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zc891101新蟲 (初入文壇)
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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). [ 發(fā)自手機版 http://www.gaoyang168.com/3g ] |
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zc891101: 金幣+10, ★★★★★最佳答案 2015-05-18 08:07:18
zc891101: 金幣+10, ★★★★★最佳答案 2015-05-18 08:07:18
| 通過胰導(dǎo)管逆向灌注TLCS (50μl,3毫摩爾)和雨蛙肽重復(fù)處理(50μg /注射,注射12次)都可以誘發(fā)具有血淀粉酶過多、胰腺水腫和炎癥、以及腺泡細胞損傷和壞死特征的急性胰腺炎(圖2 A和B)。在Gpbar1基因敲除的動物中用TLCS誘發(fā)的胰腺炎, 血淀粉酶過多, 胰腺水腫、胰腺腺泡細胞炎癥和損傷/死亡都顯著降低(p < 0.05) (圖2), 但雨蛙肽重復(fù)處理后引起的胰腺炎的個體中這些參數(shù)不因為Gpbar1基因的敲除與否有明顯差異(圖1 B)。通過胰導(dǎo)管逆向灌注50μl ,3毫摩爾�；撬徕c不引起任何像TLCS-i誘發(fā)胰腺炎的病征(即h血淀粉酶過多、水腫和腺泡的細胞受傷或死亡) (補充材料，圖2)。 |
2樓2015-05-17 08:16:22
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