本文選題：潰瘍性結(jié)腸炎 + 加味清腸解毒湯�。� 參考：《成都中醫(yī)藥大學(xué)》2016年博士論文

【摘要】：1.實驗?zāi)康耐ㄟ^觀察加味清腸解毒湯對TNBS/乙醇復(fù)制的潰瘍性結(jié)腸炎模型大鼠的炎癥細胞因子相關(guān)指標及血小板活化功能的影響來研究其治療作用和機制。2.實驗方法SPF級SD大鼠60只隨機分為空白組、模型組、西藥組、中藥高劑量組(簡稱高劑量組)、中藥中劑量組(簡稱中劑量組)、中藥低劑量組(簡稱低劑量組),每組10只。除空白組外,其余采用TNBS/乙醇復(fù)制潰瘍性結(jié)腸炎模型。第一次造模后第5周起給藥,連續(xù)兩周,空白組、模型組給予等體積生理鹽水灌胃,西藥組給予美沙拉嗪緩釋顆粒灌胃,中藥各治療組給予加昧清腸解毒湯水煎液灌胃。給藥第7天采血檢測TNF-α、TXB2、6-Keto-PGF1α含量；給藥第14天采血檢測TNF-α、TXB2、6-Keto-PGF1α、PC含量；給藥2周后處死所有動物,分別進行結(jié)腸組織病理學(xué)評分,免疫組化法檢測結(jié)腸組織IL-1β、IL-6、IL-8的表達,酶聯(lián)免疫法檢測結(jié)腸組織IL-10的表達,以及PCR檢測結(jié)腸組織TLR4、NF-κB的基因表達。3.實驗結(jié)果(1)采用TNBS/乙醇復(fù)制大鼠潰瘍性結(jié)腸炎模型,造模后實驗動物出現(xiàn)典型的腹瀉、血便、體重減輕、精神萎靡等表現(xiàn),經(jīng)治療后上述情況逐漸好轉(zhuǎn)；與模型組比較,各治療組體重恢復(fù)有統(tǒng)計學(xué)差異(P0.01,P0.05)；(2)與空白組比較,模型組結(jié)腸組織損傷符合典型的UC特征,病理學(xué)評分顯著升高(P0.01)；與模型組比較,各治療組病理學(xué)評分明顯下降(P0.01,P0.05);(3)與空白組相比,模型組大鼠結(jié)腸組織IL-1β表達明顯升高(P0.01)；與模型對照組相比,各治療組大鼠結(jié)腸組織IL-1β表達降低,(P0.05,P0.01);(4)與空白組相比,模型組大鼠結(jié)腸組織IL-6表達明顯升高(P0.01)；與模型組相比,各治療組大鼠結(jié)腸組織IL-6表達降低(P0.05)；(5)與空白組相比,模型組大鼠結(jié)腸組織IL-8表達明顯升高(P0.01)；與模型組相比,各治療組大鼠結(jié)腸組織IL-8表達降低(P0.05,P0.01)；(6)空白組不同時間點之間比較,TNF-α的表達無明顯差異(P0.05);不同時間點模型組TNF-α的表達較空白組明顯增多(P0.01)；與模型組比較,不同時間點除低劑量組之外其余治療組的TNF-α的表達下調(diào)(P0.01,P0.05)；(7)與空白組相比,模型組大鼠結(jié)腸組織IL-10含量明顯降低(P0.01)；與模型組相比,各治療組除低劑量組外IL-10的含量有所升高(P0.05,P0.01)；(8)與空白組比較,模型組大鼠結(jié)腸組織TLR4、NF-κB的mRNA表達增強(P0.01)；與模型組比較,西藥組和中藥組大鼠結(jié)腸組織中的TLR4、NF-κB的mRNA表達下降(P0.01)；西藥組與中藥組比較無顯著差異(P0.05);(9)與空白組比較,模型組大鼠PC顯著升高(P0.01)：與模型組比較,各治療組PC有所下降,其中西藥組、中藥高劑量組有統(tǒng)計學(xué)差異(P0.05)；(10)空白組組內(nèi)不同時間點比較,血漿TXB2含量無明顯差異(P0.05)；與空白組相比,模型組不同時間點血漿TXB2含量顯著升高(P0.01);與模型組比較,除低劑量組外,其余各組不同時間點血漿TXB2含量下降(P0.01,P0.05);(11)空白組組內(nèi)各時間點比較血漿6-Keto-PGF1α含量無明顯差異(P0.05);與空白組比較,模型組不同時間點血漿6-Keto-PGF1α含量升高(P0.05)；與模型組比較,各治療組不同時間點血漿6-Keto-PGF1α含量升高(P0.05,P0.01)；(12)空白組組內(nèi)不同時間點比較,TXB2/6-Keto-PGF1α比值無明顯差異(P0.05)；與空白組比較,模型組不同時間點TXB2/6-Keto-PGF1α比值顯著升高(P0.01)；與模型組比較,各治療組不同時間點TXB,/6-Keto-PGF1α比值降低(P0.01,P0.05)：4.實驗結(jié)論(1)加味清腸解毒湯具有改善實驗性潰瘍性結(jié)腸炎組織病理學(xué)評分,改善一般情況,促進實驗大鼠體重恢復(fù)的作用；(2)加味清腸解毒湯降低促炎因子IL-1β、IL-6、IL-8、TNF-α的過度表達,升高抗炎因子IL-10的表達,可能是其治療TNBS/乙醇復(fù)制的大鼠潰瘍性結(jié)腸炎的機制之一；(3)加味清腸解毒湯治療實驗性潰瘍性結(jié)腸炎的機制可能與通過抑制TLR4、 NF-κB的過度表達繼而抑制下游炎癥因子的釋放發(fā)揮抗炎作用有關(guān)；(4)加味清腸解毒湯治療實驗性潰瘍性結(jié)腸炎的機制可能與通過下調(diào)血漿TXB2水平,上調(diào)6-Keto-PGF1α含量,降低TXB2/6-Keto-PGF1α比值,降低血小板過度活化有關(guān)。
[Abstract]:1. to observe the effect of Jiawei Qing Chang Jiedu soup on the inflammatory cytokine related index and platelet activation function of TNBS/ ethanol replicating ulcerative colitis model rats, and to study its therapeutic effect and mechanism.2. experimental method SPF grade SD rats randomly divided into blank group, model group, western medicine group, high dose group of traditional Chinese medicine (Jane) The high dose group (high dose group), medium dose group (medium dose group), low dose group of traditional Chinese medicine (low dose group), 10 rats in each group. Except for the blank group, the rest used TNBS/ ethanol to copy ulcerative colitis model. After the first model, the drug was given for two weeks, the blank group was given the same volume of normal saline, and the western medicine group was given Meisha. TNF- alpha, TXB2,6-Keto-PGF1 alpha content was measured for seventh days, and the content of TNF- a, TXB2,6-Keto-PGF1 A and PC was detected by blood for fourteenth days; all animals were killed after 2 weeks of administration, and the colon histopathological score and immunohistochemical method were carried out for 2 weeks. The expression of IL-1 beta, IL-6 and IL-8 in colon tissue was measured, the expression of IL-10 in colon tissue was detected by ELISA, and PCR was used to detect TLR4 in colon tissue and the results of NF- kappa B gene expression.3. experimental results (1) the rat model of ulcerative colitis was replicated by TNBS/ ethanol. After the model, the experimental animals showed typical diarrhea, blood stool, weight loss and mental malaise. After treatment, the above conditions gradually improved; compared with the model group, the weight recovery of the treatment groups was statistically different (P0.01, P0.05). (2) compared with the blank group, the damage of the colon tissue in the model group was conformed to the typical UC characteristics, and the pathological score was significantly higher (P0.01); and compared with the model group, the pathological scores of the treatment groups were significantly decreased (P0.01, P0.05). 3) the expression of IL-1 beta in the colon tissue of the model group was significantly higher than that in the blank group (P0.01). Compared with the model control group, the expression of IL-1 beta in the colon tissue of the rats in the treatment group was reduced, (P0.05, P0.01). (4) the expression of IL-6 in the colon tissue of the model group was significantly higher than that in the blank group (P0.01). Compared with the model group, the colon group of the rats in the treatment group was compared with the model group. The expression of IL-6 was reduced (P0.05); (5) the expression of IL-8 in the colon tissue of the model group was significantly higher than that in the blank group (P0.01). Compared with the model group, the expression of IL-8 in the colon tissue of the rats in the treatment group decreased (P0.05, P0.01), and (6) there was no significant difference in the expression of TNF- a (P0.05) in the blank group at different time points (P0.05), and the model group of TNF- a at different time points. Compared with the model group, the expression of TNF- alpha in the other treatment groups was down down (P0.01, P0.05) at different time points except the low dose group. (7) the IL-10 content in the colon tissue of the model group was significantly lower than that in the blank group (P0.01). Compared with the model group, the content of IL-10 in the treatment group except the low dose group was compared with the model group. (P0.05, P0.01); (8) compared with the blank group, the colon tissue of the rats in the model group was TLR4, and the mRNA expression of NF- kappa B was enhanced (P0.01). Compared with the model group, the mRNA expression of NF- kappa B in the colon tissue of the western medicine group and the Chinese medicine group was decreased (P0.01); (9) compared with the blank group, the model was compared with the blank group. Group PC significantly increased (P0.01): compared with the model group, PC decreased in the treatment group, and there was a statistical difference between the western medicine group and the high dose group (P0.05). (10) there was no significant difference in plasma TXB2 content in the blank group at different time points (P0.05). Compared with the empty white group, the plasma TXB2 content was significantly increased in the model group at different time points (P0.0). 1): compared with the model group, the plasma TXB2 content decreased (P0.01, P0.05) at different time points except the low dose group, and (11) there was no significant difference in plasma 6-Keto-PGF1 alpha content in the blank group at all time points (P0.05). Compared with the blank group, the plasma level of 6-Keto-PGF1 alpha was increased (P0.05) in the model group (P0.05), and the treatment was compared with the model group. The plasma 6-Keto-PGF1 alpha content increased at different time points in the treatment group (P0.05, P0.01). (12) there was no significant difference in the ratio of TXB2/6-Keto-PGF1 a (P0.05) at different time points in the blank group (P0.05). Compared with the blank group, the TXB2/6-Keto-PGF1 alpha ratio in the model group increased significantly at different time points (P0.01). Compared with the model group, the different time points of the treatment groups were TXB, /6. The -Keto-PGF1 alpha ratio decreased (P0.01, P0.05):4. experimental conclusion (1) Jiawei Qing Chang Jiedu Decoction can improve the histopathological score of experimental ulcerative colitis, improve the general situation, promote the effect of weight recovery of experimental rats, and (2) the overexpression of IL-1 beta, IL-6, IL-8, TNF- a, and increase the anti inflammatory factors of the IL-1 beta, IL-6, IL-8, TNF- alpha in the proinflammatory cells. The expression of IL-10 may be one of the mechanisms for the treatment of TNBS/ ethanol replicating ulcerative colitis. (3) the mechanism of the treatment of experimental ulcerative colitis in the treatment of experimental ulcerative colitis may be related to the inhibition of the overexpression of TLR4, NF- kappa B and the inhibition of the release of the downstream inflammatory factors; (4) the flavored clearing intestine detoxification soup The mechanism of treating experimental ulcerative colitis may be related to the reduction of plasma TXB2 level, the increase of 6-Keto-PGF1 alpha content, the reduction of the ratio of TXB2/6-Keto-PGF1 a, and the reduction of platelet activation.

【學(xué)位授予單位】：成都中醫(yī)藥大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R259;R-332

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