Evodiamine Enhanced The Anti-Inflammation Effect Of Clindamycin In The Beas-2b Cells Infected With H5n1 And Pneumoniae D39 Through Creb-C/Ebp Beta Signaling Pathway

Pneumonia is a pulmonary disease among children. Evodiamine, a traditional Chinese medicine, is known for anti-inflammatory effect. This study aimed to investigate the impact of evodiamine on severe pneumonia-like cells and the underlying mechanism involved. H5N1 and pneumoniae D39 was used to induce severe pneumonia-like conditions in BEAS-2B cells. The cell viability in BEAS-2B cells after treatments with 0, 20, 40, 60, 80, and 100 mu M evodiamine was examined using MTT assays. The protein concentrations of inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-1 beta, and Toll-like receptors (TLRs) were measured by enzyme-linked immunosorbent assay methods and the protein and mRNA changes in C/EBP beta/CREB were measured using Real Time-quantitative polymerase chain reaction and Western blot methods. Our results revealed that Evodiamine significantly decreased TNF-alpha, IL-6, and IL-1 beta in BEAS-2B cells. Moreover, evodiamine markedly reduced TLR2,3,4 protein expression and the phosphorylated protein of C/EBP beta and CREB. Besides, evodiamine combined with clindamycin exerted more significant effects than clindamycin alone. Taken together, our results demonstrated that evodiamine enhanced the anti-inflammation effect of clindamycin in the BEAS-2B cells infected with H5N1 and pneumoniae D39 through CREB-C/EBP beta signaling pathway.