[Mechanisms of musk and olibanum regulating inflammatory cascade reaction triggered by chemotactic and activated monocytes]

To study the effects of drug plasma of musk and olibanum (DP-MO) on the release of inflammatory cytokines from monocytes and the expressions of the proteins associated with inflammation of prostatic or endothelial cells induced by prostate antigen (PAg) stimulation.We prepared DP-MO using SD rats and monocytes and PAgs using BALB/c mice. We pre-treated the monocytes with DP-MO at the gradient concentrations of 0, 2.5, 5, 10, and 20% for 1 hour, activated them with PAgs, and then cultured them for 96 hours, followed by detection of the release of inflammatory cytokines. We co-cultured the prostate RWPE-1 cells with the endothelial EA. hy926 cells, pre-treated them with the same gradient concentrations of DP-MO as above for 1 hour, activated with PAgs, and cultured for 96 hours. Then we determined the expression levels of the proteins associated with inflammation of RWPE-1 and EA. hy926 cells by Western blot.DP-MO decreased the levels of TNF-alpha, IL-1beta, IL-6, and IL-8 and increased that of IL-10 in a concentration-dependent manner. Significant differences were found between the 20% P-MO and PAg groups in the release of the inflammatory cytokines TNF-alpha (70.8 +/- 22.3 vs. 277.1 +/- 65.5, P0.01) , IL-113 (277.5 +/- 22.6 vs. 630.4 +/- 89.7, P0.01), IL-6 (232.7 +/- 62.7 vs. 994.2 vs. 182.3, P0.01), IL-8 (227.3 +/- 79.2 vs. 769.3 +/- 284.1, P0.01), and IL-10 (640.2 +/- 201.2 vs. 271.1 +/- 55.8, P0.01). Compared with the PAg group, the 10 and 20% P-MO groups showed remarkable decreases in the protein expression of MCP-1/CCL2 in the RWPE-1 cells (1.12 +/- 0.34 vs. 0.56 +/- 0.11 and 0.34 +/- 0.08) and that of VCAM-1 in the EA. hy926 cells (0.94 +/- 0.22 vs. 0.52 +/- 0.17 and 0.38 +/- 0.12) (P0.05 or 0.01).The compatibility of musk and olibanum can decrease the expression of MCP-1/CCL2 in prostate cells and VCAM-1 in vascular endothelial cells, blocking the adhesion of leucocytes and suppressing inflammatory response.