柴芩承气汤对急性坏死性胰腺炎大鼠胰腺核因子-κB活化的影响

目的：通过观察柴芩承气汤（Chaiqin Chengqi Decoction,CQCQD）对急性坏死性胰腺炎（acute necrotizing pancreatitis,ANP）大鼠的作用,探讨其治疗机制。方法：将30只SD大鼠随机分成3组：假手术（sham-operated,SO）组、ANP组和CQCQD治疗组。大鼠胆总管内逆向泵入3.5%牛胆酸溶液制备ANP模型。6h后分别行腹腔静脉采血送检,取胰腺组织做病理切片;酶标记免疫吸附测定法检测血浆肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）和白细胞介素-6（interleukin-6,IL-6）;HE染色光学显微镜观察胰腺组织病理情况;免疫组织化学染色SP法检测胰腺核因子-κB（nuclear factor-κB,NF-κB）的活化。结果：ANP组白细胞（white blood cell,WBC）计数和血清淀粉酶（amylase,AMY）值较SO组明显升高（P〈0.05,P〈0.01）,CQCQD组血清WBC计数和AMY水平均较ANP组有所下降（P〈0.05）。ANP组的水肿、炎症浸润、出血、坏死和总积分情况较SO组严重（P〈0.01）;CQCQD组的水肿、炎症浸润、出血和总积分水平均较ANP组降低（P〈0.05）。CQCQD组胰腺NF-κB p65阳性细胞的积分光密度（integraloptical density,IOD）值低于ANP组（P〈0.05）。结论：CQCQD可减少血清TNF-α及IL-6含量,降低胰腺NF-κB的活性,减轻胰腺病理损害。

Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kB in pancreas of rats with acute necrotizing pancreatitis

OBJECTIVE: To explore the mechanism of Chaiqin Chengqi Decoction (CQCQD) in treatment of rats with acute necrotizing pancreatitis (ANP). METHODS: Thirty SD rats were randomly divided into 3 groups: sham-operated (SO) group, ANP group and CQCQD-treated group. ANP was induced by retro-pumping 3.5% sodium cholate to common bile duct. Blood sample was collected from abdominal vein for examination and the pancreatic tissue samples were taken for making pathology section 6 hours later. The pancreatic tissue (HE staining) was observed by light microscope. The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) was detected with the method of enzyme-linked immunosorbent assay, and the activation of nuclear factor-kappaB (NF-kappaB) in pancreas was detected by immunohistochemical method. RESULTS: Compared with the SO group, there was dramatic increase in the white blood cell (WBC) counts and AMY level in the ANP group (P<0.05, P<0.01). Compared with the ANP group, the WBC counts and AMY level in CQCQD-treated group were significantly reduced (P<0.05). The edema, inflammatory infiltration, haemorrhage and necrosis scores and total pathological score in the ANP group were obviously higher than those in the SO group (P<0.01). The edema, haemorrhage and inflammatory infiltration scores and the total pathological score in CQCQD-treated group were decreased (P<0.05). The integral optical density of NF-kappaB p65 positive cells of pancreas in CQCQD-treated group was lower than that in the ANP group (P<0.05). CONCLUSION: CQCQD can reduce the content of serum TNF-alpha and IL-6, depress the activation of NF-kappaB, and lessen the pancreatic lesions.