Chen N, Xiong Q
Hua Xi Yi Ke Da Xue Xue Bao. 1990 Sep;21(4):370-4.
The effect and mechanism of phospholipase A2 (PLA2) on pancreatic parenchymal necrosis in acute pancreatitis (AP) in rats were studied. Normal saline (NS), PLA2, phosphatidylcholine (PC), and PLA2 mixed PC were respectively injected into the biliopancreatic duct of the rat. The mixture of PLA2 and PC was found to result in necrotizing AP in the rat in 12 hours after injection of the reagent. The lysophosphatidylcholine (LPC) percentage in the amount of PC and LPC and the extent of pancreatic necrosis in this group increased much more significantly than those in other three groups (over about 4 and 15 times). There is evidently positive correlation (r = 0.9001, P less than 0.01) between LPC percentage and necrosis extent. The intraductal injection of PLA2, as well as NS or PC, failed to induce severe morphological changes in the pancreases. These results suggest that PC in bile is necessary in the pathogenesis of biliary pancreatitis and that LPC originated from bile PC by PLA2 may be the initiator in pancreatic parenchymal necrosis in AP.
研究了磷脂酶A2(PLA2)对大鼠急性胰腺炎(AP)胰腺实质坏死的影响及其机制。将生理盐水(NS)、PLA2、磷脂酰胆碱(PC)以及PLA2与PC的混合物分别注入大鼠胆胰管。结果发现,PLA2与PC的混合物在注入试剂12小时后可导致大鼠发生坏死性AP。该组中PC和溶血磷脂酰胆碱(LPC)中LPC的百分比以及胰腺坏死程度比其他三组显著增加得多(约4倍和15倍以上)。LPC百分比与坏死程度之间存在明显的正相关(r = 0.9001,P < 0.01)。向导管内注射PLA2以及NS或PC均未引起胰腺严重的形态学改变。这些结果表明,胆汁中的PC在胆源性胰腺炎的发病机制中是必需的,并且由PLA2作用于胆汁PC产生的LPC可能是AP胰腺实质坏死的起始因素。