关键词: 急性呼吸窘迫综合征, 川芎嗪, 前B细胞克隆增强因子, 核因子KB

Abstract: Objective To study the protective effect of TMP(Tetramethylpyrazine) on LPS(Lipopolysaccharides )-induced inflammatory response of human type II alveolar epithelial cells (HAECII) and its corresponding mechanism in vitro. Methods HAECII (A549 cells derived from human lung adenocarcinoma cells) were cultured in vitro. Inflammation models were established using A549 cells after LPS stimulation. TMP and FK866 (a specific inhibitor for pre-B cell colony-enhancing factor), were added to intervene respectively. Expression levels regarding mRNA and protein of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β), interleukin-8 (IL-8) and PBEF(pre-B cell colony-enhancing factor) were detected by q-PCR and Western blot, respectively. The activation of NF-κB(Nuclear factor κB) was monitored using Western blot by measuring the changes in phosphorylated P65 protein levels in both nucleus and cytoplasm. Results Both the mRNA and protein levels of TNF-α, IL-1β, IL-8 and PBEF in A549 cells were significantly higher after LPS stimulation than those in the control group(P<0.001). Meanwhile, the phosphorylation of P65 protein in the nucleus and cytoplas was higher(P<0.001). The expression of the aforementioned inflammatory factors and the phosphorylation of P65 protein were significantly lower after TMP intervention than those of LPS group(P<0.05). In comparison, after FK866 was added, the expression of TNF-α, IL-1β and IL-8 and the phosphorylation of P65 protein were also decreased(P<0.01). Conclusions TMP may be involved in the reduction of PBEF expression, which therefore inhibits NF-κB activation, antagonizes alveolar epithelial cell inflammatory response.

Key words: acute respiratory disease syndrome, Tetramethylpyrazine, pre-B cell colony-enhancing factor, Nuclear factor kB