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首页> 外文期刊>Regulatory peptides. >Supramaximal cholecystokinin stimulates apoptosis and necrosis in pancreatic acinar cells: Role in pancreatitis
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Supramaximal cholecystokinin stimulates apoptosis and necrosis in pancreatic acinar cells: Role in pancreatitis

机译:超最大胆囊收缩素刺激胰腺腺泡细胞凋亡和坏死:在胰腺炎中的作用

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摘要

Cholecystokinin (CCK) is a key secretagogue for the pancreatic acinar cell; however, supramaximally stimulating concentrations of CCK-8 induce pathologic responses. Pancreatitis induced in rats and mice by supramaximal CCK-8 or its analog, cerulein, is the most widely used model of acute pancreatitis. Parenchymal cell death, in particular necrosis, is a major complication of pancreatitis; also, the severity of pancreatitis in animal models correlates directly with necrosis and inversely with apoptosis. Thus, elucidating the mechanisms that regulate the pattern of death responses may be of important therapeutic value in pancreatitis.
机译:胆囊收缩素(CCK)是胰腺腺泡细胞的关键促分泌素。但是,超刺激浓度的CCK-8会引起病理反应。超最大CCK-8或其类似物cerulein在大鼠和小鼠中诱发的胰腺炎是最广泛使用的急性胰腺炎模型。实质细胞死亡,特别是坏死,是胰腺炎的主要并发症。同样,在动物模型中胰腺炎的严重程度与坏死直接相关,与细胞凋亡相反。因此,阐明调节死亡反应模式的机制在胰腺炎中可能具有重要的治疗价值。

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