本文關鍵詞： 痛瀉要方 潰瘍性結腸炎 白細胞介素-(IL-) 白細胞介素-受體(IL-R) 基因表達 蛋白表達　出處：《中國實驗方劑學雜志》2017年11期 　論文類型：期刊論文

【摘要】：目的:觀察痛瀉要方對潰瘍性結腸炎(ulcerative colitis,UC)大鼠下丘腦中白細胞介素-6(IL-6)和白細胞介素-6受體(IL-6R)基因和蛋白表達的影響。方法:將SPF級Wistar大鼠運用復合方法進行潰瘍性結腸炎造模后,隨機分為5組:模型組,痛瀉要方低、中、高劑量(2.75,5.5,11 g·kg~(-1))組,美沙拉嗪(5-ASA)組。藥物處理大鼠21 d后麻醉處死,肉眼觀察結腸大體形態(tài)損傷并進行評分。分離各組大鼠血清,酶聯(lián)免疫吸附試驗(enzyme linked immunosorbent assay,ELISA)檢測血清中IL-6含量,分離大鼠下丘腦組織并提取總RNA后,實時熒光定量PCR(Real-time polymerase chain reaction,Real-time PCR)法檢測IL-6和IL-6R基因表達,免疫組織化學染色法檢測下丘腦組織IL-6和IL-6R的分布及蛋白表達量。結果:ELISA結果顯示,與空白組比較,模型組大鼠血清中IL-6含量明顯升高,經(jīng)過藥物處理后,藥物組血清中IL-6含量均有所下降,其中以痛瀉要方高劑量組效果最為明顯(P0.05)。Real-time PCR結果表明,模型組大鼠下丘腦組織中IL-6和IL-6R基因表達量明顯高于空白組(P0.05),經(jīng)藥物治療后,藥物組IL-6和IL-6R基因表達均有所降低,其中以5-ASA組和痛瀉要方高劑量組降低最為明顯(P0.05)。免疫組織化學染色結果表明,與空白組比較,潰瘍性結腸炎大鼠IL-6和IL-6R蛋白表達量明顯增加(P0.05),藥物處理可以降低大鼠下丘腦IL-6和IL-6R蛋白表達量,其中以5-ASA組和痛瀉要方高劑量組降低最為明顯(P0.05)。結論:痛瀉要方對2,4,6三硝基苯磺酸(2,4,6-trinitrobenzene sulfonic acid,TNBS)/乙醇法UC大鼠下丘腦組織中IL-6和IL-6R基因和蛋白的表達具有明顯抑制作用,提示痛瀉要方治療潰瘍性結腸炎的機制可能與抑制下丘腦中IL-6/IL-6R信號通路的異�；罨嘘P。
[Abstract]:Objective: to observe the effect of Tongxieyao recipe on ulcerative colitis of ulcerative colitis. Interleukin-6 (IL-6) and interleukin-6 receptor (IL-6R) in the hypothalamus of UC- rats. Methods: SPF grade Wistar rats were used to model ulcerative colitis. The rats were randomly divided into 5 groups: model group, low, medium and high dose of Tongxieyangfang (2.75 ~ 5.5g 路kg ~ (-1))) group. The rats were anesthetized and killed after 21 days of drug treatment. Gross colonic lesion was observed and evaluated with naked eye. Serum of rats in each group was separated. Enzyme linked immunosorbent assay (enzyme linked immunosorbent assay (Elisa)) was used to detect the content of IL-6 in serum. The rat hypothalamus tissue was isolated and total RNA was extracted. The real-time PCR(Real-time polymerase chain reaction was quantified by fluorescence. IL-6 and IL-6R gene expression were detected by Real-time PCR. The distribution and protein expression of IL-6 and IL-6R in hypothalamus were detected by immunohistochemical staining. The content of IL-6 in the serum of the model group was significantly higher than that of the control group. After drug treatment, the content of IL-6 in the serum of the drug group decreased. Among them, the effect of Tongxieyangfang group was the most obvious (P0.05N. Real-time PCR). The expression of IL-6 and IL-6R genes in hypothalamus of the model group was significantly higher than that of the blank group (P 0.05). The expression of IL-6 and IL-6R in the drug group was decreased, especially in the 5-ASA group and the high-dose group of Tongxieyangfang. The results of immunohistochemical staining showed that the expression of IL-6 and IL-6R in the drug group was significantly lower than that in the control group. Compared with the blank group, the expression of IL-6 and IL-6R protein increased significantly in ulcerative colitis rats (P0.05). Drug treatment can reduce the expression of IL-6 and IL-6R protein in hypothalamus of rats. Among them, 5-ASA group and Tongxieyao prescription high dose group were the most obvious decrease of P0.05.Conclusion: Tongxiieyao recipe has a significant effect on 2N 4N 6 trinitrobenzenesulfonic acid 2N 4. 6-trinitrobenzene sulfonic acid. The expression of IL-6 and IL-6R genes and proteins in the hypothalamus of UC rats was significantly inhibited by TNBS / ethanol. The results suggest that the mechanism of Tongxieyangfang in the treatment of ulcerative colitis may be related to the inhibition of abnormal activation of IL-6/IL-6R signal pathway in hypothalamus.
【作者單位】： 甘肅中醫(yī)藥大學;
【分類號】：R285.5
【正文快照】： [網(wǎng)絡出版地址]http://www.cnki.net/kcms/detail/11.3495.R.20170215.0942.024.html[網(wǎng)絡出版時間]2017-02-15 9:42潰瘍性結腸炎(ulcerative colitis,UC)是發(fā)生于結腸和直腸處的一種非特異性炎癥。由于目前較公認的致病因素有遺傳、環(huán)境、免疫紊亂等,西醫(yī)多運用激素、磺胺類，

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