【摘要】：目的：香煙煙霧提取物(CSE)誘導(dǎo)人類肺泡Ⅱ型上皮細(xì)胞(A549)核因子-κB(NF-κB)、抑制蛋白-κBα(I-κ Bα)、白細(xì)胞介素-6(IL-6)的變化后，觀察甲基強(qiáng)的松龍(Mp)對(duì)其的干預(yù)作用。方法：體外培養(yǎng)A549細(xì)胞系，根據(jù)目的和條件的不同將其分為三組：1)對(duì)照組(NS組)以無(wú)血清DMEM處理；2)刺激組(CSE組)僅以10％濃度CSE處理；3)治療組(CSE+Mp組)同上CSE刺激后加入0.015％Mp處理。于不同時(shí)間段收集各組細(xì)胞裂解物后應(yīng)用免疫組化法、免疫印跡法(Westernblot)，酶聯(lián)免疫法(ELISA)等觀察NF-κ B、I-κ B α的表達(dá)量與時(shí)間的關(guān)系及IL-6的變化。結(jié)果：組間有明顯差異：1)對(duì)照組無(wú)變化；2)刺激組CSE可導(dǎo)致NF-κ B被活化，I-κ B α從處理后15分鐘開(kāi)始后減少至30分鐘后最終消失，60-90分鐘后恢復(fù)到刺激前水平，IL-6分泌增加；3)治療組檢測(cè)到NF-κ B表達(dá)量劇降，而I-κ Bα在15-30分鐘內(nèi)始終有本底表達(dá)，60-90分鐘后恢復(fù)到刺激前水平，，IL-6分泌減少，組間比較發(fā)現(xiàn)I-κ Bα蛋白的表達(dá)水平明顯低于對(duì)照組，高于刺激組，差異有統(tǒng)計(jì)學(xué)意義。(組間：F=19.633P＜0.01時(shí)間：F=14.88P＜0.01)。結(jié)論：甲基強(qiáng)的松龍能使CSE刺激后A549細(xì)胞NF-κ B活化減少，I-κ Bα蛋白表達(dá)增加，抑制NF κ B活性，減少了炎性細(xì)胞因子IL-6的分泌從而在呼吸道炎性疾病中起抗炎作用。
[Abstract]:Objective: cigarette smoke extract (CSE) induced the nuclear factor kappa B (NF- kappa B) of human alveolar type II epithelial cells (A549), inhibition of protein kappa B alpha (I- kappa B a) and interleukin -6 (IL-6), and observed the intervention effect of methylprednisolone (Mp) on it. Methods: the extracellular culture of A549 cell lines was divided into three groups according to the different purpose and conditions. 1) 1) the control group (group NS) was treated with serum-free DMEM; 2) the stimulation group (group CSE) was treated with only 10% concentration of CSE; 3) the treatment group (group CSE+Mp) was added to the 0.015%Mp treatment after the same CSE stimulation. The immunoblotting (Westernblot) and enzyme linked immunoassay (ELISA) were used to observe the NF- kappa B, I- kappa was observed in the treatment group (CSE+Mp group) after the same CSE stimulation. The relationship between the expression of B alpha and the time and the change of IL-6. Results: there were significant differences between the groups: 1) there was no change in the control group; 2) the stimulation group CSE could lead to the activation of NF- kappa B, and the I- kappa B alpha decreased from 15 minutes after treatment to 30 minutes after the treatment, and finally disappeared after 60-90 minutes, and the secretion of IL-6 increased in the 60-90 minutes, and 3) the treatment group detected NF. The expression of kappa B was dramatically reduced, and the expression of I- kappa B alpha always had the background expression in 15-30 minutes. After 60-90 minutes, the level of IL-6 secretion was reduced. The expression level of I- kappa B alpha protein was significantly lower than that of the control group. The difference was statistically significant. (group: F=19.633P < 0.01: F=14.88P < 0.01). Conclusion: Methylprednisolone can reduce the activation of NF- kappa B in A549 cells after CSE stimulation, increase the expression of I- kappa B alpha protein, inhibit the activity of NF kappa B, and reduce the secretion of inflammatory cytokines IL-6, so as to play an anti-inflammatory role in respiratory inflammatory diseases.
【學(xué)位授予單位】：新疆醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

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