电针'足三里'对急性胰腺炎大鼠血清促炎因子及胰腺核因子-kB活性的影响

摘要

目的:探讨电针"足三里"穴治疗重症急性胰腺炎(SAP)的作用机制.方法:"只雄性SD大鼠随机分为假手术组、模型组、电针组,每组22只.通过胆胰管注射3.5%牛磺胆酸钠制作SAP模型.电针组在模型制作成功后及处死前给予电针"足三里"穴治疗各30 min,3组大鼠均于造模后3 h(n=7)、6 h(n=7)、12 h(n=8)分批处死,检测各时间点腹水量,观察胰腺病理学评分变化,并用ELISA方法检测血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6浓度的变化,运用免疫组化法检测胰腺组织核因子(NF)-k P 65表达水平.结果:各时间点模型组的胰腺组织病理评分、腹水童、血清TNF-α和IL-6浓度及胰腺NF-kB P 65表达水平均较假手术组增高(均P<0.05);电针组各时间点上述各项指标均较模型组明显降低(均P<0.05).结论:电针"足三里"穴可以减轻牛磺胆酸钠诱导的SAP大鼠胰腺病理损伤,其机制可能与抑制NF-KB的活性、降低血清促炎因子TNF-α、IL-6浓度有关.%Objective To observe the effects of electroacupuncture (EA) of "Zusanli" (ST 36) on serum TNF-oc and IL-6 contents and pancreatic nuclear factor kappa-B (NF-kB) expression in acute pancreatitis rats. Methods Sixty-six male SD rats were randomly divided into sham operation (sham). Model and EA groups (n = 22). Acute pancreatitis model was established by intra-pancreatic duct injection of 3. 5% sodium taurocholate (0. 1 mL/100 g). EA (2 Hz /100 Hz, 2 mA) was applied to bilateral ST 36 for 30 min after modeling and at the end of the experiment. The animals were killed at 3 h (n = 7), 6 h (n = 7) and 12 h (n = 8) after modeling. The expression of pancreatic NF-kB P65 was detected by immunohistochemical staining, and serum TNF-oc and IL-6 contents were determined by ELISA. The pathological changes of pancreatic tissue were displayed by H.E. Staining and the quantity of ascite was measured by electronic balance. Results The pathologic score, ascite quantity, serum TNF-oc and IL-6 contents, and pancreatic NF-kB P 65 expression levels at 3 h, 6 h and 12 h after modeling were significantly higher in the model group than in the sham group (P<0. 05). Compared with the model group, the pathologic score, ascite quantity, serum TNF-α and IL-6 contents, and pancreatic NF-kB P 65 expression levels at 3 h, 6 h and 12 h were significantly decreased in the EA group (P<0. 05). Microscopic observation displayed that the necrosis of the pancreatic acinar cells and infiltration of inflammatory cells were lighter in the EA group than in the model group. Conclusion EA at ST 36 is able to down-regulate sodium taurocholate injection induced increase of serum TNF-a and IL-6 contents, and pancreatic NF-kB P65 expression level in acute pancreatitis rats, which may contribute to its effect in relieving necrosis of the pancreatic acinar cells and infiltration of pancreatic inflammatory cells.