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短期给予CCK受体拮抗剂KSG-504对大鼠急性胰腺炎胰腺腺泡细胞再生的影响。

Effects of short-term administration of the CCK receptor antagonist, KSG-504, on regeneration of pancreatic acinar cells in acute pancreatitis in rats.

作者信息

Okumura Y, Inoue H, Fujiyama Y, Bamba T

机构信息

Department of Internal Medicine, Shiga University of Medical Science, Japan.

出版信息

J Gastroenterol. 1995 Aug;30(4):493-9. doi: 10.1007/BF02347566.

Abstract

Cholecystokinin (CCK) receptor antagonists have been reported on have an inhibitory effect on acute experimental pancreatitis, but their long-term administration is also reported to block pancreatic regeneration. We examined whether the short-term administration of KSG-504 (KSG), a synthetic CCK-A receptor antagonist, inhibited the regeneration of pancreatic acinar cells after ethionine-induced acute pancreatitis in rats. KSG (50 mg/kg), given 12 times by subcutaneous injection at 6-h intervals, prevented the reduction of protein, amylase, and trypsinogen levels, and the DNA content of the pancreas and facilitated the recovery of these values. Ornithine decarboxylase activity in pancreatic tissue and a 5-bromo-2'-deoxyuridine labeling study indicated that DNA synthesis was accelerated in rats treated with KSG. These findings suggest that the short-term administration of KSG inhibits the development of ethionine-induced acute pancreatitis and facilitates the regeneration of acinar cells.

摘要

据报道,胆囊收缩素(CCK)受体拮抗剂对急性实验性胰腺炎有抑制作用,但也有报道称长期使用会阻碍胰腺再生。我们研究了合成的CCK-A受体拮抗剂KSG-504(KSG)短期给药是否会抑制乙硫氨酸诱导的大鼠急性胰腺炎后胰腺腺泡细胞的再生。KSG(50mg/kg)以6小时的间隔皮下注射12次,可防止胰腺蛋白质、淀粉酶和胰蛋白酶原水平以及DNA含量的降低,并促进这些值的恢复。胰腺组织中的鸟氨酸脱羧酶活性和一项5-溴-2'-脱氧尿苷标记研究表明,接受KSG治疗的大鼠DNA合成加速。这些发现表明,KSG短期给药可抑制乙硫氨酸诱导的急性胰腺炎的发展,并促进腺泡细胞的再生。

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