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生长抑素及Octreotide对急性胰腺炎胰腺细胞凋亡的作用机制
引用本文:袁耀宗,龚自华,楼恺娴,涂水平,翟祖康,徐家裕. 生长抑素及Octreotide对急性胰腺炎胰腺细胞凋亡的作用机制[J]. 中国危重病急救医学, 2000, 12(7): 402-405
作者姓名:袁耀宗  龚自华  楼恺娴  涂水平  翟祖康  徐家裕
作者单位:上海第二医科大学附属瑞金医院消化内科,上海,200025
摘    要:目的:探讨生长抑素(SS)及其类似物(Octreotide)治疗小鼠急性胰腺细胞凋亡及凋亡调控基因bax,p53的作用。方法:以雨蛙肽诱导CD-1小鼠急性胰腺炎模型,并应用细胞凋亡原位标记检测(TUNEL)染色,免疫组化技术等检测胰腺细胞凋亡及凋亡调控基因bax,p53的蛋白表达,以及生长抑素及其类似物治疗后对胰腺细胞凋亡及凋亡调控基因bax和p53蛋白表达的影响。结果:HE染色见胰腺组织中典型的

关 键 词:胰腺炎 急性 细胞凋亡 生长抑素 Octreotide

Effects and mechanisms of somatostatin and Octreotide on apoptosis of pancreatic acinar cells in acute pancreatitis in mice
YUAN Yaozong,GONG Zihua,LOU Kaixian,et al.. Effects and mechanisms of somatostatin and Octreotide on apoptosis of pancreatic acinar cells in acute pancreatitis in mice[J]. Chinese critical care medicine, 2000, 12(7): 402-405
Authors:YUAN Yaozong  GONG Zihua  LOU Kaixian  et al.
Affiliation:YUAN Yaozong,GONG Zihua,LOU Kaixian,et al.Department of Gastroenterology,Ruijin Hospital,Shanghai Second Medical University,Shanghai 200025
Abstract:Objective:To investigate the effects of somatostatin (SS) and its analogues (Octreotide) on apoptosis of pancreatic acinar cells and apoptosisregulated gene bax and p53 in acute pancreatitis in mice.Methods:In caeruleininduced pancreatitis with or without treatment of SS and Octreotide in CD1 mice,apoptosis of pancreatic acinar cells was detected by terminal deoxynucleotidyltransferase mediated dUTPbiotin nick end labeling(TUNEL) method,and the expression of apoptosisregulated gene bax and p53 was detected by immunohistochemical technique.Results:Pathological results showed that there were pyknotic nuclei and apoptotic bodies in the acinar cells in pancreas.Results from the TUNEL staining showed that the apoptotic index of pancreatic acinar cells in nontreated group at 1,5 and 14 hours after the induction of acute pancreatitis was significantly lower than that of SS treated group at 1 hour and those of Octreotide treated group at 5,14 hours(all P <0 01).Immunohistochemical analysis showed that there was no positive staining cells in normal pancreatic tissues.The positive rate of p53 protein in SS treated group at 1 hour was markedly higher than that of nontreated group ( P <0 01),but there was no significant difference on the positive rate of bax protein between SS treated group and nontreated group.The positive rate of bax protein in Octreotide treated group at 5 and 14 hours was significantly higher than those of nontreated group respectively (both P <0 01),but there was no marked difference on the positive rate of p53 protein between Octreotide treated group and nontreated group.Conclusions:Induction of apoptosis in injured pancreatic acinar cells to reduce inflammatory response might be one of the mechanisms of SS and its analogues in treating acute pancreatitis in mice.The SS induced apoptosis might be related with the expression of p53 but not bax,and the induction of apoptosis by somatostatin analogues might be in relationship with the expression of bax but not p53.
Keywords:acute pancreatitis  apoptosis  somatostatin  Octreotide
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