本文選題：小兒病毒性心肌炎　切入點(diǎn)：解毒活血、益氣養(yǎng)陰　出處：《山東中醫(yī)藥大學(xué)》2016年博士論文

【摘要】：目的:探討童心康合劑治療小兒病毒性心肌炎的理論依據(jù)及免疫機(jī)制。方法:基于中醫(yī)傳承輔助平臺(tái)整理小兒病毒性心肌炎相關(guān)古代及現(xiàn)代文獻(xiàn),分析病因病機(jī)、治法方藥研究概況,探討毒瘀互結(jié),氣陰兩虛的病因病機(jī)理論,提出解毒活血,益氣養(yǎng)陰的治療原則,研制成童心康合劑。采用注射豬心肌肌球蛋白免疫Lewis大鼠建立實(shí)驗(yàn)性自身免疫性心肌炎模型,予童心康合劑干預(yù)21天后,觀察心肌病理變化,ELISA法檢測(cè)血清心肌肌鈣蛋白T、腦鈉素、γ-干擾素、白介素-2、白介素-4、白介素-6水平,免疫組化法檢測(cè)心肌白介素-2、白介素-2受體、信號(hào)轉(zhuǎn)導(dǎo)及轉(zhuǎn)錄因子5的表達(dá);藥物干預(yù)56天后,Masson染色觀察心肌纖維化,免疫組化法檢測(cè)基質(zhì)金屬蛋白酶9和抑制因子1的表達(dá)。結(jié)果:提出毒瘀互結(jié)為小兒病毒性心肌炎發(fā)病之基礎(chǔ),氣陰兩傷為發(fā)病之關(guān)鍵,邪正消長(zhǎng)變化致病情錯(cuò)綜復(fù)雜;確立解毒活血、益氣養(yǎng)陰的治則,據(jù)法研制童心康合劑。實(shí)驗(yàn)證實(shí)童心康合劑能顯著改善免疫21天實(shí)驗(yàn)性自身免疫性心肌炎模型大鼠的體重下降、減輕心肌細(xì)胞的壞死和炎性浸潤(rùn)、降低反映心肌損傷的心肌肌鈣蛋白T和心衰定量標(biāo)志物腦鈉素的水平,降低血清γ-干擾素、白介素-2水平,升高白介素-4、白介素-6水平,下調(diào)心肌組織白介素-2、白介素-2受體、信號(hào)轉(zhuǎn)導(dǎo)及轉(zhuǎn)錄因子5的表達(dá);對(duì)于免疫56天的實(shí)驗(yàn)性自身免疫性心肌炎模型大鼠有抗纖維化作用,上調(diào)心肌組織基質(zhì)金屬蛋白酶9的表達(dá),下調(diào)其抑制因子1的表達(dá)。結(jié)論:本研究認(rèn)為毒瘀互結(jié),氣陰兩虛是小兒病毒性心肌炎的重要病機(jī),提出了解毒活血,益氣養(yǎng)陰的治療原則。實(shí)驗(yàn)研究證實(shí)童心康合劑可以減輕實(shí)驗(yàn)性自身免疫性心肌炎模型大鼠的心肌炎癥,通過(guò)降低Th1細(xì)胞分泌的γ-干擾素和白介素-2,提高Th2細(xì)胞分泌的白介素-4和白介素-6水平,調(diào)節(jié)實(shí)驗(yàn)性自身免疫性心肌炎模型大鼠出現(xiàn)的Th1/Th2失衡,并調(diào)節(jié)相關(guān)白介素-2/信號(hào)轉(zhuǎn)導(dǎo)及轉(zhuǎn)錄因子5信號(hào)通路是其可能機(jī)制之一;上調(diào)心肌組織基質(zhì)金屬蛋白酶9的表達(dá),下調(diào)抑制因子1的表達(dá),發(fā)揮抗纖維化作用亦是其保護(hù)心肌的原因,為“解毒活血、益氣養(yǎng)陰”這一新策略提供實(shí)驗(yàn)依據(jù)。
[Abstract]:Objective: to explore the theoretical basis and immune mechanism of Tongxinkang mixture in the treatment of viral myocarditis in children. The general situation of the research on the prescriptions of the treatment method, the discussion on the theory of the etiology and pathogenesis of the combination of toxin and stasis, the deficiency of qi and yin, and the treatment principle of detoxifying, activating blood circulation and nourishing qi and nourishing yin. Tongxinkang mixture was prepared. Experimental autoimmune myocarditis model was established in Lewis rats immunized with porcine cardiac myosin. The model was treated with Tongxinkang mixture for 21 days. Serum levels of cardiac troponin T, brain natriuretic peptide (BNP), interferon 緯 (IFN 緯), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6) were detected by Elisa, and myocardial interleukin-2 (IL-2) and interleukin-2 receptor (IL-2R) were detected by immunohistochemistry. Signal transduction and expression of transcription factor 5, myocardial fibrosis were observed by Masson staining after 56 days of drug intervention. Results: the expression of matrix metalloproteinase 9 and inhibitor of matrix metalloproteinase 1 was detected by immunohistochemistry. Results: it was suggested that the combination of toxin and blood stasis was the basis of the pathogenesis of viral myocarditis in children, Qi and Yin injuries were the key to the development of viral myocarditis, and the changes of pathogenic factors were complicated. To establish the principle of detoxifying and promoting blood circulation and nourishing qi and nourishing yin, Tongxinkang mixture was developed according to the method. The experiment proved that Tongxinkang mixture can significantly improve the weight loss of experimental autoimmune myocarditis model rats after 21 days of immunization. The levels of cardiac troponin T and brain natriuretic peptide (BNP), a quantitative marker of heart failure, and the levels of serum interferon 緯 and interleukin-2 were decreased, and the levels of interleukin-4 and interleukin-6 were increased. Down-regulate the expression of interleukin-2, interleukin-2 receptor, signal transduction and transcription factor 5 in myocardial tissue, and have anti-fibrosis effect on experimental autoimmune myocarditis model rats immunized for 56 days. Conclusion: this study suggests that toxin and blood stasis and deficiency of qi and yin are the important pathogenesis of viral myocarditis in children. Experimental study shows that Tongxinkang mixture can reduce myocarditis in experimental autoimmune myocarditis model rats. By decreasing interferon 緯 and interleukin-2 secreted by Th1 cells, increasing the levels of interleukin-4 and interleukin-6 secreted by Th2 cells, regulating the imbalance of Th1/Th2 in experimental autoimmune myocarditis rats. Regulating the related interleukin-2 / signal transduction and transcription factor 5 signaling pathway is one of its possible mechanisms, and up-regulates the expression of matrix metalloproteinase-9 and down-regulates the expression of inhibitor of metalloproteinase-1. The anti-fibrosis effect is also the cause of myocardial protection, which provides experimental basis for the new strategy of "detoxification, promoting blood circulation, supplementing qi and nourishing yin".
【學(xué)位授予單位】：山東中醫(yī)藥大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R272

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