本文選題：淫羊藿苷 + 尿酸鈉��； 參考：《中國實驗方劑學雜志》2017年11期

【摘要】：目的:觀察淫羊藿苷(icariin,ICA)對尿酸鈉誘導的大鼠急性痛風性關節(jié)炎(gouty arthritis,GA)的影響,并探討其相關的作用機制。方法:SD大鼠72只,雄雌各半,隨機分為正常組,模型組,淫羊藿苷低、中、高劑量組(20,40,80 mg·kg~(-1)),秋水仙堿組(1.5 mg·kg~(-1)),每組12只,按分組預給藥5 d后在大鼠右踝關節(jié)腔內(nèi)注射3.0%尿酸鈉溶液100μL復制大鼠GA模型,繼續(xù)給藥48 h,期間測量右踝關節(jié)周徑并作步態(tài)評分。造模48 h后麻醉動物,蘇木素-伊紅染色觀察關節(jié)腔積液涂片和關節(jié)滑膜白細胞浸潤情況,酶聯(lián)免疫吸附測定(ELISA)測定關節(jié)囊和滑膜組織中白細胞介素-1β(IL~(-1)β),白細胞介素-6(IL-6),腫瘤壞死因子-α(TNF-α)和前列腺素E_2(PGE_2)含量。蛋白質(zhì)免疫印跡(Western blot)測定關節(jié)囊和滑膜組織環(huán)氧化酶-2(COX-2)蛋白含量。結(jié)果:模型組大鼠關節(jié)周圍組織腫脹,步態(tài)跛行,關節(jié)積液和滑膜組織中大量白細胞浸潤,炎癥因子IL~(-1)β,IL-6,TNF-α均顯著高于正常組,PGE_2含量明顯升高(P0.05),關節(jié)囊和滑膜組織COX-2蛋白表達升高(P0.05);與模型組比較,ICA低、中、高劑量組可明顯改善GA模型大鼠關節(jié)腫脹和步態(tài)異常,顯著降低白細胞浸潤和IL~(-1)β,IL-6,TNF-α,PGE_2含量,明顯降低COX-2蛋白表達(P0.05)。結(jié)論:ICA可通過抑制炎癥反應改善尿酸鈉誘導的大鼠急性GA癥狀。
[Abstract]:Aim: to observe the effect of icariin Icariin (ICA) on acute gouty arthritis GA1 induced by sodium uric acid in rats, and to explore its mechanism. Methods 72 male and half male Sprague-Dawley rats were randomly divided into normal group, model group, low icariin group, middle and high dose group (20 ~ 4080 mg 路kg ~ (-1) and colchicine group (n = 12), and colchicine group (n = 12). The rat GA model was established by injecting 3.0% sodium uric acid solution into the right ankle joint of rats after 5 days of preadministration according to the group. The rats were given the drug for 48 hours. The circumference of the right ankle joint was measured and the gait score was scored. After 48 hours of modeling, hematoxylin eosin staining was used to observe the joint effusion smear and synovial leukocyte infiltration in anesthetized animals. The contents of interleukin-1 尾 -l), interleukin-6 (IL-6), tumor necrosis factor- 偽 (TNF- 偽) and prostaglandin E2PGE2) in the synovial tissues were determined by Elisa. Western blot was used to detect the content of cyclooxygenase-2 (COX-2) protein in synovium and articular capsule. Results: in the model group, the periarticular tissue swelling, gait claudication, massive leukocyte infiltration in joint effusion and synovial tissue were observed. The level of IL-6 TNF- 偽 was significantly higher than that of PGE2 in normal group, and the expression of COX-2 protein in articular capsule and synovial tissue was higher than that in control group, which was lower than that in model group, and the swelling of joints and abnormal gait in GA model rats were significantly improved in high dose group. The leukocyte infiltration and IL-6TNF- 偽 PGE2 content were significantly decreased, and the expression of COX-2 protein was significantly decreased (P 0.05). ConclusionICA can ameliorate acute GA symptoms induced by sodium uric acid by inhibiting inflammatory reaction in rats.
【作者單位】： 遵義醫(yī)學院基礎藥理教育部重點實驗室暨特色民族藥教育部國際合作聯(lián)合實驗室;
【基金】：貴州省淫羊藿開發(fā)利用科技創(chuàng)新人才團隊項目[黔科合人才團隊(2015)4023號]
【分類號】：R285.5

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本文編號：1814285