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目的研究己酮可可碱(PTX)干预大鼠胰腺纤维化及其可能的机制。方法通过对大鼠胰管内注射2%三硝基苯磺酸(TNBS)的方法制备大鼠胰腺纤维化模型。Wister大鼠18只,随机分为模型组、PTX干预组、正常对照组,每组各6只。PTX干预组大鼠术后第2d开始腹腔注射PTX,剂量为6mg/kg.d。模型组腹腔注射等量生理盐水,3组大鼠均于术后第4周处死取胰腺。采用免疫组化技术检测治疗前后胰腺组织中α-平滑肌肌动蛋白(α-SMA)、血小板衍化生长因子(PDGF)、磷酸化细胞外信号调节激酶(P-ERK1/2)的含量同时做组织胶原纤维染色,部分胰腺组织液氮冻存,以Western blot方法检测α-SMA的表达。结果模型组发生胰腺纤维化,PTX干预组有轻度纤维化。PTX干预组α-SMA、PDGF、P-ERK1、P-ERK2在基质细胞核中的表达均低于模型组(P<0.001)。胶原纤维染色显示PTX治疗组胶原面积百分比明显低于模型组(P<0.01)。结论 PTX有抗大鼠胰腺纤维化的作用,其可能通过抑制ERK信号传导通路发挥作用。
Objective To investigate the effects of pentoxifylline (PTX) on pancreatic fibrosis in rats and its possible mechanism. Methods Rat pancreatic fibrosis model was established by injecting 2% trinitrobenzene sulfonic acid (TNBS) into the pancreatic duct of rats. Eighteen Wister rats were randomly divided into model group, PTX intervention group and normal control group with 6 rats in each group. The rats in PTX intervention group were injected intraperitoneally with PTX at the second day after the operation, and the dose was 6mg / kg.d. The model group was given intraperitoneal injection of normal saline, and the rats in the three groups were sacrificed at the fourth week after operation to take the pancreas. The contents of α-smooth muscle actin (α-SMA), platelet-derived growth factor (PDGF) and phosphorylated extracellular signal-regulated kinase (P-ERK1 / 2) in pancreatic tissue before and after treatment were detected by immunohistochemistry Collagen fibers were stained and some pancreatic tissues were frozen in liquid nitrogen. The expression of α-SMA was detected by Western blot. Results The model group had pancreatic fibrosis, and the PTX intervention group had slight fibrosis. The expression of α-SMA, PDGF, P-ERK1 and P-ERK2 in PTX intervention group was lower than that in model group (P <0.001). Collagen staining showed that the percentage of collagen area in PTX treated group was significantly lower than that in model group (P <0.01). Conclusions PTX can prevent the pancreatic fibrosis in rats, which may play a role by inhibiting the ERK signal transduction pathway.