Tanshinone IIA ameliorates lipopolysaccharide-induced inflammatory response in bronchial epithelium cell line BEAS-2B by down-regulating miR-27a.

BACKGROUND: Bronchopneumonia is a common lower respiratory tract inflammatory disease, which is one of main causes of death in infants and young children. Tanshinone IIA (Tan) is a naturally derived anti-inflammatory compound, which has been used for some inflammatory diseases.

OBJECTIVE: Tan was expected to inhibit lipopolysaccharide (LPS)-induced inflammatory damage in human bronchial epithelium cell line BEAS-2B.

METHODS: BEAS-2B cells were stimulated with LPS to mimic an in vitro model of bronchopneumonia. Cell viability and apoptosis were respectively assessed by CCK-8 assay and flow cytometry. The pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) were analyzed by qRT-PCR and quantified by ELISA. Relative miR-27a expression and Bcl-2 expression were detected by qRT-PCR. Cyclin D1 expression, Bcl-2 expression, and main factors in PI3K/AKT and JNK signaling pathways were analyzed by Western blotting. Dual luciferase activity assay was conducted to analyze the target gene of miR-27a.

RESULTS: Treatment of LPS inhibited cell viability, suppressed expression of Cyclin D1, promoted apoptosis, and enhanced secretions of IL-1β, IL-6 and TNF-α, whereas, all effects were reversed by Tan treatment. Moreover, miR-27a expression was decreased by Tan. Tan protected BEAS-2B cells by down-regulating miR-27a. Bcl-2 was a direct target of miR-27a and Bcl-2 overexpression attenuated the cell injury-promoting effect of miR-27a. PI3K/AKT and JNK signaling pathways were inhibited via action of Tan-miR-27a axis.

CONCLUSION: Overall, Tan could protect BEAS-2B cells against LPS-induced inflammation damage via inactivating PI3K/AKT and JNK pathways by down-regulating miR-27a.