الملخص
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.
الملخص
Sepsis is still a major cause of death among neonates and its morbidity rate remain high nowadays.Because of the atypical symptoms and extremely dangerous progress in neonatal sepsis,early diagnosis and treatment are requisite.But the unique biomarkers are lacking meanwhile.Recent study shows that PBEF influences individual susceptibility,severity and outcome in sepsis.This review synthesizes the research of PBEF in neonatal sepsis in order to provide the evidence of reliable biomarker to diagnose and treat neonatal sepsis in the early stage.
الملخص
Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the salvage pathway for the biosynthesis of nicotinamide adenine dinucleotide (NAD+) from nicotinamide. NAMPT is also a cytokine that inhibits the apoptosis of neutrophils under various inlfammatory stimuli, regulates various diseases and closely associates with the progression and prognosis of cancers. However, it is still not clear whether the cytokine-like function of NAMPT is interrelated with the biosynthesis enzyme activity of NAD+. This article aims to provide novel insights for inflammation and cancers treatment by reviewing the function of NAMPT in inflammation, carcinogenesis, cancer progression and its inhibitors, APO866/FK866.