Laboratoire de recherche en inflammation et physiologie des granulocytes, Université du Québec, INRS-Institut Armand-Frappier, Laval, QC, Canada.
J Inflamm (Lond). 2012 May 28;9(1):19. doi: 10.1186/1476-9255-9-19.
Esenbeckia leiocarpa, a wide spread native Brazilian tree, was reported recently to possess anti-inflammatory effects in vivo, but the mechanisms involved are still not fully understood and its role in neutrophils is poorly documented. The aim of this study was to compare the effects of a crude hydroalcoholic extract (CHE) and an alkaloid-enriched (Alk) fraction obtained from Esenbeckia leiocarpa bark on human neutrophils by investigating the effect of each fraction alone or in a mixture with classical neutrophil agonists. CHE inhibited intracellular reactive oxygen species (ROS) production but increased the extracellular superoxide (O2-) production, while Alk increased the former and also slightly increased O2- production. We found that CHE and Alk also induced phagocytosis accompanied by Syk activation, adhesion and degranulation. However, neither CHE nor Alk potentiated the effect of classical neutrophil agonists, namely the cytokines GM-CSF for phagocytosis and TNF-α for adhesion or N-formyl-methionyl-leucyl-phenylalanine (fMLP) for degranulation. In addition, based on catalase treatment, CHE and Alk induced neutrophil apoptosis by a hydrogen peroxide (H2O2)-dependent mechanism. Since the elimination of apoptotic neutrophils by professional phagocytes is important for the resolution of inflammation, the ability of CHE and Alk to induce neutrophil apoptosis has to be considered as one possible mechanism associated with the anti-inflammatory activity of these fractions previously reported in vivo.
巴西原产的广布树种 Leiocarpa esenbeckii 最近被报道具有体内抗炎作用，但相关机制仍不完全清楚，其在中性粒细胞中的作用也鲜有记载。本研究旨在通过研究各部分单独或与经典中性粒细胞激动剂混合时的作用，比较从 Leiocarpa esenbeckii 树皮中获得的粗水醇提取物 (CHE) 和富含生物碱 (Alk) 的部分对人中性粒细胞的影响。 CHE 抑制细胞内活性氧 (ROS) 的产生，但增加细胞外超氧化物 (O2-) 的产生，而 Alk 则增加前者，并略微增加 O2- 的产生。我们发现 CHE 和 Alk 还诱导吞噬作用，同时伴有 Syk 激活、黏附和脱颗粒。然而，无论是 CHE 还是 Alk，都不能增强经典中性粒细胞激动剂的作用，即细胞因子 GM-CSF 促进吞噬作用和 TNF-α 促进黏附和 N-甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸 (fMLP) 促进脱颗粒作用。此外，基于过氧化氢酶处理，CHE 和 Alk 通过依赖于过氧化氢 (H2O2) 的机制诱导中性粒细胞凋亡。由于专业吞噬细胞清除凋亡中性粒细胞对于炎症的消退很重要，因此 CHE 和 Alk 诱导中性粒细胞凋亡的能力必须被视为与这些部分体内抗炎活性相关的一种可能机制。
