慢性胰腺炎大鼠肝脏IKK-β表达及药物的干预作用

Expression of Hepatic IKK-β in Chronic Pancreatitis Rat Model and Intervening Effect of Medicine

目的:观察慢性胰腺炎大鼠肝脏核因子-κB(nuclear factor-κB,NF-κB)抑制因子(inhibitor nuclear factor-kappa B,IκB)的激酶抑制剂-β(inhabit kappa B kinase-beta,IKK-β)表达变化及药物的干预作用。方法:制备慢性胰腺炎大鼠模型后随机分为模型组、罗格列酮组、柴胡疏肝散组,并设对照组。进行葡萄糖耐量试验,RT-PCR法检测肝脏IKK-βmRNA水平,Western blot法检测IKK-β蛋白表达变化。结果:模型组大鼠的糖耐量异常,肝脏IKK-β的mRNA水平和蛋白表达较对照组显著增加(P<0.05),罗格列酮组和柴胡疏肝散组IKK-β的表达较模型组显著降低(P<0.05)。结论:慢性胰腺炎大鼠肝脏IKK-β的表达增加,可能是胰源性糖尿病发生的一个重要机制;罗格列酮和柴胡疏肝散对其表达有抑制作用。

Objective To observe the expression of hepatic IKK-βin chronic pancreatitis rats and the intervention effect of medication. Methods Chronic pancreatitis rat model was established by injection of oleic acid into the pancreatic duct, then 40 rats were divided into model group, rosiglitazone group, and ChaihuShuganSan（柴胡疏肝散） group randomLy, with a control group. Glucose tolerance test was carried out. The level of hepatic IKK-βmRNA was determined by reverse transcription polymerase chain reaction （RT-PCR）. Expression of hepatic IKK-βwas observed by Western blot. Results Compared with the control group, glucose tolerance of the model group was abnormal, the hepatic IKK-βmRNA level and expression was increased significantly. While compared with the model group, the expression of IKK-βin medication groups was decreased significantly. Conclusion Chronic pancreatitis causes the expression of IKK-βincreasing, which might be an important mechanism leading to pancreatogenic diabetes. Rosiglitazone and ChaihuShugansan can inhibit the expression of IKK-β.