本文關(guān)鍵詞： 胰性腦病 多巴胺 多巴胺受體 氧自由基 炎性因子　出處：《實(shí)用醫(yī)學(xué)雜志》2017年18期 　論文類型：期刊論文

【摘要】：目的探討腦內(nèi)多巴胺受體在胰性腦病中表達(dá)的作用,為進(jìn)一步闡明胰性腦病的發(fā)病機(jī)制奠定基礎(chǔ)。方法胰膽管逆行注射5%�；悄懰徕c誘發(fā)大鼠胰性腦病模型。觀察胰腺和腦的病理改變;稱重測(cè)定腦組織含水量;化學(xué)比色法測(cè)定腦組織勻漿超氧化物歧化酶活性和丙二醛含量;免疫組化染色(SP法)觀察腦組織腫瘤壞死因子-α(TNF-α)、白細(xì)胞介素-1β(IL-1β)、酪氨酸羥化酶和多巴胺受體-2的表達(dá)情況。結(jié)果光鏡下顯示3、6、12 h模型組胰腺有不同程度的炎性細(xì)胞浸潤(rùn)和腺泡細(xì)胞壞死;腦組織中神經(jīng)元水腫,炎性細(xì)胞浸潤(rùn),微血管內(nèi)白細(xì)胞附壁。與對(duì)照組比較,3、6、12 h模型組腦組織中超氧化物歧化酶活性均明顯降低(均P0.01),丙二醛含量均明顯升高(P0.01);與對(duì)照組比較,3、6、12 h模型組大鼠腦組織含水量均增高(均P0.05);與對(duì)照組比較,3、6、12 h模型組腦組織TNF-α、IL-1β、酪氨酸羥化酶和多巴胺受體-2表達(dá)均明顯增多(均P0.01)。結(jié)論胰性腦病的發(fā)病可能與大量氧自由基和炎性因子透過血腦屏障進(jìn)入中樞,致腦內(nèi)多巴胺生成增加及受體上調(diào)有關(guān)。
[Abstract]:Objective to investigate the expression of dopamine receptor in pancreatic encephalopathy. Methods Rat pancreatic encephalopathy model was induced by retrograde injection of 5% sodium taurocholate. The water content of brain tissue was measured by weighing. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in brain homogenate were determined by chemical colorimetry. The tumor necrosis factor- 偽 (TNF- 偽) and interleukin-1 尾 (IL-1 尾) in brain tissue were observed by immunohistochemical staining (SP method). Results the expression of tyrosine hydroxylase and dopamine receptor -2 was observed under light microscope. Neuronal edema, inflammatory cell infiltration and leukocyte attachment in the microvessel were observed in brain tissue compared with control group (P < 0.05). The activity of superoxide dismutase (SOD) in brain tissue of 12h model group was significantly decreased (P0.01), and the content of malondialdehyde (MDA) was significantly increased. Compared with the control group, the water content of brain tissue in the model group was significantly higher than that in the control group (P 0.05). Compared with the control group, TNF- 偽 and IL-1 尾 in the brain tissue of the model group were compared with that of the control group for 12 h. The expression of tyrosine hydroxylase and dopamine receptor -2 were significantly increased (P 0.01). Conclusion the pathogenesis of pancreatic encephalopathy may be associated with a large number of oxygen free radicals and inflammatory factors passing through the blood-brain barrier into the center. Increased dopamine production and up-regulation of receptors in the brain.
【作者單位】： 西南醫(yī)科大學(xué)解剖學(xué)教研室;四川衛(wèi)生康復(fù)職業(yè)學(xué)院解剖學(xué)教研室;西南醫(yī)科大學(xué)附屬中醫(yī)醫(yī)院藥劑科;
【基金】：四川省衛(wèi)生廳科研項(xiàng)目(編號(hào):070226)
【分類號(hào)】：R576;R747.9
【正文快照】： 胰性腦病(pancreatic encephalopathy,PE)是指胰腺炎并發(fā)意識(shí)模糊及幻覺等神經(jīng)精神癥狀,多發(fā)生于重癥急性胰腺炎(severe acute pancreatitis,SAP),其病死率達(dá)10%~66.7%[1-2]。有關(guān)PE的發(fā)病機(jī)制目前尚未完全闡明。SAP時(shí),白細(xì)胞被過度激活,產(chǎn)生大量的氧自由基(oxygen free radic

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