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作 者:范志宁[1] 刘训良[1] 熊观瀛[1] 文卫[1] 缪林[1]
机构地区:[1]南京医科大学第一附属医院胰腺外科,江苏省南京市210029
出 处:《世界华人消化杂志》2006年第9期912-915,共4页World Chinese Journal of Digestology
摘 要:目的:结合胆管压力的变化来探讨胰腺炎轻重程度与胆胰管梗阻时间及腺泡细胞凋亡的关系.方法:采用结扎胆胰管的方法制成胰腺炎模型.分别于梗阻后4、8、12 h以及解除梗阻后1、3 d分别测定胆管压力.流式细胞分析法检测胰腺腺泡细胞Annexin V-FITC/PI和 Caspase-3的表达.结果:与正常对照组(16.42±1.03)相比,随着梗阻时间的延长,胆管压力明显增高(4,8, 12 h分别为49.98±3.05,90.20±8.66,589.00 ±60.10),而在解除梗阻后,压力迅速下降并在1 d即恢复正常(1,3 d分别为17.50±2.84, 16.37±0.46),变化显著(P<0.01).AnnexinV- FITC/PI检测显示梗阻4 h时细胞凋亡较多, 至梗阻12 h时,腺泡细胞凋亡明显减少而坏死增加;在解除梗阻后,随着时间的延长凋亡明显增多,坏死逐渐减少,变化显著(P<0.01). Caspase-3检测显示在梗阻4 h时凋亡表达最高,梗阻8 h已明显减少,12 h则以坏死为主要表达方式;解除梗阻后1 d仍以坏死为主,到第3天则表现出大量的凋亡,变化显著 (P<0.01).结论:胆管压力升高引起的胆胰液返流是胰腺炎的发病机制之一,并可引起胰腺腺泡细胞的凋亡减少,而早期恢复正常胆胰管压力可使细胞凋亡增多,有效的阻止急性胰腺炎的病情发展.AIM: To analyze the correlations of the degrees of acute pancreatitis with the duration of bilepancreatic duct obstruction (BPDO) and acinar cell apoptosis by observing the change of bile duct pressure. METHODS: The model of acute pancreatitis was established by ligation of bile-pancreatic duct. Bile duct pressure was examined 4, 8, and 12 h after BPDO as well as 1 and 3 d after removal of BPDO. Flow cytometry was used to detect the acinar cell apoptosis (AnnexinV-FITC/PI assay) and the expression of Caspase-3. RESULTS: Compared with that in control group (16.42 ± 1.03), the pressure of bile-pancreatic duct increased with the prolonging of obstruction duration (49.98 ± 3.05, 90,20 ± 8.66, 589.00 ± 60.10 for 4, 8, 12 h after obstruction, respectively). When BPDO was removed, the pressure decreased and returned to the normal level within 1 d (17.50 ± 2.84, 16.37 ± 0.46 for 1 and 3 d after removal of obstruction, respectively), and the difference was significant (P 〈 0.01). AnnexinV- FITC/PI assay showed that the number of apoptotic cells increased significantly 4 h after BPDO, but it decreased while the number of dead cells increased 12 h after BPDO. However, after removal of BPDO, acinar cell apoptosis increased while cell death decreased markedly with the prolonging of BPDO (P 〈 0.01). Caspase-3 detection confirmed that apoptosis reached the peak at 4 h, and then decreased gradually. Cell death was mostly observed at 12 h. One day after removal of BPDO, cell death still covered the most percentage, but 3 d later, apoptosis was significantly observed (P 〈 0.01). CONCLUSION: Enhancement of bile duct pressure is one of the mechanisms in the pathogenesis of acute pancreatitis, which leads to a decrease of acinar cell apoptosis. It is effective to resume the enhanced pressure to normal level at the early stage in the prevention of the disease from development,
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