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Retrograde intraductal infusion of TLCS (50 μl, 3 mM) and repeated administration ofcaerulein (50 μg/injection, 12 injections) each induce acute pancreatitis that is characterized by hyperamylasemia, pancreatic edema, inflammation, and acinar cell injury/necrosis (Fig. 2Aand B). In TLCS-induced pancreatitis, hyperamylasemia, pancreatic edema, pancreaticinflammation and acinar cell injury/death are all significantly reduced (p<0.05) whenGpbar1 has been deleted (Fig. 2A) but, when pancreatitis is induced by caeruleinadministration, none of these parameters of pancreatitis severity are altered by genetic deletionof Gpbar1 (Fig. 1B). None of the features of TLCS-induced pancreatitis (i.e. hyperamylasemia,edema, and acinar cell injury/death) are observed when 50 μl of 3 mM Na-taurocholate, ratherthan TLCS, is infused into the pancreatic duct (Suppl. Fig. 2A). [ 发自手机版 https://muchong.com/3g ] |
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genhunter
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zc891101: 金币+10, ★★★★★最佳答案 2015-05-18 08:07:18
zc891101: 金币+10, ★★★★★最佳答案 2015-05-18 08:07:18
| 通过胰导管逆向灌注TLCS (50μl,3毫摩尔)和雨蛙肽重复处理(50μg /注射,注射12次)都可以诱发具有血淀粉酶过多、胰腺水肿和炎症、以及腺泡细胞损伤和坏死特征的急性胰腺炎(图2 A和B)。在Gpbar1基因敲除的动物中用TLCS诱发的胰腺炎, 血淀粉酶过多, 胰腺水肿、胰腺腺泡细胞炎症和损伤/死亡都显著降低(p < 0.05) (图2), 但雨蛙肽重复处理后引起的胰腺炎的个体中这些参数不因为Gpbar1基因的敲除与否有明显差异(图1 B)。通过胰导管逆向灌注50μl ,3毫摩尔牛磺酸钠不引起任何像TLCS-i诱发胰腺炎的病征(即h血淀粉酶过多、水肿和腺泡的细胞受伤或死亡) (补充材料，图2)。 |
2楼2015-05-17 08:16:22
