Tetramethylpyrazine inhibits LPS-inducedinflammation of human type Ⅱ alveolar epithelial cells
- VernacularTitle:川芎嗪抑制LPS诱导的人Ⅱ型肺泡上皮细胞炎性反应
- Author:
Xiaoyong HU
;
Fachun ZHOU
- Keywords:
acute respiratory disease syndrome;
tetramethylpyrazine;
pre-B cell colony-enhancing factor;
nuclear factor κB
- From:
Basic & Clinical Medicine
2017;37(6):839-844
- CountryChina
- Language:Chinese
-
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.Methods HAECⅡ (A549 cells derived from human lung adenocarcinoma cells) were cultured in vitro.Inflammation model was 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 level of mRNA, 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 examined by Western blot to find the changes in phosphorylated P65 protein level in both nucleus and cytoplasm.Results Both the mRNA and protein level 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 inter-vention 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.
