Salidroside protects LPS-induced injury in human thyroid follicular epithelial cells by upregulation of MiR-27a

Abstract Aims Hypothyroidism is a common endocrine disease without standard treatment. Salidroside (SAL) has various positive biological activities. In this study, experiments were performed to investigate whether SAL had protective effects on LPS-induced cell inflammatory injury. Main methods The human thyroid follicular epithelial cells (Nthy-ori 3-1) stimulated by LPS were treated with SAL and/or transfected with miR-27a inhibitor. Cell viability and cell apoptosis were detect by Cell Counting Kit-8 assay and flow cytometry, respectively. The expression of Cyclin D1 and apoptosis-related proteins, Notch proteins and NF-κB pathways related proteins were all measured by western blot. The expression of miR-27a and inflammatory chemokines MCP-1, IL-6 and TNF-α was examined by qRT-PCR. The protein weight of MCP-1, IL-6 and TNF-α was detected by ELISA. Key findings LPS treatment induced cell injury by decreasing cell viability, and inducing cell apoptosis and inflammatory chemokines MCP-1, IL-6 and TNF-α. In addition, SAL alleviated LPS-induced cell injury by increasing cell viability, and decreasing cell apoptosis and inflammatory chemokines MCP-1, IL-6 and TNF-α. SAL upregulated miR-27a expression and further study showed that miR-27a downregulation impaired the protective effects of SAL. SAL downregulated the expression of Notch1/2, and phosphorylation of p65 and IκBα. Significance SAL protects against LPS-induced injury in human thyroid follicular epithelial cells by upregulation of miR-27a. This process might be via inactivating Notch and NF-κB pathways.