Department of Pathophysiology, Shaanxi University of Traditional Chinese Medicine, Xianyang 712046, Shaanxi Province, China.
World J Gastroenterol. 2011 Apr 14;17(14):1825-30. doi: 10.3748/wjg.v17.i14.1825.
To study the effect of breviscapine (Bre) on activity of protein kinase Cα (PKCα) and nuclear factor (NF)-κB in pancreas, and the mechanism of Bre attenuating acute pancreatitis (AP).
One hundred and eight rats were randomly divided into acute necrotizing pancreatitis (ANP) group, Bre group (ANP + Bre group) and sham operation (SO) group, 36 rats in each group. ANP model was induced by a retrograde injection of 4% sodium deoxycholate into the bilio-pancreatic duct. Fifteen minutes after the ANP model was induced, the rats in Bre group were intraperitoneally injected with Bre (0.4 mg/100 g body weight or 0.1 mL/100 g body weight). Survival time and mortality of rats were calculated. Serum amylase and malondialdehyde levels were measured, volume of ascites was recorded and morphology of pancreas and lung was evaluated at 1, 5 and 10 h, after the ANP model was induced, respectively. Expressions of PKCα and subunit p65 of NF-κB in pancreas were detected by immunohistochemistry and Western blotting.
The life span of rats was longer and the mortality was lower in Bre group than in ANP group 13.51 ± 5.46 vs. 25.36 ± 8.11 (P < 0.05). The amylase and MDA levels as well as the volume of ascites were lower and the pathological changes in pancreas and lung were less in Bre group than ANP group (P < 0.05), indicating that the pancreatitis is less severe in Bre group than ANP group. The activation of PKCα and NF-κB p65 in pancreas was induced rapidly and reached their peak at 1 h or 5 h after ANP, but their activity in Bre group was significantly inhibited.
Bre exerts its therapeutic effect on AP by inhibiting the activation of PKCα and NF-κB p65 in pancreas.
研究灯盏花素（Bre）对胰腺蛋白激酶 Cα（PKCα）和核因子（NF）-κB活性的影响，并探讨 Bre 减轻急性胰腺炎（AP）的机制。
108 只大鼠随机分为急性坏死性胰腺炎（ANP）组、Bre 组（ANP+Bre 组）和假手术（SO）组，每组 36 只。通过逆行胰胆管注射 4%脱氧胆酸钠诱导 ANP 模型。在诱导 ANP 模型后 15 分钟，Bre 组大鼠腹腔注射 Bre（0.4mg/100g 体重或 0.1mL/100g 体重）。计算大鼠的生存时间和死亡率。分别在诱导 ANP 模型后 1、5 和 10 小时测量血清淀粉酶和丙二醛水平，记录腹水量，并评价胰腺和肺的形态。通过免疫组织化学和 Western 印迹法检测胰腺中 PKCα 和 NF-κB p65 亚单位的表达。
Bre 组大鼠的生存期较长，死亡率较低，13.51±5.46 比 25.36±8.11（P<0.05）。Bre 组的淀粉酶和 MDA 水平以及腹水量较低，胰腺和肺的病理变化较轻，与 ANP 组相比（P<0.05），提示 Bre 组胰腺炎的严重程度低于 ANP 组。胰腺中 PKCα 和 NF-κB p65 的激活迅速，在 ANP 后 1 小时或 5 小时达到峰值，但 Bre 组的活性明显受到抑制。
Bre 通过抑制胰腺中 PKCα 和 NF-κB p65 的激活对 AP 发挥治疗作用。
