摘要：
Objective To investigate the expression of dopamine receptor in brain of rats with pancreatic encephalopathy and provide a theoretical basis to reveal pathogenesis of pancreatic encephalopathy. Methods A rat model of experimental pancreatic encephalopathy was induced by retrograde injection of 5％sodium taurocholate into the pancreatic duct. The pathological changes of pancreas and brain were detected. The water content in brain tissue was determined. The superoxide dismutase activity and malondialdehyde content in brain tissue homogenate were detected by the chemical colorimetry. Levels of TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 were detected by immunohistochemistry(SP method). Results Cerebral sulcus was shallow,ventricle was small-er and the superficial veins were dilated and congested. The inflammatory cell infiltration and pancreatic acinar cell necrosis in the pancreas and neuron edema ,inflammatory cell infiltration ,microvessel adherent leukocytes in brain were observed by light microscope in model groups at 3,6,12 hours. Compared with the control group. The activities of superoxide dismutase in brain tissue in model groups at 3,6,12 hours were significantly decreased (P < 0.01). The level of malondialdehyde and the water content of brain tissue were significantly increased (P <0.01 ,respectively). Compared with the control group ,levels of brain TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 in model groups at 3,6,12 hours were significantly increased(P < 0.01,respectively).Conclusions The incidence of pancreatic encephalopathy may be related to the influx of oxygen free radical and inflammatory factors,invading nerve center by blood-brain barrier and inducing the increased production of dopa-mine and the upregulation of dopamine receptor in brain.%目的 探讨脑内多巴胺受体在胰性脑病中表达的作用,为进一步阐明胰性脑病的发病机制奠定基础.方法 胰胆管逆行注射5％牛磺胆酸钠诱发大鼠胰性脑病模型.观察胰腺和脑的病理改变;称重测定脑组织含水量;化学比色法测定脑组织匀浆超氧化物歧化酶活性和丙二醛含量;免疫组化染色(SP法)观察脑组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、酪氨酸羟化酶和多巴胺受体-2的表达情况.结果 光镜下显示3、6、12 h模型组胰腺有不同程度的炎性细胞浸润和腺泡细胞坏死;脑组织中神经元水肿,炎性细胞浸润,微血管内白细胞附壁.与对照组比较,3、6、12 h模型组脑组织中超氧化物歧化酶活性均明显降低(均P<0.01),丙二醛含量均明显升高(P<0.01);与对照组比较,3、6、12 h模型组大鼠脑组织含水量均增高(均P<0.05);与对照组比较,3、6、12 h模型组脑组织TNF-α、IL-1β、酪氨酸羟化酶和多巴胺受体-2表达均明显增多(均P<0.01).结论 胰性脑病的发病可能与大量氧自由基和炎性因子透过血脑屏障进入中枢,致脑内多巴胺生成增加及受体上调有关.
