本文選題：12-脂加氧酶　切入點(diǎn)：病毒性心肌炎　出處：《吉林大學(xué)》2012年博士論文　論文類型：學(xué)位論文

【摘要】：病毒性心肌炎（viral myocarditis，VMC）是兒科臨床常見(jiàn)的心血管疾病，近年發(fā)病有上升趨勢(shì)，并且已成為青少年不明原因猝死的主要原因之一，不僅如此，慢性VMC還可導(dǎo)致擴(kuò)張性心肌病的發(fā)生，嚴(yán)重危害小兒生命健康。因VMC發(fā)病機(jī)制尚未完全闡明，至今國(guó)內(nèi)外對(duì)VMC尚無(wú)特效的治療方法。 12-脂加氧酶(12-LO)是一類以非血紅素鐵蛋白為輔基的多功能酶，屬于脂質(zhì)酶家族中的一種，廣泛分布于機(jī)體各部分，具有多種生物功能；12-LO又是一種重要的信號(hào)分子，能夠促進(jìn)細(xì)胞的增殖，通過(guò)機(jī)體氧化應(yīng)激反應(yīng)和炎癥反應(yīng)，參與多種疾病病理過(guò)程，并在心血管方面具有重要作用，參與了高血壓、動(dòng)脈粥樣硬化等疾病的病理過(guò)程。但目前國(guó)內(nèi)外對(duì)12-LO與病毒性心肌炎的關(guān)系尚無(wú)研究。本研究通過(guò)采用BALB/C小鼠腹腔注射柯薩奇B3病毒（CVB3）的經(jīng)典制作病毒性心肌炎模型的方法，建立病毒性心肌炎小鼠模型。通過(guò)半定量RT-PCR方法、免疫組織化學(xué)方法確定了12-LO在VMC發(fā)病過(guò)程中的作用，證實(shí)了12-LO與VMC發(fā)病過(guò)程中心肌病理積分、肌酸激酶同工酶質(zhì)量(CK-MB mass)等指標(biāo)呈正相關(guān)，并與細(xì)胞內(nèi)游離鈣（Ca2+）、一氧化氮(NO)進(jìn)行相關(guān)分析，發(fā)現(xiàn)12-LO可能是NO和細(xì)胞內(nèi)Ca2+的促發(fā)因子。并應(yīng)用12-LO抑制劑黃芩素對(duì)病毒性心肌炎小鼠進(jìn)行干預(yù)，有效的降低了VMC小鼠心肌中12-LO的表達(dá)，減輕VMC病情，表明12-LO抑制劑黃芩素對(duì)小鼠病毒性心肌炎具有一定的治療效果。結(jié)果說(shuō)明12-LO在小鼠病毒性心肌炎發(fā)病過(guò)程中有重要作用，通過(guò)降低CVB3感染后小鼠心肌組織12-LO的表達(dá)可減輕VMC病情，，為病毒性心肌炎的臨床治療應(yīng)用提供了理論和實(shí)驗(yàn)依據(jù)。 本研究創(chuàng)新點(diǎn):探討12－LO在VMC中的作用，并觀察12－LO抑制劑黃芩素對(duì)VMC小鼠動(dòng)物模型的干預(yù)作用。
[Abstract]:Viral myocarditis (VMC) is a common cardiovascular disease in pediatric clinic. In recent years, the incidence of viral myocarditis is on the rise, and it has become one of the main causes of sudden death in adolescents. Not only that, chronic VMC can also lead to the occurrence of dilated cardiomyopathy. The pathogenesis of VMC has not been fully elucidated and there is no effective treatment for VMC at home and abroad. 12- lipoxygenase (12-LOA) is a kind of multifunctional enzyme with non-heme ferritin as the cogroup, which belongs to the lipase family and is widely distributed in various parts of the body. 12-LO is a kind of important signal molecule with various biological functions. It can promote cell proliferation, participate in many pathological processes through oxidative stress and inflammation, play an important role in cardiovascular, and participate in hypertension. However, the relationship between 12-LO and viral myocarditis has not been studied at home and abroad. The method of making viral myocarditis model by intraperitoneal injection of coxsackie B3 virus CVB3 into BALB/C mice was used in this study. The role of 12-LO in the pathogenesis of VMC was determined by semi-quantitative RT-PCR method and immunohistochemical method, and the pathological integrals of 12-LO and VMC in the pathogenesis of VMC were confirmed. Creatine kinase isoenzyme (CK-MB) was positively correlated with intracellular free Ca ~ (2 +) (Ca ~ (2 +)) and nitric oxide (no). It was found that 12-LO may be the stimulating factor of no and intracellular Ca2, and the intervention of baicalin, a 12-LO inhibitor, on viral myocarditis mice could effectively reduce the expression of 12-LO in the myocardium of VMC mice and alleviate the condition of VMC. The results showed that the 12-LO inhibitor baicalin had a certain therapeutic effect on viral myocarditis in mice. The results showed that 12-LO had an important role in the pathogenesis of viral myocarditis in mice. By reducing the expression of 12-LO in the myocardium of mice infected with CVB3, the condition of VMC can be alleviated, which provides theoretical and experimental basis for the clinical treatment of viral myocarditis. The purpose of this study was to investigate the role of 12-LO in VMC and to observe the effects of baicalin, a 12-LO inhibitor, on VMC mice.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類號(hào)】：R285.5;R725.4

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