内毒素对肠黏膜微血管内皮细胞内分泌一氧化氮和内皮素的影响

The Respective Effects of LPS on the Intestinal Mucosa Microvascular Endothelial Cells Secreting NO and ET

目的是研究内毒素(lipopolysaccharide;LPS)导致肠黏膜微血管内皮细胞损伤的作用机制。将所培养的肠黏膜微血管内皮细胞分为空白对照组和LPS组,每组按时间分为4个亚组:3h、6h、9h、12h。空白对照组加维持培养液,LPS组加1μg/mlLPS培养液,在CO2培养箱内静置培养。结果表明,一氧化氮(NO)分泌明显升高,3h后达到高峰,随后逐渐降低,而内皮素(endothelin;ET)分泌急剧升高,9h后达到高峰,随后又开始逐渐降低,但一直保持在较高的水平。所以引起了NO和ET的升高可能是LPS导致肠黏膜微血管内皮细胞的损伤机制。

The aim： To research on the functional mechanism of LPS damaging intestinal mucosa microvascular endothelial cells. The way： Divide the intestinal mucosa micro vascular endothelial ceils fostered into blank control group and LPS group and further divide each group into four minor groups according to the time： 3h, 6h, 9h, 12h. Add feeding medium into the blank control group while fill 1μtg/ml LPS nutrient liquid into LPS group. After that, put them into CO2 incubators and cultivate them statically. Result： The secretion of NO rises obviously and arrives at the peak in three hours before it lowers gradually. The secretion of ET rises rapidly and arrives at the peak in 9 hours, then it begins to lower gradually, however, it always stays at a high level. Conclusion： the functional mechanism of LPS damaging intestinal mucosa microvascular endothelial cells may be that LPS leads to the rise in the secretion of NO and ET.