 1.21,P＜0.05) were all increased significantly at 3 hours post LPS stimulation compared with blank control group,reached the peak at 12 hours (TNF-α:605.09 ± 57.13,IL-1β:377.09 ± 28.55,IL-6:558.04 ± 77.45,all P＜0.01),and descended at 24 hours (TNF-α:281.95 ± 41.61,IL-1β:263.17 ± 51.36,IL-6:438.74 ±79.94) but the levels remained significantly higher than blank control group (all P＜0.01).The expression of miR-132 started to rise at 3 hours after LPS stimulation compared with blank control group [(1.12 ± 0.11) folds,P=0.995],and presented a gradual increasing trend at 6,12,24 hours [(5.98 ± 0.65),(7.64 ± 0.53),(8.92 ±0.83) folds,all P＜0.01].Conclusion The expression of miR-132 increased gradually over time after LPS-induced inflammation of rat alveolar macrophages,suggesting that miR-132 may be involved in regulation of rat alveolar macrophages inflammatory response. Key words: MicroRNA-132;  Lipopolysaccharide;  Alveolar macrophage;  Inflammatory response