论文部分内容阅读
目的:探讨不同浓度麝香配伍乳香含药血浆(DP-M&O)对单核细胞分泌TNF-α、IL-1β、IL-6、IL-8、IL-10水平的影响,了解麝香配伍乳香在治疗前列腺炎中抗炎作用的机理。方法:制备小鼠脾脏单核细胞,细胞培养后分加入2.5%、5%、10%、20%浓度的DP-M&O预处理1 h后,加入小鼠前列腺抗原(PAgs)诱导活化单核细胞。阳性对照组加入脂多糖(LPS)处理。阴性对照组加入等体积DMEM完全培养基。培养96 h后收集各组上清,ELISA法检测单核细胞分泌的炎症因子TNF-α、IL-1β、IL-6、IL-8、IL-10的水平。结果:与空白对照组比较,经PAgs刺激诱导后,各组小鼠单核细胞的炎症因子释放增加,除IL-10的升高明显低于阳性对照LPS组外,其他TNF-α、IL-1β、IL-6、IL-8均明显增高;2.5%DP-M&O预处理后,虽然炎症因子有改变的趋势,但与PAgs组比较,差异无统计学意义(P>0.05);随着DP-M&O浓度增加,对TNF-α、IL-1β、IL-6、IL-8降低及IL-10升高作用更明显,呈剂量依赖性改变,在20%DP-M&O预处理后,TNF-α、IL-1β、IL-6、IL-8分别降低了74.4%、56.0%、76.6%、70.5%,IL-10上升了236.1%。结论:DP-M&O具有直接抑制前炎症因子产生的作用,其中对IL-1β的抑制作用最强;可促进IL-10的升高,从而抑制单核巨噬细胞释放炎症介质,减少PAgs诱导活化导致的TNF-α、IL-1β、IL-6、IL-8的分泌释放。
OBJECTIVE: To investigate the effects of different concentrations of musk and frankincense drug-containing plasma (DP-M & O) on monocyte secretion of TNF-α, IL-1β, IL-6, IL-8 and IL- Anti-inflammatory mechanism of prostatitis. Methods: Mice spleen mononuclear cells were prepared. After pretreatment with 2.5%, 5%, 10%, 20% DP-M & O for 1 h, the mouse prostatic antigens (PAgs) . The positive control group was treated with lipopolysaccharide (LPS). Negative control group was added equal volume of DMEM complete medium. The supernatants of all groups were collected after 96 h culture, and the levels of TNF-α, IL-1β, IL-6, IL-8 and IL-10 secreted by monocytes were detected by ELISA. Results: Compared with the blank control group, the release of inflammatory cytokines in monocytes increased after stimulation with PAgs. The levels of IL-10 and TNF-α, IL- 1β, IL-6 and IL-8 were significantly higher than those of PAgs group (P> 0.05). However, there was no significant difference between the two groups (P> 0.05) The effect of TNF-α, IL-1β, IL-6, IL-8 and IL-10 on IL-10 and IL-10 was more obvious in a dose-dependent manner after the pretreatment with 20% DP-M & α, IL-1β, IL-6 and IL-8 decreased by 74.4%, 56.0%, 76.6% and 70.5%, respectively. IL-10 increased by 236.1%. Conclusions: DP-M & O can directly inhibit the production of proinflammatory cytokines, and its inhibitory effect on IL-1β is the strongest. It can promote the increase of IL-10 and inhibit the release of inflammatory mediators by monocytes and decrease the activation of PAgs Resulting in the secretion and release of TNF-α, IL-1β, IL-6 and IL-8.