Otamiri T
Clinical Research Center, University Hospital, Linköping, Sweden.
Food Chem Toxicol. 1989 Jun;27(6):399-402. doi: 10.1016/0278-6915(89)90146-4.
Phospholipase C from Clostridium perfringens, when injected into a closed loop of the rat small intestine in vivo, caused an increase in the activity of intraluminal N-acetyl-beta-glucosaminidase and mucosal permeability to sodium fluorescein, indicating damage to the mucosa. Phospholipase C also caused an influx of granulocytes (neutrophils) into the mucosa, as shown by the myeloperoxidase activity--a granulocyte neutrophil marker, and increased localized lipid peroxidation. Pretreatment of animals with quinacrine, a known inhibitor of phospholipase A2, prevented the increases in the luminal N-acetyl-beta-glucosaminidase activity, mucosal permeability, malondialdehyde and myeloperoxidase activity after deposition of phospholipase C in the gut lumen. It is concluded that phospholipase C might impair the function of the mucosal barrier and increase the permeability of the gut to undesirable molecules and pathogens. Part of its action may be mediated via phospholipase A2 activation since pretreatment with quinacrine afforded protection.
将产气荚膜梭菌的磷脂酶C注入大鼠小肠的体内闭合肠袢时，会导致肠腔内N-乙酰-β-氨基葡萄糖苷酶活性增加以及黏膜对荧光素钠的通透性增加，表明黏膜受到损伤。磷脂酶C还会导致粒细胞（中性粒细胞）流入黏膜，髓过氧化物酶活性显示了这一点——髓过氧化物酶是粒细胞中性粒细胞的标志物，同时局部脂质过氧化增加。用已知的磷脂酶A2抑制剂喹吖因对动物进行预处理，可防止在肠腔内注入磷脂酶C后肠腔N-乙酰-β-氨基葡萄糖苷酶活性、黏膜通透性、丙二醛和髓过氧化物酶活性的增加。得出的结论是，磷脂酶C可能损害黏膜屏障的功能，并增加肠道对不良分子和病原体的通透性。其部分作用可能是通过磷脂酶A2的激活介导的，因为用喹吖因预处理可提供保护作用。
