發(fā)布時間：2018-05-21 06:38

  本文選題：脾虛證 + 白色念珠菌��； 參考：《遼寧中醫(yī)藥大學(xué)》2016年博士論文

【摘要】：目的:對正常及脾虛小鼠經(jīng)口感染白色念珠菌,通過檢測小鼠糞便中活菌數(shù)和小腸組織病理改變,觀察脾虛小鼠對白色念珠菌的易感性;通過檢測小腸黏膜固有層CD4+T和CD8+T細(xì)胞亞群分布,分析脾虛小鼠經(jīng)口感染白色念珠菌對CD4+T和CD8+T細(xì)胞亞群分布的影響;通過檢測小腸組織中IL-4、IL-10、IL-12、IFN-γm RNA及蛋白表達(dá)水平,推測脾虛小鼠感染白色念珠菌后Th1/Th2平衡的變化;通過檢測小腸組織中穿孔素、顆粒酶基因及蛋白表達(dá)水平,闡述經(jīng)口感染白色念珠菌小鼠CTL細(xì)胞通過穿孔素/顆粒酶途徑殺傷靶細(xì)胞的機(jī)制。材料與方法:健康SPF級昆明種小白鼠60只,隨機(jī)分為兩組:空白組(30只)和脾虛造模組(30只)。對脾虛造模組小鼠采用飲食失節(jié)加勞倦過度的方法制備脾虛小鼠模型。模型制備成功后,再次將空白組小鼠隨機(jī)均分為2組:正常對照組和正常+白色念珠菌組;將脾虛造模組小鼠隨機(jī)均分為2組:脾虛模型組和脾虛+白色念珠菌組。實驗第1天起,采用的飲食失節(jié)加勞倦過度復(fù)合因素造模法制備小鼠脾氣虛泄瀉模型。給脾虛造模組小鼠單日喂飼甘藍(lán),并強(qiáng)制性游泳至耐力極限(指小鼠游泳至無力游動,經(jīng)驅(qū)趕仍不能繼續(xù)游動,且出現(xiàn)身體向腹側(cè)蜷曲、發(fā)抖、欲溺水等征象);雙日施加豬油0.2m L/10g體重,灌胃,并正常進(jìn)食,連續(xù)14天。正常對照組小鼠正常飼養(yǎng)。實驗14天后,按照脾虛模型宏觀診斷標(biāo)準(zhǔn)對脾虛造模組小鼠進(jìn)行模型評價。脾虛模型制備成功后,次日對正常+白色念珠菌組和脾虛+白色念珠菌組小鼠經(jīng)口感染白色念珠菌,白色念珠菌濃度為2×108/m L,劑量為0.2m L/10g體重,正常對照組和脾虛模型組小鼠給予等量生理鹽水經(jīng)口灌胃,染菌后,各組小鼠均正常飼養(yǎng),至實驗第35天,即染菌后的第21天,處死各組小鼠,進(jìn)行相關(guān)指標(biāo)檢測。采用HE染色及電鏡的方法,觀察小鼠小腸黏膜的病理變化及超微結(jié)構(gòu)改變;檢測糞便中活菌數(shù)及念珠菌種類;采用流式細(xì)胞術(shù)檢測各組小鼠小腸黏膜固有層中T淋巴細(xì)胞亞群的分布;采用western-blot法和RT-PCR法檢測各組小鼠小腸組織中IL-4、IL-10、IL-12、IFN-γ蛋白及基因表達(dá)水平;采用western-blot法、免疫熒光法和RT-PCR法檢測各組小鼠小腸組織中Perforin、Granzyme蛋白及基因表達(dá)水平。結(jié)果:1.各組小鼠小腸黏膜形態(tài)學(xué)改變:正常對照組小鼠小腸黏膜完整,絨毛排列整齊,肌層薄厚均勻適中。脾虛模型組小鼠與正常對照組比較,小腸黏膜比較完整,偶見小腸絨毛排列不整齊等改變。正常+白色念珠菌組和脾虛+白色念珠菌組小鼠均顯示出不同程度的病變,尤以脾虛+白色念珠菌組小鼠病理改變最為明顯,主要表現(xiàn)為絨毛缺失,排列不整齊,黏膜下層有炎性細(xì)胞浸潤。2.各組小鼠小腸超微結(jié)構(gòu)改變:正常對照組小鼠小腸微絨毛排列整齊,細(xì)胞內(nèi)細(xì)胞器豐富,線粒體、內(nèi)質(zhì)網(wǎng)、核糖體清晰可見。脾虛模型組小鼠小腸微絨毛略短,但排列尚比較整齊。正常+白色念珠菌組小鼠小腸微絨毛稀疏,長短不一,細(xì)胞質(zhì)內(nèi)線粒體腫脹、偶見空泡樣改變。脾虛+白色念珠菌組小鼠小腸微絨毛明顯減少,排列紊亂,線粒體明顯腫脹,嵴消失,呈空泡樣改變,內(nèi)質(zhì)網(wǎng)擴(kuò)張,表面核糖體脫落。3.各組小鼠糞便中活菌數(shù)檢測結(jié)果顯示:與正常對照組比較,脾虛模型組、脾虛+白色念珠菌組小鼠糞便中活菌數(shù)顯著增高(P0.01或P0.05),有統(tǒng)計學(xué)差異,與脾虛模型組比較,脾虛+白色念珠菌組小鼠糞便中活菌數(shù)顯著升高(P0.01),有統(tǒng)計學(xué)差異。4.各組小鼠糞便中念珠菌種類檢測結(jié)果顯示:正常對照組熱帶念珠菌和克柔念珠菌偶有生長,檢出率均為10%。正常+白色念珠菌組小鼠糞便中以白念菌檢出率最高,為50%,光滑念珠菌檢出率為20%,克柔念珠菌檢出率為10%。脾虛模型組小鼠以熱帶念珠菌檢出率最高,為30%,其次為光滑念珠菌,為20%。脾虛+白色念珠菌組小鼠以白色念珠菌檢出率最高,為40%,其次為光滑念珠菌(30%)和克柔念珠菌(20%)。5.各組小鼠腸黏膜固有層CD3+T細(xì)胞的檢測結(jié)果顯示:各組小鼠腸黏膜固有層CD3+T細(xì)胞組間比較無統(tǒng)計學(xué)差異。與正常對照組比較,正常+白色念珠菌組、脾虛模型組及脾虛+白色念珠菌組小鼠小腸黏膜固有層中CD4+T細(xì)胞比例均不同程度下降。與正常+白色念珠菌組比較,脾虛+白色念珠菌組小鼠小腸黏膜固有層CD4+T細(xì)胞百分比顯著下降(P0.01)。與脾虛模型組比較,脾虛+白色念珠菌組小鼠小腸黏膜固有層CD4+T細(xì)胞百分比顯著下降(P0.01)。正常對照組、正常+白色念珠菌組、脾虛模型組間比較,小鼠小腸黏膜固有層中CD8+T細(xì)胞比例無統(tǒng)計學(xué)差異,但均與脾虛+白色念珠菌組比較,有統(tǒng)計學(xué)差異(P0.05或P0.01)。與正常對照組比較,其余三組小鼠小腸黏膜固有層中CD4+T/CD8+T比值均有不同程度下降,有顯著性差異(P0.01);正常+白色念珠菌組與脾虛+白色念珠菌組比較,有統(tǒng)計學(xué)差異(P0.01);脾虛模型組與脾虛+白色念珠菌組比較,有統(tǒng)計學(xué)差異(P0.01)。6.各組小鼠小腸組織中IFN-γm RNA及蛋白的表達(dá)水平顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中IFN-γm RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組IFN-γm RNA及蛋白表達(dá)水平顯著降低(P0.01),而脾虛+白色念珠菌組IFN-γm RNA及蛋白表達(dá)水平顯著升高(P0.01);與脾虛模型組比較,脾虛+白色念珠菌組IFN-γm RNA及蛋白表達(dá)水平顯著升高(P0.05)。7.各組小鼠小腸組織中IL-4 m RNA及蛋白表達(dá)水平檢測結(jié)果顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中IL-4 m RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組及脾虛+白色念珠菌組IL-4 m RNA及蛋白表達(dá)水平顯著降低(P0.01);與脾虛模型組比較,脾虛+白色念珠菌組IL-4 m RNA及蛋白表達(dá)水平顯著升高(P0.01)。8.各組小鼠小腸組織中IL-12 m RNA及蛋白表達(dá)水平檢測結(jié)果顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中IL-12 m RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組IL-12 m RNA及蛋白表達(dá)水平顯著降低(P0.01),而脾虛+白色念珠菌組IL-12 m RNA及蛋白表達(dá)水平顯著升高(P0.05);與脾虛模型組比較,脾虛+白色念珠菌組IL-12 m RNA及蛋白表達(dá)水平顯著升高(P0.01或0.05)。9.各組小鼠小腸組織中IL-10 m RNA及蛋白表達(dá)水平檢測結(jié)果顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中IL-10 m RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組及脾虛+白色念珠菌組IL-10 m RNA及蛋白表達(dá)水平顯著降低(P0.01);與脾虛模型組比較,脾虛+白色念珠菌組IL-10 m RNA及蛋白表達(dá)水平顯著升高(P0.01或0.05)。10.各組小鼠小腸組織中Perforin m RNA及蛋白的表達(dá)水平結(jié)果顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中Perforin m RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組Perforin m RNA及蛋白表達(dá)水平顯著降低(P0.01),而脾虛+白色念珠菌組Perforin m RNA及蛋白表達(dá)水平顯著升高(P0.01);與脾虛模型組比較,脾虛+白色念珠菌組Perforin m RNA及蛋白表達(dá)水平顯著升高(P0.01)。11.各組小鼠小腸組織中Granzyme B m RNA及蛋白表達(dá)水平檢測結(jié)果顯示:與正常對照組比較,正常+白色念珠菌組、脾虛模型組、脾虛+白色念珠菌組小鼠小腸組織中Granzyme B m RNA及蛋白表達(dá)水平顯著升高(P0.01);與正常+白色念珠菌組比較,脾虛模型組Granzyme B m RNA及蛋白表達(dá)水平顯著降低(P0.01或P0.05);與脾虛模型組比較,脾虛+白色念珠菌組Granzyme B m RNA及蛋白表達(dá)水平顯著升高(P0.01)。結(jié)論:1.脾虛證小鼠腸道念珠菌群紊亂。經(jīng)口感染白色念珠菌后,糞便活菌數(shù)明顯增加,加重腸道的念珠菌群紊亂及小腸組織的病理改變。2.脾虛小鼠的CD4+T/CD8+T比例發(fā)生改變。經(jīng)口感染白色念珠菌后,CD4+T、CD8+T亞群分布變化更為明顯,機(jī)體的免疫功能受損更為明顯。3.白色念珠菌感染時,機(jī)體的體液免疫及細(xì)胞免疫功能均發(fā)生變化,但以細(xì)胞免疫為主。4.經(jīng)口感染白色念珠菌可引起小鼠小腸局部CTL的活化,導(dǎo)致Perforin和Granzyme表達(dá)水平的升高。脾虛加重了機(jī)體白色念珠菌感染病情,Perforin和Granzyme高表達(dá)水平可能是脾虛小鼠感染白色念珠菌的發(fā)生機(jī)制之一。
[Abstract]:Objective: To observe the oral Candida albicans infection in normal and spleen asthenia mice, by detecting the number of living bacteria in the feces and pathological changes of small intestine in mice, the susceptibility to Candida albicans in spleen asthenia mice was observed. By detecting the distribution of CD4+T and CD8+T cell subsets in the propria of the small intestinal mucosa, the oral Candida albicans infected by the spleen asthenia mice on CD4+T and CD8+T were analyzed. The influence of the distribution of cell subsets; by detecting the level of IL-4, IL-10, IL-12, IFN- gamma m RNA and protein expression in the small intestinal tissue, the changes of Th1/Th2 balance after infection with Candida albicans in spleen asthenia mice were estimated. By detecting the perforin, Granzyme gene and protein expression in small intestine tissues, the passage of the oral Candida albicans CTL cells through oral infection was introduced. The mechanism of perforin / granzyme pathway killing target cells. Materials and methods: 60 healthy Kunming mice were randomly divided into two groups: blank group (30) and spleen deficiency model (30 rats). The spleen asthenia mice model was prepared by diet loss and overfatigue in spleen deficiency model mice. After the model preparation was successful, the blank group was reduced to a small group. The rats were randomly divided into 2 groups: normal control group and normal + Candida albicans group. The spleen asthenia model mice were randomly divided into 2 groups: spleen deficiency model group and spleen asthenia + Candida albicans group. After the first day of experiment, the model of spleen deficiency and tiredness was used to produce spleen deficiency diarrhea model in mice. Brassica oleracea, and compulsory swimming to the endurance limit (refers to the mice swimming to the inability to swim, still can not continue to swim, and the body to the abdominal crouching, shivering, drowning and other signs); double day to apply the lard 0.2m L/10g weight, gavage, and normal feeding for 14 days, normal control group normal feeding. 14 days after the experiment, according to spleen asthenia model After the spleen deficiency model was successfully prepared, the normal + Candida albicans group and the spleen asthenia + Candida albicans group were infected with Candida albicans, the concentration of Candida albicans was 2 x 108/m L, and the dose was 0.2m L/10g, and the normal control group and the spleen deficiency model group were given the same amount. The normal saline was fed through the mouth. After dyeing the bacteria, all the mice were kept normally, and the mice were killed for thirty-fifth days, that is, twenty-first days after the infection, the mice were killed and the related indexes were detected. The pathological changes and ultrastructural changes of the small intestinal mucosa were observed by HE staining and electron microscopy, and the number of living bacteria and Candida species in the feces was detected. Flow formula was used. The distribution of T lymphocyte subsets in the small intestinal mucosa propria of each group was detected by cell operation, and the levels of IL-4, IL-10, IL-12, IFN- gamma protein and gene expression were detected by Western-blot and RT-PCR methods. Western-blot, immunofluorescence and RT-PCR methods were used to detect Perforin, Granzyme eggs in small intestine tissues of mice in each group. The expression level of Rhizoma Bletillae gene. Results: 1. the morphological changes of small intestinal mucosa of mice in each group: the small intestinal mucosa of the normal control group was complete, the villi were arranged well and the muscularis thickness was evenly and moderately. The small intestine mucosa was more complete in the spleen deficiency model group than the normal control group. The mice of the spleen deficiency + Candida albicans group showed different degrees of pathological changes, especially in the spleen deficiency and Candida albicans group, the most obvious pathological changes were the loss of the villus, the irregular arrangement, the small intestinal ultrastructure of the mice in each group of.2. groups with inflammatory cell infiltration in the submucosa: the small intestinal microvilli in the normal control group were arranged neatly and finely. The intracellular organelles were abundant, mitochondria, endoplasmic reticulum and ribosome were clearly visible. The small intestinal microvilli in the mice of the spleen deficiency model group were slightly shorter, but the small intestinal microvilli in the normal + Candida albicans group were sparse and different, the mitochondria were swollen in the cytoplasm, and the vacuoles like changes were seen in the cytoplasm. The results showed that the number of living bacteria in the spleen asthenia model group and the spleen asthenia + Candida albicans group increased significantly (P0.01 or P0.05) in the feces of the mice of the spleen asthenia and Candida albicans (P0.01 or P0.05). Compared with the spleen deficiency model group, the number of living bacteria in the feces of spleen asthenia + Candida albicans increased significantly (P0.01), and there was a statistical difference in the detection of Candida species in the feces of.4. mice: the normal control group of Candida tropicalis and Candida kuriuri were even growing, and the detection rates were all white in the feces of 10%. normal + Candida albicans. The detection rate of Candida albicans was the highest, the detection rate of Candida smooth Candida was 20%, the detection rate of Candida Kurus in 10%. spleen deficiency model group was the highest, 30%, followed by Candida albicans. The detection rate of Candida albicans in 20%. spleen asthenia + Candida albicans group was the highest, 40%, followed by Candida smooth Candida (30%) and krou. The detection of intestinal mucosa propria CD3+T cells in each group of.5..5. showed that there was no statistical difference between the groups of intestinal mucosa propria in each group. Compared with the normal control group, the proportion of CD4+T cells in the small intestinal mucosa of normal + Candida albicans group, spleen deficiency model group and spleen asthenia + Candida albicans group was different Compared with the normal + Candida albicans group, the percentage of CD4+T cells in the small intestinal mucosa propria of the spleen asthenia + Candida albicans group decreased significantly (P0.01). Compared with the spleen deficiency model group, the percentage of CD4+T cells in the small intestinal mucosa propria of spleen asthenia + Candida albicans decreased significantly (P0.01). Normal control group, normal + Candida albicans group, Compared with the spleen deficiency model group, the proportion of CD8+T cells in the small intestinal mucosa propria of mice was not statistically different, but compared with the spleen asthenia + Candida albicans group, there were statistical differences (P0.05 or P0.01). Compared with the normal control group, the ratio of CD4+T/CD8+ T in the propria of the small intestinal mucosa of the other three groups decreased in varying degrees, there was significant difference (P0.01 Compared with the spleen asthenia and Candida albicans group, the normal + Candida albicans group had statistical difference (P0.01), the spleen deficiency model group and the spleen asthenia + Candida albicans group had statistical difference (P0.01) the expression level of IFN- gamma m RNA and protein in the small intestinal tissues of.6. mice showed that the normal + Candida albicans group and the spleen deficiency model were compared with the normal control group. The expression level of IFN- gamma m RNA and protein in small intestinal tissue of spleen asthenia + Candida albicans group increased significantly (P0.01). Compared with normal + Candida albicans group, IFN- gamma m RNA and protein expression level in spleen deficiency model group decreased significantly (P0.01), but IFN- gamma m RNA and protein expression level in spleen asthenia + Candida albicans group increased significantly (P0.01), and spleen deficiency model. IFN- gamma m RNA and protein expression level in the group of spleen deficiency and Candida albicans increased significantly (P0.05) and the expression level of IL-4 m RNA and protein expression in small intestinal tissues of each group of.7. mice showed that: compared with the normal control group, normal + Candida albicans, spleen deficiency model group, spleen asthenia + Candida albicans group mice small intestinal tissue IL-4 m RNA and protein Compared with normal + Candida albicans group, the expression level of IL-4 m RNA and protein in spleen asthenia model group and spleen deficiency + Candida albicans group decreased significantly (P0.01), and the expression of IL-4 m RNA and protein in spleen asthenia + Candida albicans group was significantly higher than that in spleen asthenia model group (P0.01) and IL-12 m in small intestine tissues of mice in each group of spleen asthenia + Candida albicans (P0.01).8. group (P0.01) The results of RNA and protein expression showed that: compared with the normal control group, the expression level of IL-12 m RNA and protein in small intestinal tissues of normal + Candida albicans group, spleen deficiency model group and spleen deficiency + Candida albicans group increased significantly (P0.01), compared with normal + Candida albicans group, the expression level of IL-12 m RNA and protein in spleen deficiency model group decreased significantly. The level of IL-12 m RNA and protein expression in spleen asthenia and Candida albicans increased significantly (P0.05), and the expression level of IL-12 m RNA and protein expression in spleen asthenia + Candida albicans group was significantly increased (P0.01 or 0.05) in spleen asthenia + Candida albicans group (P0.01 or 0.05), IL-10 m and protein expression in small intestine tissues of mice in each group showed that the results showed that the normal control group was with the normal control group. Compared with normal + Candida albicans group, spleen deficiency model group, spleen asthenia + Candida albicans group, the expression level of IL-10 m RNA and protein increased significantly (P0.01). Compared with normal + Candida albicans group, the IL-10 m RNA and protein expression level of spleen asthenia model group and spleen deficiency + Candida albicans group decreased significantly (P0.01); compared with the spleen deficiency model group, the expression level of the spleen deficiency and Candida albicans group was significantly lower than that of the spleen deficiency model group. IL-10 m RNA and protein expression level of spleen asthenia + Candida albicans increased significantly (P0.01 or 0.05) the expression level of Perforin m RNA and protein in small intestine tissues of.10. mice showed that: compared with normal control group, normal + Candida albicans group, spleen deficiency model group, spleen deficiency + Candida albicans group mice small intestine tissue Perforin m RNA and The level of protein expression increased significantly (P0.01). Compared with the normal + Candida albicans group, the expression level of Perforin m RNA and protein in the spleen deficiency model group decreased significantly (P0.01), but the expression level of Perforin m RNA and protein in the spleen asthenia + Candida albicans group increased significantly (P0.01), and the spleen asthenia + Candida albicans group Perforin m RNA and protein compared with the spleen deficiency model group. The expression level of Granzyme B m RNA and protein expression in small intestine tissues of mice in each group was significantly increased (P0.01). The results showed that the Granzyme B m RNA and protein expression level in the small intestinal tissues of normal + Candida albicans, spleen deficiency model and spleen asthenia + Candida albicans increased significantly (P0.01) and normal + with normal control group. Compared with the group of Candida albicans, the expression level of Granzyme B m RNA and protein in the spleen deficiency model group was significantly decreased (P0.01 or P0.05). Compared with the spleen deficiency model group, the Granzyme B m RNA and protein expression level of the spleen asthenia + Candida albicans group increased significantly (P0.01). Conclusion: 1. spleen asthenia mice with intestinal candidiasis disorder. After oral Candida albicans infection, feces The number of living bacteria increased significantly, the disorder of Candida albicans in the intestine and the pathological changes of small intestinal tissue changed the CD4+T/CD8+T ratio in.2. spleen asthenia mice. After oral Candida albicans infection, the distribution of CD4+T and CD8+T subgroups was more obvious, and the immune function of the body was more obvious in.3. Candida albicans infection, body humoral immunity and The cellular immune function changes, but the oral Candida albicans infected with cellular immune.4. can cause the activation of local CTL in the small intestine of mice, which leads to the increase of the expression level of Perforin and Granzyme. Spleen deficiency aggravates the disease of Candida albicans, and the high level of Perforin and Granzyme may be the white Candida infection in mice with spleen deficiency. One of the mechanisms of bacteria.
【學(xué)位授予單位】：遼寧中醫(yī)藥大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R-332;R519.3

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