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血清补体系统——急性胰腺炎的一个介质。

The serum complement system--a mediator of acute pancreatitis.

作者信息

Seelig R, Ehemann V, Tschahargane C, Seelig H P

出版信息

Virchows Arch A Pathol Anat Histol. 1975;365(3):193-9. doi: 10.1007/BF00434038.

Abstract

The role of the complement system in the initial membrane lesion of acute pancreatitis was investigated. In the experimental sodium-taurocholate pancreatitis of the rat a sudden and steady decline of serum complement was observed. The deposition of C3 component of complement in acute pancreatitis could be demonstrated by immunofluorescence. To rule out mere deposition or activation of complement in the interstitial exsudative fluid, single acinar cells of rat and rabbit pancreatic tissue were prepared and transfered to culture medium. In contrast to heat inactivated serum and C6 deficient serum these cells were lysed by trypsin activated fresh serum. Consequently, an acute pancreatitis could be induced by activating exclusively the complement system by injection of cobra venom factor into the pancreatic duct of rats. The activated complement system is thought to be responsible for initial membrane lesion in exsudative inflammation, as could be shown in acute pancreatitis.

摘要

研究了补体系统在急性胰腺炎初始膜损伤中的作用。在大鼠实验性牛磺胆酸钠胰腺炎中,观察到血清补体突然且持续下降。通过免疫荧光可证实补体C3成分在急性胰腺炎中的沉积。为排除补体仅在间质渗出液中沉积或激活,制备了大鼠和兔胰腺组织的单个腺泡细胞并转移至培养基中。与热灭活血清和C6缺陷血清不同,这些细胞被胰蛋白酶激活的新鲜血清裂解。因此,通过向大鼠胰管注射眼镜蛇毒因子仅激活补体系统可诱发急性胰腺炎。如在急性胰腺炎中所示,激活的补体系统被认为是渗出性炎症初始膜损伤的原因。

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