本文關(guān)鍵詞：脾氣虛證模型大鼠心功能變化及其機(jī)制的研究　出處：《遼寧中醫(yī)藥大學(xué)》2016年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 脾氣虛證 心功能 腦納肽 環(huán)磷酸腺苷 堿性成纖維生長因子

【摘要】：目的:中醫(yī)學(xué)基本理論認(rèn)為,脾臟“為后天之本”“氣血生化之源”,是提供后天生命活動(dòng)所需物質(zhì)最重要器官。而“脾主運(yùn)化、統(tǒng)血”是脾臟的核心功能�，F(xiàn)代醫(yī)學(xué)已明確,維系生命活動(dòng)最基本物質(zhì)是三磷酸腺苷(ATP)為代表的能量物質(zhì)。而ATP的來源與生成則包括了物質(zhì)的消化與吸收、血液的運(yùn)輸、跨膜物質(zhì)轉(zhuǎn)運(yùn)以及以線粒體為平臺(tái)的氧化磷酸化等生物學(xué)過程。因此,“脾主運(yùn)化、統(tǒng)血”功能與現(xiàn)代醫(yī)學(xué)能量代謝的生物學(xué)過程有著密切的內(nèi)在聯(lián)系。但中醫(yī)學(xué)理論認(rèn)為,“脾主運(yùn)化與統(tǒng)血”是脾臟象的兩個(gè)不同核心功能,“脾統(tǒng)血”包含了“生血、行血、攝血”作用。我們根據(jù)中醫(yī)學(xué)理論與現(xiàn)代醫(yī)學(xué)能量代謝的生物學(xué)過程及其機(jī)制,認(rèn)為脾生血應(yīng)與血液成分的生成有關(guān);脾攝血?jiǎng)t與止血和凝血機(jī)制有關(guān)。而對(duì)于“行血”則提出以下科學(xué)假說:“脾統(tǒng)血”功能可能屬于“脾主運(yùn)化”功能的一部分,即物質(zhì)消化與吸收后,通過血液循環(huán)系統(tǒng)向全身組織細(xì)胞輸送的部分功能,其機(jī)制可能是脾氣虛導(dǎo)致了BNP的變化,進(jìn)而影響了c AMP-PKA通路,導(dǎo)致心功能發(fā)生了變化。本工作目的,運(yùn)用電生理學(xué)及分子生物學(xué)技術(shù),觀察脾氣虛證模型大鼠心功能變化,并探討其可能的分子生物學(xué)機(jī)制,旨在闡明中醫(yī)學(xué)“脾主運(yùn)化、統(tǒng)血”,特別是“運(yùn)化”與行血功能之間關(guān)系的科學(xué)內(nèi)涵同時(shí),為臨床“從脾論治”心血管疾病提供實(shí)驗(yàn)依據(jù)。方法:1.實(shí)驗(yàn)動(dòng)物與分組由本溪實(shí)驗(yàn)動(dòng)物中心(遼寧長生生物科技有限公司)購入30只SPF級(jí)雄性SD大鼠,體重200±10g,許可證號(hào)SCXK(遼-2010-0001),進(jìn)行一周時(shí)間適應(yīng)性飼養(yǎng)后,隨機(jī)分為正常組和脾氣虛模型組兩組,每組各15只。2.脾氣虛證模型復(fù)制與評(píng)價(jià):大鼠脾氣虛證模型復(fù)制方法根據(jù)中醫(yī)學(xué)病因基本理論,參照《中藥新藥臨床研究指導(dǎo)原則》[1]和《中醫(yī)實(shí)驗(yàn)動(dòng)物模型方法學(xué)》[2]中制備脾虛模型的方法,運(yùn)用飲食不節(jié)加勞倦內(nèi)傷復(fù)合因素復(fù)制脾氣虛證大鼠模型。即24小時(shí)自由飲食水,禁食不禁水48小時(shí);同時(shí)每天進(jìn)行游泳25分鐘,水溫在35℃~37℃之間,室溫保持在23±1℃;連續(xù)造模2周后進(jìn)行模型評(píng)價(jià)。脾氣虛證模型成模評(píng)價(jià)方法:依據(jù)文獻(xiàn)[3]分別對(duì)模型大鼠宏觀表征主要癥狀,神疲、乏力、食少納呆、身體消瘦、便軟腹瀉等進(jìn)行了量化,剔除沒有達(dá)到標(biāo)準(zhǔn)大鼠。正常組正常飲食水,沒有施加刺激因素。3.核心指標(biāo)檢測方法3.1左心功能檢測:采用小動(dòng)物超聲影像系統(tǒng)進(jìn)行大鼠心功能檢測;該系統(tǒng)由加拿大Visua Sonics公司購入,型號(hào)VEVO2100超高分辨率。于模型組造模成功后,禁食24小時(shí),分別檢測正常組及模型組大鼠左心功能,檢測部位選擇大鼠房室環(huán),參照小動(dòng)物超聲心動(dòng)圖儀器內(nèi)部設(shè)定的的心電圖既有模式連接儀器。連接完成后,調(diào)整儀器參數(shù):動(dòng)態(tài)量程(Dynamic range),60d B;顯示地圖(Display map),CS;掃描速率(Sweep speed),1000Hz;對(duì)等(Contrast),50;亮度(Brightness)50。等待大鼠呼吸平穩(wěn),心電圖能夠清楚的展現(xiàn)出來后,開始記錄大鼠10秒鐘的超聲心動(dòng)圖,儀器隨機(jī)從10秒鐘的片段中選取3段進(jìn)行測量,給出平均值,從而獲得各組大鼠的左室射血分?jǐn)?shù)(LVEF)、左室收縮末期容積(ESV)、左室每搏輸出量(SV)、左室舒張末期容積(EDV)的平均值。3.2.取材及分子生物學(xué)指標(biāo)檢測:取材方法:實(shí)驗(yàn)結(jié)束后,兩組大鼠禁止飲食24小時(shí),選用20%氨基甲酸乙酯溶液對(duì)大鼠進(jìn)行麻醉,大鼠腹部備皮,解剖,5ml注射器抽取大鼠腹主動(dòng)脈血;隨后用醫(yī)用剪刀剪開胸腔后,取大鼠心臟,醫(yī)用手術(shù)刀迅速切取心臟組織,根據(jù)檢測指標(biāo)要求分別進(jìn)行采血即組織樣本制備。采用常規(guī)HE染色方法觀察心臟組織形態(tài)學(xué)變化;透射電鏡檢測心肌組織細(xì)胞形態(tài)學(xué)改變。采用Elisa法測定血清及心肌組織BNP、c AMP的含量;采用免疫組化法測心肌細(xì)胞BNP受體蛋白的表達(dá)。采用蛋白質(zhì)印跡法(Western Blot)測定心肌中BNP的表達(dá);采用Q-PCR方法檢測b FGF、PKA m RNA表達(dá)。4.統(tǒng)計(jì)方法:本實(shí)驗(yàn)所有數(shù)據(jù)統(tǒng)計(jì)學(xué)分析處理都由SPSS 13.0統(tǒng)計(jì)軟件進(jìn)行,并用均數(shù)±標(biāo)準(zhǔn)差(`x±s)的方式表達(dá)數(shù)據(jù)結(jié)果,采用校正t檢驗(yàn)(方差不齊時(shí))或獨(dú)立樣本t檢驗(yàn)(方差齊時(shí))比較計(jì)量資料,以P0.05為差異具有統(tǒng)計(jì)學(xué)意義。結(jié)果:1.大鼠心功能檢測結(jié)果:與正常組比較,脾氣虛證模型組大鼠心臟左室收縮末期容積(ESV)數(shù)值明顯升高(P0.05);而左室舒張末期容積(EDV)、左室射血分?jǐn)?shù)(LVEF)、左室每搏輸出量(SV)則明顯低于正常組(P0.05)。2.心肌組織HE染色結(jié)果:正常組大鼠心肌細(xì)胞纖維結(jié)構(gòu)顯示較為清楚、心肌纖維排列方式整齊、心肌細(xì)胞橫向紋路清晰,并無出現(xiàn)炎癥細(xì)胞的浸潤現(xiàn)象,心肌細(xì)胞結(jié)構(gòu)為正常;脾氣虛證模型組大鼠心肌萎縮,細(xì)胞排列方式紊亂、細(xì)胞壞死,存在細(xì)胞脂肪變性及渾濁等變化。3.心肌組織透射電鏡檢測結(jié)果:正常組心肌細(xì)胞排列正常,肌膜結(jié)構(gòu)清晰,心肌纖維排列尚規(guī)則,Z線可見。肌纖維內(nèi)線粒體豐富,結(jié)構(gòu)完好,線粒體無腫脹、變性及壞死;間質(zhì)未見纖維組織增生及炎細(xì)胞浸潤。模型組肌纖維排列疏松(水腫),偶見閏板分離,部分肌絲溶解;肌絲A帶、I帶結(jié)構(gòu)不清,Z線仍可見;線粒體較豐富,但大小不一,線粒體基質(zhì)電子密度增高。4.BNP、c AMP含量檢測結(jié)果:與正常組比較,脾氣虛證模型組大鼠血清及心肌組織中BNP、c AMP含量均明顯升高,具有統(tǒng)計(jì)學(xué)意義(P0.05)。5.BNP受體表達(dá)檢測結(jié)果:大鼠心肌組織中BNP受體表達(dá),多見于細(xì)胞膜,細(xì)胞胞漿亦有表達(dá)但較少,呈棕黃色為陽性表達(dá)。正常組大鼠心肌細(xì)胞染色表現(xiàn)為弱陽性,而脾氣虛證模型組的陽性物表達(dá)的細(xì)胞數(shù)明顯多于正常組;與正常組比較,脾氣虛證模型組其心肌細(xì)胞中BNP的IOD值明顯升高,且差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。6、PKA與b FGF m RNA表達(dá)檢測結(jié)果:目的基因得到有效擴(kuò)增,因目的基因的擴(kuò)增曲線走勢符合S型曲線。熔解曲線中顯示沒有出現(xiàn)雜峰,只有一個(gè)峰值,說明目的基因的定量測定可以采用該體系。對(duì)比兩組間PKA及b FGF m RNA的表達(dá)情況,脾氣虛證模型組比正常組具有明顯的增加(P0.05)。本實(shí)驗(yàn)結(jié)果顯示,脾氣虛證模型大鼠的“脾主運(yùn)化”功能損傷時(shí),其左室收縮末期容積增大,舒張末期容積、每搏輸出量等均發(fā)生變化,特別是左心射血分?jǐn)?shù)發(fā)生改變,表明脾氣虛“運(yùn)化”功能發(fā)生障礙時(shí),心臟射血功能也明顯受到影響,即表現(xiàn)為“行血”功能下降。本結(jié)果支持了“脾統(tǒng)血”功能可能屬于“脾主運(yùn)化”功能一部分的假說�？偨Y(jié)本實(shí)驗(yàn)結(jié)果可以認(rèn)為,脾氣虛證,“脾主運(yùn)化”功能失職時(shí)其“統(tǒng)血”功能也受到影響,其可能機(jī)制之一是由于心肌組織BNP及其受體表達(dá)上調(diào),激動(dòng)了c AMP-PKA通路并通過b FGFm RNA過度表達(dá),從而造成心肌組織形態(tài)學(xué)發(fā)生改變,最終導(dǎo)致其左心室射血功能下降。結(jié)論:1、脾氣虛證模型大鼠左心室射血功能明顯降低。其中左室收縮末期容積(ESV)升高;左室舒張末期容積(EDV)、左室射血分?jǐn)?shù)(LVEF)、左室每搏輸出量(SV)則明顯降低。2、脾氣虛證模型大鼠心肌組織萎縮,炎癥細(xì)胞浸潤、其肌纖維排列紊亂、肌絲與核發(fā)生溶解;線粒體大小不均。3、脾氣虛證模型大鼠心肌組織與血清中BNP含量增加,其心肌細(xì)胞BNP受體表達(dá)上調(diào)。4、脾氣虛證模型大鼠心肌組織c AMP含量升高、PKA及b FGFm RNA表達(dá)上調(diào)。
[Abstract]:Objective: TCM basic theory, "the spleen is the acquired" the source of Qi and blood ", is to provide the required material acquired life activities. The most important organs and spleen transport, the blood" is the core function of spleen. Modern medicine has been clear, sustain the life of the most basic activities of substances (ATP ATP) as the representative of the energy sources and generate ATP. It includes the matter digestion and absorption of blood transport, transmembrane transport and mitochondrial oxidative phosphorylation as a platform for other biological processes. Therefore, the "spleen transport, the blood biological process function and energy metabolism in modern medicine there is a close relationship. But the theory of traditional Chinese medicine thinks," spleen transport and blood "are two different core functions as the" spleen, splenic blood "contains" blood, blood, blood ". According to our medical theory and Biological process and mechanism of modern medicine, energy metabolism, blood and spleen that should generate blood components; spleen blood intake is related to blood coagulation and hemostasis mechanism. For the "blood" is to put forward the following hypothesis: "the spleen blood" may be a part of "spleen transport". The substance of digestion and absorption, part of the function of transport to body tissues through the blood circulation system, which may be the mechanism of spleen deficiency leads to the change of BNP, thereby affecting the C AMP-PKA pathway, leading to the changes of heart function. The objective of this work, the use of electrophysiology and molecular biology technology to observe the changes of heart function model rats with spleen deficiency syndrome, and to explore its possible molecular mechanism, to learn "spleen transport clarificate, the blood", especially the scientific connotation of "the relationship between transport and blood function at the same time, for the clinical" On the treatment of cardiovascular diseases and provide experimental evidence from the spleen. Methods: 1. experimental animal and group by Benxi Experimental Animal Center (Liaoning Changsheng biotechnology limited company) bought 30 male SD SPF rats, weight 200 + 10g, license No. SCXK (Liaoning -2010-0001), a week after adaptive feeding time. Were randomly divided into normal group and spleen qi deficiency model group two groups, 15 rats in each group of.2. replication and evaluation: the model of spleen qi deficiency in spleen qi deficiency rats model according to the basic theory of the etiology of traditional Chinese medicine, preparation method for reference "method of spleen deficiency model of clinical research on new drugs of experimental animal medicine guidelines of >[1] and >[2] in model" in the use of improper diet and internal root composite factors to copy the model of spleen qi deficiency rats. 24 hours of free food and water, but the water fasting for 48 hours; at the same time every day to swim for 25 minutes, the temperature between 35 DEG ~37 DEG, keep at room temperature In 23 - 1 DEG C; was evaluated after 2 weeks of continuous modeling. The model of spleen qi deficiency model evaluation methods: Based on literature [3] were the main symptoms, rat model of macro characterization of lassitude, weakness, anorexia, body weight loss, diarrhea and other soft is quantified, excluding did not reach the standard of rats. The normal group with normal diet water, no stimulus detection factor.3. 3.1 core indicators of left ventricular function detected by small animal imaging system of rat cardiac function detection; the system by the Canadian Visua Sonics company purchased VEVO2100 type ultra high resolution. In the model group after modeling, fasting for 24 hours, respectively, left heart the function of the normal group and the model group rats were detected, rat atrioventricular ring detection site, according to small animal echocardiography instrument set the ECG model as connecting instrument. The connection is completed, the adjustment of the instrument parameters: dynamic range (Dynamic range), 60d B (Display map); map display, CS; scanning rate (Sweep speed), 1000Hz (Contrast, 50); equivalence; brightness (Brightness) 50. rats for respiration, ECG can be clearly demonstrated after the start of rats was recorded 10 seconds of ultrasonic cardiogram. The instrument from 10 randomly selected 3 seconds of footage segments were measured, gives the average value, so as to obtain the rats left ventricular ejection fraction (LVEF), left ventricular end systolic volume (ESV), left ventricular stroke volume (SV), left ventricular end diastolic volume (EDV) of the average detection.3.2. material and molecular biology index: sampling method: after the end of the experiment, two groups of rats to prohibit eating for 24 hours, with 20% urethane solution on rats were anesthetized rat abdominal skin, anatomy, 5ml syringe from rat abdominal aortic blood; followed by medical scissors after thoracic, from rat heart medical, surgical Rapid knife cut heart tissue, according to the detection requirements for blood or tissue samples were prepared by conventional HE. Observe the morphological changes of heart tissue staining; cell morphology change detection of myocardial tissue by transmission electron microscopy. The determination of serum and myocardial tissue BNP by Elisa method, the content of C AMP; the expression of BNP in myocardial cell receptor test protein by Western blot method. (Western Blot) expression of myocardial BNP were determined by Q-PCR method; detection of B FGF PKA, m RNA expression of.4. statistical methods: the statistical analysis of all data processing by the statistical software SPSS 13, and the mean and standard deviation (`x + S). Expression of the results, the correction of t test (variance missing) or independent samples t test (Fang Chaqi) measurement data are compared with P0.05, the difference was statistically significant. Results: the cardiac function of 1. rats respectively. Results: compared with normal group, spleen qi deficiency model rats, left ventricular end systolic volume (ESV) were significantly increased (P0.05); left ventricular end diastolic volume (EDV), left ventricular ejection fraction (LVEF), left ventricular stroke volume (SV) was significantly lower than that of normal group (P0.05).2. myocardial tissue HE staining results: normal rat myocardial cell fiber structure shows more clearly, the arrangement of myocardial fiber neat, myocardial cells transverse lines clear, there is no infiltration of inflammatory cells, myocardial cell structure is normal; spleen qi deficiency model group rat myocardial atrophy, cell arrangement disorder, cell necrosis. The cellular fatty degeneration and turbidity changes of.3. in myocardial tissue by electron microscopy results: normal myocardial cells were normal, muscle membrane structure clear, myocardial fibers still rules, the Z line is visible. In skeletal muscle fibers rich in mitochondria and mitochondrial structure intact, no The swelling, degeneration and necrosis; no interstitial fibrous tissue hyperplasia and inflammatory cell infiltration. The model group loosely arranged muscle fibers (edema), occasionally intercalated plate separation, part of myofilament dissolved; filaments A band, I band structure is not clear, the Z line is still visible; mitochondria were abundant, but not the size of a line. Mitochondrial matrix increased electron density.4.BNP, c test results of AMP content: compared with the normal group, spleen qi deficiency model rats serum and myocardial tissue BNP, C content of AMP were increased significantly, with statistical significance (P0.05).5.BNP receptor expression results: expression of BNP receptor in rat myocardium, found in the cell membrane the cytoplasm was also expressed, but less, brownish yellow positive expression. Normal rats myocardial cells were weakly positive, the number of cells and expression of spleen qi deficiency model group were significantly higher than the normal group; comparing with normal group, spleen qi deficiency model group, the cardiac muscle fine Cell BNP of IOD increased obviously, and the difference was statistically significant (P0.05).6, PKA B and FGF m test results: the expression of RNA gene was effectively amplified, because the amplification curve of target gene in line with the trend of the S curve. The melting curve shows no impurity peaks, only one peak, indicating the quantitative determination the target gene can be used in the system. The expression of PKA and B were compared between two groups of FGF m of RNA, spleen qi deficiency model group significantly increased than normal group (P0.05). The experimental results show that the model of spleen qi deficiency rats "spleen transport function injury, the left ventricular end systolic increased volume, end diastolic volume, stroke volume and change, especially the left ventricular ejection fraction changes showed that spleen deficiency" transport "dysfunction, cardiac ejection function was significantly affected by the performance of the" blood "function Drop. The results support the "splenic blood" function may belong to the spleen transport function part of the hypothesis. The experimental results can be summarized that "spleen deficiency syndrome, spleen transport function of dereliction of duty on the part of its" the blood "function is also affected, one of the mechanisms may be due to the upregulation of BNP expression and its receptors in cardiac muscle tissue, excited C AMP-PKA pathway by B FGFm overexpression of RNA, resulting in myocardial tissue morphological changes, resulting in the left ventricular ejection function decreased. Conclusion: 1. The left ventricular ejection function of spleen qi deficiency model rats decreased obviously. The left ventricular end systolic volume (ESV) increased; left ventricular end diastolic volume (EDV), left ventricular ejection fraction (LVEF), left ventricular stroke volume (SV) decreased.2, myocardial tissue in the rat model of spleen qi deficiency atrophy, inflammatory cell infiltration, the muscle fibers arranged in disorder, myofilament and nuclear dissolution; The size of mitochondria was not equal to.3. In the spleen qi deficiency syndrome rats, the BNP content in myocardium and serum increased, the expression of BNP receptor in cardiac myocytes increased by.4, and the C AMP content in myocardial tissue increased, the expression of PKA and B FGFm RNA increased in rats with spleen qi deficiency syndrome.

【學(xué)位授予單位】：遼寧中醫(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)】：R-332;R228

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2 趙t

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