本文選題：脾氣虛證 + 針刺�。� 參考：《大連醫(yī)科大學(xué)》2017年博士論文

【摘要】：背景:脾氣虛證(Syndrome of Deficiency of Spleen-Qi,SDSQ)是臨床上最常見的虛證之一,臨床上主要是以進餐后胃部飽脹不適、消瘦乏力、倦怠易疲勞、面色枯黃無血色、大便稀溏等為臨床表現(xiàn)�，F(xiàn)代西方醫(yī)學(xué)研究證實:脾氣虛證的主要表現(xiàn)是胃腸道運動功能、消化吸收功能、內(nèi)分泌功能和免疫功能等多系統(tǒng)、多因素的紊亂。然而消化道運動功能的恢復(fù)是消化吸收功能、內(nèi)分泌和免疫功能低下等系統(tǒng)恢復(fù)的前提條件。胃腸道運動功能的恢復(fù)既是糾正胃腸道損害的最初始同時也是最關(guān)鍵的一步。促進胃腸道動力的治療能夠有效的治療胃腸道運動功能、消化吸收功能、內(nèi)分泌和免疫功能障礙等。所以說,探討脾氣虛證胃腸道運動功能障礙的本質(zhì),研究治療脾氣虛證胃腸道運動功能障礙的有效方法變得十分必要。針灸作為祖國醫(yī)學(xué)中一種傳統(tǒng)的治療方法,在中國應(yīng)用已有兩千多年的歷史。在臨床實踐中,越來越多的研究顯示,針刺足三里、天樞穴可以糾正胃腸道運動功能紊亂,有效的治療脾氣虛證,在治療功能性胃腸道疾病方面有著自己獨特的優(yōu)勢,但確切的機制仍不十分清楚,需要進一步的研究。目的:通過苦寒瀉下結(jié)合耗氣破氣的方法建造脾氣虛證大鼠模型,以脾氣虛證大鼠小腸腸神經(jīng)-Cajal間質(zhì)細胞-平滑肌細胞網(wǎng)絡(luò)為研究對象,觀察脾氣虛證大鼠小腸腸神經(jīng)-Cajal間質(zhì)細胞-平滑肌細胞網(wǎng)絡(luò)的損傷,研究脾氣虛證的發(fā)病機制。然后對脾氣虛證大鼠進行針刺足三里、天樞穴進行治療,觀察針灸對脾氣虛證大鼠小腸腸神經(jīng)-Cajal間質(zhì)細胞-平滑肌細胞網(wǎng)絡(luò)損傷的修復(fù)作用,進一步探索針刺足三里、天樞穴治療脾氣虛證的作用機制。方法:選取清潔級成年Wistar大鼠,雌雄不限,參考中國中醫(yī)科學(xué)院陳小野教授的方法,先通過體質(zhì)篩選,再采用苦寒瀉下結(jié)合耗氣破氣的方法建造脾氣虛證大鼠動物模型。將大鼠分為對照組、模型組、自然恢復(fù)組、假針刺穴位組(針刺非經(jīng)非絡(luò)穴位組)、針刺天樞穴治療組、針刺足三里穴治療組、針刺足三里+天樞穴聯(lián)合治療組。造模成功及治療結(jié)束后,采用頸椎脫臼法處死大鼠,打開腹腔切取小腸的近幽門端用于實驗。本實驗研究分為以下三部分:第一部分、通過觀察一般行為學(xué)變化、監(jiān)測體重、測定尿d-木糖排泄率、大體解剖觀察、測定胃排空率、測定小腸推進率、病理學(xué)he染色觀察、透射電鏡超微結(jié)構(gòu)檢測、免疫熒光標記激光掃描共聚焦顯微鏡檢測等方法來觀察脾氣虛證大鼠小腸腸神經(jīng)-icc-平滑肌網(wǎng)絡(luò)的形態(tài)學(xué)變化和針刺足三里、天樞穴的修復(fù)作用。第二部分、通過免疫熒光雙重標記激光掃描共聚焦顯微鏡檢測的方法來觀察脾氣虛證大鼠小腸腸神經(jīng)-icc之間的信號傳導(dǎo)通路的損傷和針刺足三里、天樞穴的修復(fù)作用。第三部分、通過免疫組織化學(xué)、westernblotting、qpcr等方法來觀察脾氣虛證大鼠小腸icc-平滑肌之間的信號傳導(dǎo)通路的損傷和針刺足三里、天樞穴的修復(fù)作用。通過三部分實驗來探索脾氣虛證所導(dǎo)致的胃腸道運動功能障礙的實質(zhì)和針刺足三里、天樞穴治療脾氣虛證的作用機制。結(jié)果:1.與正常對照組相比,脾氣虛證模型組大鼠的一般行為學(xué)表現(xiàn)明顯變差,大體解剖肉眼觀察小腸蠕動明顯緩慢,小腸組織he病理學(xué)表現(xiàn)小腸組織結(jié)構(gòu)明顯破壞,icc的超微結(jié)構(gòu)遭到嚴重破壞,體重增長明顯緩慢,尿d-木糖排泄率、胃排空率、小腸推進率均明顯降低,腸神經(jīng)系統(tǒng)的pgp9.5神經(jīng)纖維、ach神經(jīng)纖維、sp神經(jīng)纖維、vip神經(jīng)纖維、no神經(jīng)纖維、icc、smc、ens-icc-smc網(wǎng)絡(luò)的數(shù)量明顯減少,結(jié)構(gòu)遭到明顯破壞(p0.05),而模型組、自然恢復(fù)組、假針刺組三組之間相互比較,無明顯差異(p0.05)。與模型組相比,天樞組、足三里組略有好轉(zhuǎn)(p0.05),但天樞組、足三里組兩組之間比較,無明顯差異(p0.05)。與天樞組、足三里組相比,聯(lián)合治療組效果明顯好轉(zhuǎn)(p0.05),但仍低于正常對照組(p0.05)。總體來說,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。2.與正常對照組相比,脾氣虛證模型組大鼠小腸腸神經(jīng)-icc之間的信號傳導(dǎo)通路,主要有ach神經(jīng)纖維的m受體、sp神經(jīng)纖維的nk受體、no神經(jīng)纖維的受體-鳥苷酸環(huán)化酶(sgc)、vip神經(jīng)纖維的vpac受體、pka、pkc、cgk/pkg數(shù)量明顯減少,其信號通路g蛋白偶聯(lián)受體-camp-pka途徑、g蛋白偶聯(lián)受體-磷脂酶c(plc)-pkc途徑、sgc-cgmp-pkg途徑明顯遭到破壞(p0.05),而模型組、自然恢復(fù)組、假針刺組三組之間相互比較,無明顯差異(p0.05)。與模型組相比,天樞組、足三里組略有好轉(zhuǎn)(p0.05),但天樞組、足三里組兩組之間比較,無明顯差異(p0.05)。與天樞組、足三里組相比,聯(lián)合治療組效果明顯好轉(zhuǎn)(p0.05),但仍低于正常對照組(p0.05)。總體來說,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。3.與正常對照組相比,脾氣虛證模型組大鼠小腸icc-平滑肌之間的信號傳導(dǎo)通路,主要是縫隙連接和縫隙連接蛋白43數(shù)量明顯減少,信號傳導(dǎo)途徑明顯破壞(p0.05),而模型組、自然恢復(fù)組、假針刺組三組之間相互比較,無明顯差異(p0.05)。與模型組相比,天樞組、足三里組略有好轉(zhuǎn)(p0.05),但天樞組、足三里組兩組之間比較,無明顯差異(p0.05)。與天樞組、足三里組相比,聯(lián)合治療組效果明顯好轉(zhuǎn)(p0.05),但仍低于正常對照組(p0.05)。總體來說,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。結(jié)論:1.脾氣虛證時,大鼠一般行為學(xué)表現(xiàn)明顯變差,體重增長緩慢,尿d-木糖排泄率明顯降低,大體解剖觀察小腸蠕動明顯緩慢,胃排空率明顯降低,小腸推進率明顯降低,小腸病理學(xué)he染色觀察小腸組織結(jié)構(gòu)明顯破壞,icc超微結(jié)構(gòu)明顯破壞,小腸的pgp9.5神經(jīng)纖維、ach神經(jīng)纖維、sp神經(jīng)纖維、no神經(jīng)纖維、vip神經(jīng)纖維、icc、smc數(shù)量明顯減少,網(wǎng)絡(luò)結(jié)構(gòu)明顯破壞。針刺足三里和天樞穴治療后,可明顯修復(fù)脾氣虛證的損傷,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。2.脾氣虛證時,大鼠小腸腸神經(jīng)-icc之間的信號傳導(dǎo)通路,主要有ach神經(jīng)纖維的m受體、sp神經(jīng)纖維的nk受體、no神經(jīng)纖維的受體-鳥苷酸環(huán)化酶(sgc)、vip神經(jīng)纖維的vpac受體、pka、pkc、cgk/pkg數(shù)量明顯減少,其信號通路g蛋白偶聯(lián)受體-camp-pka途徑、g蛋白偶聯(lián)受體-磷脂酶c(plc)-pkc途徑、sgc-cgmp-pkg途徑明顯破壞。針刺足三里和天樞穴治療后,可明顯修復(fù)脾氣虛證的損傷,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。3.脾氣虛證時,大鼠小腸ICC-平滑肌之間的信號傳導(dǎo)通路-縫隙連接、縫隙連接蛋白43的數(shù)量明顯減少,信號傳導(dǎo)途徑明顯破壞。針刺足三里和天樞穴治療后,可明顯修復(fù)脾氣虛證的損傷,其基本趨勢為:模型組≈自然恢復(fù)組≈假針刺組天樞組≈足三里組聯(lián)合組正常組。
[Abstract]:Background: spleen qi deficiency syndrome (Syndrome of Deficiency of Spleen-Qi, SDSQ) is one of the most common deficiency syndrome in clinical. The main clinical manifestations are stomach distention, fatigue, fatigue, dull complexion, loose stool and so on. Modern western medical research confirms that the main manifestation of spleen qi deficiency syndrome is gastrointestinal tract. Movement function, digestion and absorption function, endocrine function and immune function and many other systems, multiple factors disorder. However, the recovery of digestive tract motor function is the precondition for the recovery of digestive and absorption functions, endocrine and immune function. The recovery of gastrointestinal motility is both the initial and the most important to correct gastrointestinal damage. The key step is to promote the treatment of gastrointestinal motility, which can effectively treat gastrointestinal motility, digestion and absorption, endocrine and immune dysfunction. Therefore, it is necessary to explore the essence of gastrointestinal motility dysfunction in spleen qi deficiency syndrome and to study the effective methods of treating gastrointestinal motility dysfunction in spleen qi deficiency syndrome. As a traditional treatment method in Chinese medicine, it has been used in China for more than two thousand years. In clinical practice, more and more studies have shown that acupuncture at Zusanli, Tianshu point can correct gastrointestinal motility disorders, effectively treat spleen qi deficiency syndrome, and have its own unique advantages in the treatment of functional gastrointestinal diseases. But the exact mechanism is still not very clear, and further study is needed. Objective: to build a rat model of spleen qi deficiency syndrome by using the method of bitter cold and diarrhea combined with gas consumption and gas breaking, taking the mesenteric smooth muscle cell network of the intestinal nerve -Cajal as the research object in the spleen Qi deficiency rats, and observing the -Cajal interstitial cells of the intestinal nerve of the small intestine of the spleen qi deficiency rats. The mechanism of smooth muscle cell network was studied and the pathogenesis of spleen qi deficiency syndrome was studied. Then the rats of spleen qi deficiency syndrome were treated with acupuncture at Zusanli and Tianshu acupoint for treatment. The repair effect of acupuncture on the damage of mesenteric -Cajal stromal cells - smooth muscle cell network in the intestinal nerve of rats with spleen qi deficiency syndrome was observed, and the acupuncture at Zusanli and Tianshu point were used to treat the deficiency of Spleen Qi. Methods: to select the clean adult Wistar rats, the male and female rats are not limited. Referring to the methods of Professor Chen Xiaoye of Chinese Academy of Chinese medicine, the rat model of spleen qi deficiency syndrome is constructed by physical screening, and then using the method of bitter cold diarrhea and gas consumption breaking gas. The rats are divided into the control group, the model group, the natural recovery group and the false acupuncture point. Group (acupuncture non meridian acupoint group), acupuncture Tianshu acupoint treatment group, acupuncture Zusanli treatment group, acupuncture Zusanli + Tianshu point combined treatment group. After the success of the model and the end of the treatment, the cervical dislocated method was used to kill the rats and open the intraperitoneal incision of the proximal pylorus for the actual test. The experimental study was divided into the following three parts: the first part After observing general behavioral changes, monitoring body weight, measuring urine d- xylose excretion rate, gross anatomical observation, measuring gastric emptying rate, measuring small intestine propulsion rate, pathological HE staining, ultrastructural examination of transmission electron microscope, and immunofluorescent laser scanning confocal microscopy to observe -icc- level of intestinal nerve in small intestine of rats with Spleen Qi deficiency syndrome The morphological changes of smooth muscle network and the effect of acupuncture on Zusanli and Tianshu point. The second part is to observe the damage of the signal transduction pathway between the -icc of the intestinal nerve in the small intestine of rats with spleen qi deficiency syndrome by the method of double immunofluorescence double labeling laser scanning confocal microscopy, and the repair effect of the acupuncture point in the Zusanli and the Tianshu point. Third parts. By means of immunohistochemistry, westernblotting, qPCR and other methods to observe the damage of the signal transduction pathway between icc- smooth muscle in the small intestine of spleen qi deficiency rats and the repair effect of acupuncture at Zusanli and Tianshu point. The essence of the gastrointestinal motility dysfunction caused by spleen qi deficiency syndrome and the acupuncture at Zusanli, Tianshu and Tianshu are explored by three parts of experiments. Results: 1. compared with the normal control group, the general behavior of the rats in the model group of spleen qi deficiency syndrome was significantly worse than that in the normal control group, and the small intestinal peristalsis was obviously slowed down by the gross anatomy of the naked eye. The he pathology of the small intestine showed the obvious destruction of the small intestine structure, the ultrastructure of the ICC was seriously damaged and the weight increased obviously. Slow, urinary d- xylose excretion rate, gastric emptying rate and small intestinal propulsion rate decreased significantly. The number of PGP9.5 nerve fiber, ACh nerve fiber, SP nerve fiber, VIP nerve fiber, no nerve fiber, ICC, SMC, ens-icc-smc network in the intestinal nervous system decreased significantly, and the structure was obviously destroyed (P0.05), while the model group, natural recovery group, and false acupuncture group were three groups. Compared with the model group, there was a slight improvement in the Tianshu group and Zusanli group (P0.05), but there was no significant difference between the two groups in the Tianshu group and the Zusanli group (P0.05). Compared with the Tianshu group, the effect of the combined treatment group was better than the Zusanli group (P0.05), but it was still lower than that of the normal control group (P0.05). Overall, the base of the group was the base of the group (P0.05). Compared with the normal control group, the normal group.2. of the Zusanli group of the Zusanli group was compared with the normal control group, and the signal transduction pathway between the -icc of the intestinal and intestinal nerve in the model group of spleen qi deficiency syndrome group was mainly the M receptor of ACh nerve fiber, the NK receptor of SP nerve fiber, the receptor of no nerve fiber receptor cyclization of guanosine acid. The number of VPAC receptors, PKA, PKC, cgk/pkg decreased significantly in SGC, PKA, PKC, cgk/pkg, G protein coupled receptor -camp-pka pathway, G protein coupled receptor phospholipase C (PLC) -pkc pathway, and the model group, natural recovery group and false acupuncture group were compared with each other, and there was no significant difference. Compared with the model group, Tianshu group and Zusanli group had a slight improvement (P0.05), but there was no significant difference between the two groups in the Tianshu group and the Zusanli group (P0.05). Compared with the Tianshu group and Zusanli group, the effect of the combined treatment group was obviously improved (P0.05), but still lower than the normal group (P0.05). Compared with the normal control group, the signal transduction pathway between the icc- smooth muscle of the small intestine of the model group of spleen qi deficiency syndrome group and the normal group of the combination group of the Zusanli group of the Tianshu group of the sham acupuncture group, the signal transduction pathway of the gap junction and the gap junction protein 43 was significantly reduced, the signal transduction pathway was obviously broken (P0.05), and the model group, the natural recovery group, and the false acupuncture group were used in the model group of spleen qi deficiency syndrome group. There was no significant difference between the three groups (P0.05). Compared with the model group, the Tianshu group and Zusanli group had a slight improvement (P0.05), but there was no significant difference between the Tianshu group and the Zusanli group (P0.05). Compared with the Tianshu group and Zusanli group, the effect of the combined treatment group was obviously improved (P0.05), but still lower than that of the normal control group (P0.05). Conclusion: 1. when spleen qi deficiency syndrome, the general behavior of the rats was significantly worse, the body weight increased slowly, the urine d- xylose excretion rate decreased significantly, the gross anatomic observation of the small intestinal peristalsis was slow, the gastric emptying rate was significantly reduced and the small intestine was pushed. The small intestinal pathology HE staining showed that the structure of small intestine was obviously destroyed and the ultrastructure of ICC was obviously destroyed. The PGP9.5 nerve fibers of the small intestine, ACh nerve fiber, SP nerve fiber, no nerve fiber, VIP nerve fiber, ICC, SMC were obviously reduced, and the network structure was obviously destroyed. The basic trend of the syndrome of qi deficiency syndrome of the spleen qi deficiency syndrome was as follows: the signal transduction pathway between the -icc of the intestinal nerve of the small intestine in the normal group of the combination group of the Zusanli group of the Zusanli group and the normal group of the Zusanli group was.2., mainly including the M receptor of the ACh nerve fiber, the NK receptor of the SP nerve fiber, the receptor of the no nerve fiber receptor - guanosine ring. SGC, the number of VPAC receptors, PKA, PKC, cgk/pkg in VIP nerve fibers obviously decreased. The signal pathway of G protein coupled receptor -camp-pka pathway, G protein coupled receptor phospholipase C (PLC) -pkc pathway was significantly destroyed. After acupuncture at Zusanli and Tianshu acupoints, the damage of spleen qi deficiency syndrome could be obviously repaired. The basic trend was the model. The signal transduction pathway - gap junction between the ICC- smooth muscle of the small intestine of the rat's small intestine, the number of gap junction protein 43 decreased obviously, and the signal transduction pathway was obviously destroyed. After the acupuncture foot three li and Tianshu acupoint treatment, the spleen qi could be obviously repaired after the treatment of the acupuncture at the point of.3.. The basic trend of deficiency syndrome was: model group, natural recovery group, pseudo acupuncture group, Tianshu group, Zusanli group and normal group.
【學(xué)位授予單位】：大連醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2017
【分類號】：R245

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7 陳小野,周永生,樊雅莉,張宇鵬,蔣小麗,鄒世潔,崔成德,喬文彪,李玉梅,王肅,王左原,邵德彬,王麗芳,龐大本,池旭生;脾氣虛證動物模型規(guī)范化的初步研究[J];中國醫(yī)藥學(xué)報;2001年04期

8 陳易新,陳家旭,季紹良;脾氣虛證基礎(chǔ)研究的理論探討[J];中國醫(yī)藥學(xué)報;2002年07期

9 吳英鋒;脾氣虛證研究現(xiàn)狀[J];天津醫(yī)科大學(xué)學(xué)報;2003年01期

10 包素珍;鄭銘鋒;毛海燕;;脾氣虛證的本質(zhì)研究[J];中華中醫(yī)藥學(xué)刊;2007年08期

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3 柳和培;唐黨生;侯燕鳴;王淑蘭;;驢脾氣虛證的超微結(jié)構(gòu)研究(一)[A];第四次全國電子顯微學(xué)會議論文摘要集[C];1986年

4 陳達理;周立紅;;脾氣虛證纖溶、凝血、血小板活化指標的臨床研究[A];全國中西醫(yī)結(jié)合基礎(chǔ)理論學(xué)術(shù)研討會論文集[C];2004年

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6 陳達理;周立紅;;脾氣虛證纖溶、凝血、血小板活化狀態(tài)的臨床研究[A];中國中西醫(yī)結(jié)合學(xué)會第十四次全國消化系統(tǒng)疾病學(xué)術(shù)研討會論文匯編[C];2002年

7 危北海;陳言言;張聲生;;脾氣虛證的病理生理學(xué)及其相關(guān)客觀實驗指標的研究[A];中國中西醫(yī)結(jié)合學(xué)會第十八次全國消化系統(tǒng)疾病學(xué)術(shù)會議暨2006年全國中西醫(yī)結(jié)合消化系統(tǒng)疾病進展學(xué)習(xí)班論文匯編[C];2006年

8 柳和培;侯燕鳴;長曉楓;王淑蘭;;大白鼠脾氣虛證超微結(jié)構(gòu)定量計測研究[A];第六次全國電子顯微學(xué)會議論文摘要集[C];1990年

9 孫豐雷;;脾氣虛證與糖尿病及其慢性并發(fā)癥的關(guān)系和臨床干預(yù)[A];第六次中國中西醫(yī)結(jié)合糖尿病學(xué)術(shù)會議論文匯編[C];2002年

10 柳和培;侯燕鳴;長曉楓;;脾氣虛證大白鼠膈肌的超微結(jié)構(gòu)研究[A];海峽兩岸電子顯微學(xué)研討會論文專集[C];1992年

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