本文選題：心梗后心室重構(gòu) + 瘀熱證��； 參考：《湖北中醫(yī)藥大學(xué)》2016年博士論文

【摘要】：理論研究辛開苦降立法于《黃帝內(nèi)經(jīng)》,成方完備于《傷寒論》,對(duì)后世具有深遠(yuǎn)的影響�！秱摗分行灵_苦降法具有調(diào)節(jié)開闔樞、協(xié)調(diào)臟腑等功用,廣泛運(yùn)用于寒熱錯(cuò)雜痞證、上熱下寒證、痰熱互結(jié)證、瘀熱互結(jié)證等證候之中,對(duì)后世脾胃學(xué)說及溫病學(xué)說的形成有一定的影響。心梗后心室重構(gòu)是心梗發(fā)生后心室出現(xiàn)的一系列變化,應(yīng)歸屬于中醫(yī)學(xué)胸痹、心痛、心悸等范疇。中醫(yī)學(xué)對(duì)該病的認(rèn)識(shí),病因主要有外感六淫、情志內(nèi)傷、飲食不節(jié)、年老體衰、久患他病等,病機(jī)可歸結(jié)為本虛標(biāo)實(shí),本虛是指心、肺、脾、腎等臟氣血陰陽的虧損,標(biāo)實(shí)主要是指痰濁、瘀血、水濕的停聚。課題組通過研究歷代文獻(xiàn),并結(jié)合臨床觀察,認(rèn)為隨著人們生活方式、飲食、體質(zhì)等的變化,熱邪在該類疾病中的影響越來越突出。因此提出了瘀熱相互膠結(jié)、相互促進(jìn)使病情不斷演變發(fā)展的觀點(diǎn),并總結(jié)出以《傷寒論》辛開苦降法為主治療該類疾病的思路。以辛開苦降法為基礎(chǔ),結(jié)合現(xiàn)代的藥理研究,擬定了宣痹散結(jié)方,其具有活血化瘀、清熱散結(jié)之功。在多年的臨床運(yùn)用和臨床研究中已顯示出卓越的療效。心室重構(gòu)的現(xiàn)代機(jī)制研究主要有血流動(dòng)力學(xué)改變、神經(jīng)內(nèi)分泌的激活、炎癥反應(yīng)、細(xì)胞凋亡、心肌纖維化等。實(shí)驗(yàn)研究目的本課題主要研究基于《傷寒論》辛開苦降法組方的宣痹散結(jié)方對(duì)心梗后心室重構(gòu)瘀熱證大鼠的防治作用與機(jī)制,并為目前正在作為新藥開發(fā)的該方提供實(shí)驗(yàn)研究支持。方法1.宣痹散結(jié)方對(duì)大鼠疾病和證候的干預(yù)研究。對(duì)Wistar大鼠采用結(jié)扎冠狀動(dòng)脈前降支的方法建立急性心肌梗死模型,存活大鼠喂養(yǎng)4周后即可出現(xiàn)明顯的心室重構(gòu),對(duì)模型B組和宣痹散結(jié)方B組兩組大鼠再以角叉菜膠和活性干酵母制作瘀熱模型。對(duì)心室重構(gòu)的研究主要通過心功能、心臟指數(shù)、形態(tài)學(xué)等參數(shù)來觀察。對(duì)瘀熱證的觀察主要選用心率、體溫、血常規(guī)、血清中炎癥因子表達(dá)水平、血流變等指標(biāo)。2.宣痹散結(jié)方對(duì)血清中炎癥因子的干預(yù)研究。運(yùn)用ELISA法檢測心梗后心室重構(gòu)模型大鼠血清中IL-6、IL-10、TNF-α等炎癥因子的表達(dá)水平,以揭示其對(duì)大鼠心梗后心室重構(gòu)的作用機(jī)制。3.宣痹散結(jié)方對(duì)大鼠血清中與纖維化相關(guān)因子的干預(yù)研究。運(yùn)用ELISA法檢測各組大鼠血清中TGF-β1、MMP-9、TIMP-1、HYP等與纖維化相關(guān)因子的表達(dá)水平。4.宣痹散結(jié)方對(duì)心梗后心室重構(gòu)蛋白表達(dá)的干預(yù)研究。運(yùn)用Western blotting法測定各組大鼠心肌組織中COL1、P-smad3、smad7等蛋白的表達(dá)。5.宣痹散結(jié)方對(duì)心梗后心室重構(gòu)m RNA表達(dá)的干預(yù)研究。采用實(shí)時(shí)熒光定量PCR分析法檢測各組大鼠心肌組織中NF-κB、smad3、smad7、TGF-β1等因子m RNA的表達(dá)。結(jié)果對(duì)心室重構(gòu)的影響:1心功能:同模型A組比較,宣痹散結(jié)方A組可明顯提高大鼠心臟射血分?jǐn)?shù)、但對(duì)心室腔無明顯干預(yù)作用;同模型A組比較,卡托普利可減小舒張期和收縮期的心室腔內(nèi)徑,但對(duì)心室射血分?jǐn)?shù)無改善作用。2光鏡和電鏡顯示:模型A組心肌可見明顯壞死灶,心肌細(xì)胞腫脹,炎性粒細(xì)胞浸潤,心肌線粒體腫脹�？ㄍ衅绽托陨⒔Y(jié)方能夠減輕心肌細(xì)胞腫脹,減輕炎性細(xì)胞浸潤,改善心肌線粒體病理變化。3通過Masson染色觀察發(fā)現(xiàn)卡托普利和宣痹散結(jié)方能顯著減輕心室重構(gòu)后心肌纖維化程度。對(duì)證候的影響:1心率:同模型A組比較,模型B組心率顯著加快,同模型B組比較,宣痹散結(jié)方B組心率顯著降低。2體溫:同模型A組相比,模型B組大鼠在注射活性干酵母后6小時(shí)體溫明顯升高,9小時(shí)最明顯;同模型B組相比,宣痹散結(jié)方B組大鼠體溫降低顯著。3血常規(guī):同模型A組比較,模型B組大鼠的血紅蛋白濃度明顯升高,與模型B組相比,宣痹散結(jié)方B組大鼠的紅細(xì)胞壓積明顯降低。4血流變:同模型A組相比,模型B組大鼠全血黏度中、高切升高顯著,同模型B組相比,宣痹散結(jié)方B組大鼠的全血黏度低切、中切、紅細(xì)胞壓積明顯降低。5血清中炎癥因子:同模型A組比較,模型B組大鼠血清中IL-6、TNF-α的表達(dá)顯著升高,與模型B組相比,宣痹散結(jié)方B組的IL-10表達(dá)明顯升高。作用機(jī)制研究:1宣痹散結(jié)方對(duì)心梗后心室重構(gòu)大鼠血清中炎癥因子IL-6、TNF-α的病理性表達(dá)上調(diào)具有抑制作用,而對(duì)IL-10的表達(dá)具有促生作用。2對(duì)TGF-β1、MMP-9的表達(dá)有抑制作用,而對(duì)TIMP-1有促生作用。3對(duì)COL1、P-smad3蛋白表達(dá)有下調(diào)作用,對(duì)smad7蛋白表達(dá)具有上調(diào)作用。4對(duì)NF-κBm RNA、TGF-β1m RNA、smad3m RNA的表達(dá)有下調(diào)作用,對(duì)smad7m RNA有上調(diào)作用。結(jié)論1.以《傷寒論》辛開苦降法為基礎(chǔ)的宣痹散結(jié)方對(duì)心梗后心室重構(gòu)大鼠的心室重構(gòu)和瘀熱證均能有效地治療和改善。2.宣痹散結(jié)方對(duì)NF-k B、IL-6、TNF-α等促使心室重構(gòu)的炎癥因子有下調(diào)和抑制作用,而對(duì)炎癥抑制因子IL-10有促生作用,提示其可通過抑制NF-k B所介導(dǎo)的IL-6等炎癥因子所誘發(fā)的免疫炎性反應(yīng),從而對(duì)心室重構(gòu)和瘀熱證起到防治作用。3.宣痹散結(jié)方對(duì)TGF-β1、MMP-9、COL1、smad3、P-smad3等促使心室重構(gòu)的纖維化因子有下調(diào)和抑制作用,而對(duì)抑制纖維化的因子TIMP-1、smad7有促生作用,提示宣痹散結(jié)方可作用于TGFβ1-smad通路,從而發(fā)揮其抗心室重構(gòu)的作用。4.宣痹散結(jié)方,可作用于NF-k B通路以消除心室重構(gòu)過程中的免疫炎性反應(yīng),并作用于TGFβ1-Smad通路以減輕心肌纖維化,同時(shí)對(duì)心室重構(gòu)中的瘀熱證候亦具有顯著的改善作用,提示心室重構(gòu)中的NF-k B、TGFβ1-Smad信號(hào)轉(zhuǎn)導(dǎo)通路的活化與瘀熱證的病機(jī)發(fā)展具有潛在相關(guān)性。
[Abstract]:The theoretical study was made in the "Huangdi Neijing", complete in the "Huangdi Neijing", complete in the "Treatise on typhoid fever", and has a profound influence on later generations. There is a certain influence on the formation of the theory of febrile disease. Ventricular remodeling after myocardial infarction is a series of changes in the ventricular appearance after the onset of myocardial infarction. It should belong to the category of chest pain, heart pain and palpitation in traditional Chinese medicine. The main causes of the disease are six prostitution, internal injury, diet, old age and disease, and the pathogenesis can be attributed to the deficiency of this disease. It refers to the loss of the dirty Qi and blood of the heart, lung, spleen and kidney, which mainly refers to phlegm, blood stasis and water dampness. By studying the literature of the past generation and combining with clinical observation, the subject group thinks that the influence of heat is more and more prominent in this kind of disease with the changes of people's lifestyle, diet and physique. Cementation and mutual promotion of the viewpoint of continuous evolution and development of the disease, and summed up the thought of treating this kind of disease mainly by "the theory of typhoid fever" and "Xin Kai bitterness". Based on the method of "Xin Kai bitterness" and modern pharmacological research, it has drawn up the prescription of Xuan Bi San, which has the function of activating blood and removing stasis and clearing away heat and nodding. It has been used in clinical and clinical studies for many years. The modern mechanism of ventricular remodeling mainly includes hemodynamic changes, neuroendocrine activation, inflammatory response, cell apoptosis, myocardial fibrosis, etc. The effect and mechanism of treatment and research support are provided for the new drug that is currently being developed as a new drug. Method 1. the intervention study on the disease and syndrome of rats in 1. Xuan Bi San. The acute myocardial infarction model was established by ligating the anterior descending coronary artery of the coronary artery in the rats. The survival rats were able to have obvious ventricular remodeling after 4 weeks of feeding. The model B group and the two groups of rats in group B of Xuan Bi Jie Fang were used to make the blood stasis model with carrageenan and active dry yeast. The study of ventricular remodeling was mainly observed by cardiac function, cardiac index, morphology and other parameters. Heart rate, body temperature, blood routine, expression level of inflammatory factors and blood rheology were mainly used to observe the syndrome of blood stasis. The intervention study of the serum inflammatory factors in 2. Xuan Bi Jie Fang. The expression level of IL-6, IL-10, TNF- alpha and other inflammatory factors in the serum of ventricular remodeling model rats after myocardial infarction was detected by ELISA method in order to reveal the mechanism of its effect on ventricular remodeling after myocardial infarction in rats. The intervention study on the serum and fibrosis related factors in the rat serum.3. ELISA method was used to detect the expression level of TGF- beta 1, MMP-9, TIMP-1, HYP and the expression level of fibrosis related factors.4. Xuan Bi Jie Fang on ventricular remodeling after myocardial infarction. The Western blotting method was used to determine the expression of COL1, P-smad3, Smad7 and other proteins in each group of rats. The intervention study of the expression of M RNA in the posterior ventricular remodeling. The expression of NF- kappa B, Smad3, Smad7, TGF- beta 1 and other factors m RNA was detected by real-time fluorescence quantitative PCR analysis. The effect on ventricular remodeling: 1 cardiac function: compared with the model A group, the PBI group could significantly increase the ejection fraction of the rat heart, but to the ventricular cavity No significant intervention; compared with the model A group, Kato Pury could reduce the diastolic and systolic ventricular inner diameter, but there was no improvement on the ventricular ejection fraction by.2 light microscopy and electron microscopy: the myocardium in the model A group showed obvious necrotic foci, myocardial cell swelling, inflammatory granulocyte soaking, myocardial mitochondria swelling. Kato Pury and Xuan Bi Sanjie prescription Can reduce the swelling of myocardial cells, reduce inflammatory cell infiltration, improve the pathological changes of myocardial mitochondria.3 through Masson staining observation found that Kato Pury and Xuan Bi San can significantly reduce the degree of myocardial fibrosis after ventricular remodeling. The impact of syndrome: 1 heart rate: compared with the model A group, the heart rate of the model B group is significantly faster than the model B group, The heart rate of group B of Xuan Bi Sanjie group was significantly reduced by.2 temperature: compared with the model A group, the body temperature of the model B rats increased obviously at 6 hours after the injection of active dry yeast, and the most obvious in the 9 hours. Compared with the model B group, the hypothermia of the rats in group B of the Xuan Bi Sanjie group was significantly.3 blood routine: compared with the model A group, the hemoglobin concentration in the model B group was significantly higher than that of the model A group. Compared with the model B group, the hematocrit of the rats in group B of Xuan Bi Jie Fang group obviously decreased the blood rheology of.4: compared with the model A group, the high shear increased significantly in the whole blood viscosity of the model B group. Compared with the model B group, the whole blood viscosity of the B group of the Xuan Bi Sanjie group was lower than that of the model B group, and the red cell pressure product obviously reduced the inflammatory factors in the.5 serum: the ratio of the model A group to the model A group was significantly lower than that of the model group. The expression of IL-6 and TNF- a in the serum of model B rats increased significantly. Compared with the model B group, the IL-10 expression of B group in the Xuan Bi Sanjie group was significantly increased. The mechanism of action study: 1 Xuan Bi Sanjie prescription inhibited the up regulation of the pathological expression of inflammatory factor IL-6, TNF- a in the serum of ventricular remodeling rats after myocardial infarction, and the expression of IL-10 was promoted. The effect of.2 on the expression of TGF- beta 1 and MMP-9 inhibited the expression of TIMP-1, while.3 had a down-regulation effect on COL1, P-smad3 protein expression and the up regulation of Smad7 protein expression, and the expression of NF- kappa Bm RNA was up. The foundation of Xuan Bi Sanjie Fang can effectively treat and improve the ventricular remodeling and stasis heat syndrome of ventricular remodeling rats after myocardial infarction, which can effectively reduce and inhibit the inflammatory factors of.2. B, IL-6, TNF- A and so on, while promoting the growth of the inflammatory inhibitory factor IL-10, suggesting that it can inhibit IL-6 through the inhibition of NF-k B. The immune inflammatory response induced by inflammatory factors, thus the prevention and control of ventricular remodeling and stasis heat syndrome,.3. Xuan Bi Sanjie Fang has a down-regulation and inhibition effect on TGF- beta 1, MMP-9, COL1, Smad3, P-smad3 and other fibrosis factors that promote ventricular remodeling, but has a stimulating effect on the inhibition of fibrosis, TIMP-1 and Smad7, suggesting that Xuan Bi San can be used as a prescription. The use of TGF beta 1-smad pathway, thus exerting its anti ventricular remodeling effect,.4. Xuan Bi square, can act on the NF-k B pathway to eliminate the inflammatory response in the process of ventricular remodeling, and act on the TGF beta 1-Smad pathway to reduce myocardial fibrosis, and also have a significant improvement in the syndrome of blood stasis in ventricular remodeling, suggesting ventricular weight. The activation of NF-k B, TGF 1-Smad signaling pathway is correlated with pathogenesis of stasis heat syndrome.

【學(xué)位授予單位】：湖北中醫(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)】：R222.2

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