Schisandrin B Attenuates Inflammation in LPS-Induced Sepsis Through miR-17-5p Downregulating TLR4

• DOI: 10.1007/s10753-018-0931-3
• Publication Date: 2018-12-01T15:50:30Z
• Authors: Zhi-Rong Ji; Wei-Liang Xue; Ling Zhang
• Keywords: Inflammation; Lipopolysaccharides; 0301 basic medicine; Tumor Necrosis Factor-alpha; Macrophages; Interleukin-1beta; Anti-Inflammatory Agents; Down-Regulation; Lignans; 3. Good health; Toll-Like Receptor 4; Cyclooctanes; Mice; MicroRNAs; 03 medical and health sciences; Sepsis; Animals; Polycyclic Compounds

To investigate the mechanism of Schisandrin B (Sch B) on the inflammation in LPS-induced sepsis. Sepsis mouse model was established by injecting LPS. qRT-PCR and western blot were used to measure the expression of miR-17-5p and TLR4. ELISA was used to test the concentrations of IL-1β and TNF-α. Sch B could increase miR-17-5p expression, promote inflammation, and decrease TLR4 expression in sepsis mice and LPS-induced macrophages. Moreover, miR-17-5p could negatively regulate TLR4. Overexpression of miR-17-5p suppressed the concentrations of inflammatory factors (IL-1β and TNF-α) in LPS induced-macrophages, while pcDNA-TLR4 could change the inhibition effect. Additionally, miR-17-5p inhibitor changed the inhibitory effects of Sch B on TLR4 expression and the concentrations of IL-1β and TNF-α in LPS induced-macrophages. Sch B could attenuate inflammation in LPS-induced sepsis through miR-17-5p downregulating TLR4.