腹腔感染后低白蛋白血症的分子机理和防治实验研究

Molecular mechanism and therapy of hypoalbuminemia in peritoneal infection

腹腔感染常伴有低白蛋白血症，为探讨其发生机理和防治方法，作者应用ＲＴ－ＰＣＲ方法，在大鼠体内体外进行了实验研究。结果显示：（１）腹腔感染后白蛋白ｍＲＮＡ显著下降，是发生低白蛋白血症的重要原因，而内毒素是重要的介导因素。（２）内毒素在体内显著抑制白蛋白ｍＲＮＡ表达，其机理系通过剌激非实质细胞产生ＴＮＦ、ＩＬ－１、ＩＬ－６而起作用。（３）ＴＮＦ、ＩＬ－１、ＩＬ－６显著抑制肝细胞白蛋白ｍＲ－ＮＡ表达，但以局部作用为主。（４）代谢激素对白蛋白合成有重要的调节，但在感染时它们的变化并非导致低白蛋白血症的原因。（５）生长激素和黄芪多糖在体外可明显减轻内毒素对白蛋白合成的抑制，并显著提高腹腔感染大鼠血浆白蛋白水平。作者认为，本研究结果表明，低白蛋白血症的发生机理是：腹腔感染引起内毒素吸收，内毒素刺激ｋｕｐｆｅｒ细胞等非实质细胞，产生ＴＮＦ、ＩＬ－１、ＩＬ－６等介质，它们作用于肝细胞抑制白蛋白ｍＲＮＡ表达，最终导致低白蛋白血症。减少内毒素吸收是重要防治环节，重组生长激素和黄芪多糖有明显的防治效果。

Albumin mRNA expression was studied by the use of reverse transcriptional polymerase chain reaction(RT PCR) to determine the molecular mechanism in peritoneal infection.Albumin mRNA content markedly decreased.Endotoxin inhibited albumin mRNA expression in vivo probably by stimulating TNF,IL 1,and IL 6 production.Changes of the hormone levels were not the cause of hypoalbuminemia in infection.Reconbined growth hormone and astragalus polysaccharides alleviated inhibition albumin synthesis inhibition increasing albumin serum concentration in rats with peritoneal infection.The results suggested that hypoalbuminemia is associated with endotoxemia during sepsis,which inhibites hepatocytes albumin synthesis probably by stimulating nonparenchymal cells to produce TNF,IL 1,and IL 6.