紅霉素對(duì)煙草煙霧刺激下沉默信息調(diào)節(jié)因子1（SIRT1）的影響
發(fā)布時(shí)間：2018-09-01 19:35
【摘要】：第一部分：紅霉素對(duì)煙草煙霧暴露下人巨噬細(xì)胞釋放活性氧及炎癥因子的作用目的：1.觀察煙草煙霧刺激對(duì)人巨噬細(xì)胞產(chǎn)生活性氧的影響,以及紅霉素能否調(diào)控由煙草煙霧暴露介導(dǎo)的人巨噬細(xì)胞活性氧(Reactive oxygen species, ROS)釋放。2.觀察煙草煙霧刺激條件下,人巨噬細(xì)胞釋放的白細(xì)胞介素6(interleukin 6, IL-6)、白細(xì)胞介素8(interleukin 8, IL-8)、腫瘤壞死因子a (tumor necrosis factor a, TNF-α)水平改變,以及紅霉素對(duì)于煙草煙霧暴露下人巨噬細(xì)胞釋放炎癥因子水平的影響。方法：研究對(duì)象為人淋巴瘤單核細(xì)胞株U937,經(jīng)10nM佛波酯(phorbol 12-myristate 13-acetate, PMA)誘導(dǎo)24h后,U937轉(zhuǎn)換成巨噬細(xì)胞,用香煙煙霧提取物(cigarette smoke extract, CSE)刺激人巨噬細(xì)胞。用四甲基偶氮唑藍(lán)(MTT)法檢測(cè)CSE及紅霉素對(duì)細(xì)胞最適宜作用濃度。細(xì)胞分組：對(duì)照組,CSE組(加入1%CSE孵育24h),CSE+紅霉素24h組(1μg/ml紅霉素預(yù)孵育24h后,加入1%CSE繼續(xù)刺激24h),CSE+紅霉素48h組(1μg/ml紅霉素預(yù)孵育48h后,加入1%CSE繼續(xù)刺激24h)。各細(xì)胞組在紅霉素(Erythromycin, EM)、CSE干預(yù)下,以2',7'-二氯二氫熒光素二乙酯(2',7'-dichlorofluorescin-diacetate, DCFH-DA, 10mM)作為熒光探針,流式細(xì)胞術(shù)檢測(cè)各組細(xì)胞中ROS水平。用酶聯(lián)免疫吸附法(ELISA)檢測(cè)各實(shí)驗(yàn)組細(xì)胞上清液中IL-6、IL-8、 TNF-α釋放水平。結(jié)果：1%濃度的CSE能顯著上調(diào)人巨噬細(xì)胞ROS的釋放(P0.01),紅霉素(lug/ml)預(yù)孵育24h、48h能抑制1%CSE對(duì)細(xì)胞ROS的上調(diào)作用(p0.01),SIRT1特異性抑制劑(NAM)顯著上調(diào)人巨噬細(xì)胞ROS的釋放(P0.01)；CSE 1%增加人巨噬細(xì)胞釋放IL-6、IL-8、TNF-α,紅霉素(lug/ml)預(yù)孵育24h減少IL-6、TNF-α釋放(p0.01)。紅霉素(lug/ml)預(yù)孵育48h對(duì)人巨噬細(xì)胞釋放IL-6、IL-8、TNF-α的抑制作用更加明顯(p0.01)。結(jié)論：1.煙草煙霧刺激引起人巨噬細(xì)胞釋放活性氧增多,紅霉素抑制氧化應(yīng)激機(jī)制之一是通過(guò)抑制活性氧釋放。2.煙草煙霧刺激促進(jìn)人巨噬細(xì)胞釋放IL-6、IL-8、TNF-α增加,紅霉素抑制炎癥機(jī)制之一通過(guò)抑制人巨噬細(xì)胞釋放IL-6、IL-8、TNF-α。第二部分：紅霉素對(duì)煙草煙霧刺激下人巨噬細(xì)胞內(nèi)SIRT1、NF-κB蛋白表達(dá)及兩種蛋白之間的相互作用目的：觀察人巨噬細(xì)胞中SIRT1及NF-κB蛋白表達(dá)在煙草煙霧暴露條件下的改變,以及紅霉素對(duì)煙草煙霧刺激條件下SIRT1和NF-κB蛋白表達(dá)產(chǎn)生何種影響。觀察人巨噬細(xì)胞中SIRT1及NF-κB蛋白是否存在相互作用,以及在煙草煙霧暴露、紅霉素治療下,存在何種相互作用關(guān)系。方法：1.用10nmol/ml PMA孵育24h可將人淋巴瘤單核細(xì)胞株U937誘導(dǎo)分化成巨噬細(xì)胞,用CSE刺激巨噬細(xì)胞,制造細(xì)胞在煙草煙霧暴露氧化應(yīng)激模型。分為：對(duì)照組,CSE組,CSE+紅霉素24h組,CSE+紅霉素48h組,NF-κB蛋白特異性抑制劑PDTC組(20nM PDTC預(yù)孵育24h后加入1%CSE繼續(xù)孵育24h),SIRT1特異性抑制劑NAM組(20mM NAM孵育24h)。用western blot (WB)方法檢測(cè)各組細(xì)胞中NF-κB、SIRT1蛋白表達(dá)。2.將U937誘導(dǎo)分化成巨噬細(xì)胞后,對(duì)細(xì)胞分組并進(jìn)行實(shí)驗(yàn)。分為：對(duì)照組,CSE組,CSE+紅霉素24h組,CSE+紅霉素48h組。提取各組細(xì)胞總蛋白,先用免疫共沉淀(co-immunoprecipitation, Co-IP)進(jìn)行蛋白沉淀,再用westernblot (WB)方法檢測(cè)各組細(xì)胞中NF-κB、SIRT1蛋白表達(dá)。結(jié)果：1.CSE暴露會(huì)導(dǎo)致人巨噬細(xì)胞中SIRT1蛋白表達(dá)明顯下降,并能增加NF-κB蛋白表達(dá),經(jīng)紅霉素預(yù)孵育24h后再予CSE刺激,能促進(jìn)人巨噬細(xì)胞中SIRT1蛋白表達(dá)升高,同時(shí)抑制NF-κB蛋白表達(dá)升高,經(jīng)紅霉素預(yù)孵育48h后,對(duì)人巨噬細(xì)胞中SIRT1蛋白表達(dá)升高以及對(duì)NF-κB蛋白的抑制作用更加明顯。結(jié)果：1.CSE暴露會(huì)導(dǎo)致人巨噬細(xì)胞中SIRT1蛋白表達(dá)明顯下降,增加NF-κB蛋白表達(dá),經(jīng)紅霉素預(yù)孵育24h、48h,均促進(jìn)人巨噬細(xì)胞中SIRT1蛋白表達(dá)升高,同時(shí)抑制NF-κB蛋白表達(dá)升高,其中48h組更明顯。2.經(jīng)Co-IP檢測(cè),SIRT1和NF-κB蛋白在人巨噬細(xì)胞內(nèi)存在直接相互作用,CSE刺激可導(dǎo)致SIRT1蛋白表達(dá)減少,從而促進(jìn)NF-κB蛋白表達(dá)增加,經(jīng)紅霉素預(yù)孵育24h、48h,可增加人巨噬細(xì)胞中SIRT1蛋白表達(dá),抑制NF-κB蛋白表達(dá)。結(jié)論：1煙草煙霧導(dǎo)致炎癥的機(jī)制可能是通過(guò)氧化應(yīng)激抑制人巨噬細(xì)胞SIRT1蛋白表達(dá),進(jìn)而促進(jìn)NF-κB蛋白表達(dá),從而促進(jìn)炎癥介質(zhì)IL-6、IL-8、 TNF-α釋放。2.紅霉素抑制氧化應(yīng)激誘導(dǎo)的炎癥機(jī)制可能是通過(guò)紅霉素增加SIRT1蛋白表達(dá),進(jìn)而抑制NF-κB蛋白表達(dá),從而抑制炎癥介質(zhì)釋放。第三部分：紅霉素對(duì)煙草煙霧暴露小鼠肺組織以及肺組織中SIRT1與NF-κB蛋白作用目的：觀察煙草煙霧暴露對(duì)小鼠肺組織的影響,以及紅霉素對(duì)煙草煙霧暴露小鼠肺組織的作用。觀察受煙草煙霧暴露刺激小鼠的肺組織中SIRT1及NF-κB蛋白表達(dá)的改變,以及紅霉素對(duì)煙草煙霧刺激下對(duì)小鼠肺組織內(nèi)SIRT1及NF-κB蛋白表達(dá)的作用。方法：將8周大小的雄性BALB/c小鼠分為：對(duì)照組,煙草煙霧暴露組,紅霉素治療組。煙草煙霧暴露組每天煙草煙霧暴露2h,持續(xù)12w,紅霉素治療組在煙草煙霧暴露前用紅霉素(100mg/kg-day)灌胃治療,余處理同煙草煙霧暴露組。建模到期后取右肺組織切片行HE染色,剩余肺組織行westernblot檢測(cè)各組小鼠肺組織中NF-κB、SIRT1蛋白表達(dá)。結(jié)果：1.煙草煙霧暴露小鼠肺組織中出現(xiàn)炎癥,支氣管周圍炎癥細(xì)胞聚集,肺組織出現(xiàn)肺氣腫表現(xiàn)。紅霉素治療組炎癥反應(yīng)較煙草煙霧暴露組減輕,肺氣腫表現(xiàn)減輕。2.煙草煙霧暴露小鼠肺組織中SIRT1蛋白較對(duì)照組明顯減少,NF-κB蛋白明顯增加。紅霉素治療組小鼠肺組織中SIRT1蛋白較對(duì)照組減少,但較煙草煙霧暴露組表達(dá)增加。結(jié)論：1.紅霉素減輕煙草煙霧暴露引起的小鼠肺組織炎癥,可能與紅霉素上調(diào)肺組織SIRT1蛋白表達(dá),抑制肺組織中NF-κB蛋白表達(dá)相關(guān)。2.紅霉素減輕小鼠肺氣腫,可能與紅霉素促進(jìn)SIRT1表達(dá)相關(guān)。
[Abstract]:Part I: Effects of erythromycin on the release of reactive oxygen species (ROS) and inflammatory factors from human macrophages exposed to tobacco smoke. Objective: 1. To observe the effects of tobacco smoke on the production of reactive oxygen species (ROS) in human macrophages and whether erythromycin can regulate the release of ROS from human macrophages mediated by tobacco smoke exposure. To observe the changes of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-A (TNF-a) released by human macrophages under tobacco smoke stimulation, and the effect of erythromycin on the release of inflammatory factors from human macrophages under tobacco smoke exposure. METHODS: Human lymphoma monocyte U937 was induced by 10 nM phorbol 12-myristate 13-acetate (PMA) for 24 hours. U937 was transformed into macrophages and stimulated by cigarette smoke extract (CSE). The optimum concentration of CSE and erythromycin on human lymphoma cells was determined by MTT assay. Cell groups: control group, CSE group (incubated with 1% CSE for 24 hours), CSE + erythromycin 24 hours group (incubated with 1 ug / ml erythromycin for 24 hours, added 1% CSE for 24 hours), CSE + erythromycin 48 hours group (incubated with 1 ugh / ml erythromycin for 48 hours, added 1% CSE for 24 hours). Cell groups were treated with Erythromycin (EM), CSE and 2', 7'-dichlorodihydrofluorescence. Optical diethyl ester (2', 7'-dichlorofluorescin-diacetate, DCFH-DA, 10mM) was used as a fluorescent probe to detect the ROS level in the cells of each group. The levels of IL-6, IL-8 and TNF-a in the supernatant of the cells of each experimental group were detected by enzyme-linked immunosorbent assay (ELISA). Results: CSE at 1% concentration could significantly up-regulate the release of ROS from human macrophages (P 0.01). Erythromycin (lug / ml) could inhibit the up-regulation of ROS by 1% CSE (p0.01), SIRT1 specific inhibitor (NAM) could significantly increase the release of ROS by human macrophages (p0.01), and 1% CSE could increase the release of IL-6, IL-8, TNF-a, and erythromycin (lug / ml) by 48 h after pre-incubation. Conclusion: 1. Tobacco smoke stimulates the release of reactive oxygen species from human macrophages. One of the mechanisms of erythromycin inhibiting oxidative stress is through inhibiting the release of reactive oxygen species. 2. Tobacco smoke stimulates the release of IL-6, IL-8, TNF-a from human macrophages, and erythromycin. One of the mechanisms of inhibiting inflammation is by inhibiting the release of IL-6, IL-8 and TNF-alpha from human macrophages. Part II: The effect of erythromycin on the expression of SIRT1, NF-kappa B protein in human macrophages stimulated by tobacco smoke and the interaction between the two proteins. To observe the interaction between SIRT1 and NF-kappa B protein in human macrophages and the interaction between SIRT1 and NF-kappa B protein in tobacco smoke exposure and erythromycin treatment. Methods: 1. Human lymphoma monocytes were incubated with 10 nmol/ml PMA for 24 hours. U937 cells were induced to differentiate into macrophages and stimulated with CSE to produce a model of oxidative stress induced by tobacco smoke exposure. The cells were divided into control group, CSE group, CSE + erythromycin 24 h group, CSE + erythromycin 48 h group, NF-kappa B protein specific inhibitor PDTC group (20nM PDTC pre-incubated for 24 h and added 1% CSE for 24 h), SIRT1 specific inhibitor NA. After U937 was induced to differentiate into macrophages, the cells were divided into control group, CSE group, CSE + erythromycin 24 h group and CSE + erythromycin 48 h group. The expression of NF-kappa B and SIRT1 protein was detected by Western blot (WB). Results: 1. The expression of SIRT1 protein in human macrophages was significantly decreased and the expression of NF-kappa B protein was increased after exposure to CSE. The expression of SIRT1 protein in human macrophages was stimulated by CSE 24 hours after incubation with erythromycin. After incubation with erythromycin for 48 hours, the expression of SIRT1 protein and the inhibition of NF-kappa B protein in human macrophages were increased. Results: 1. The expression of SIRT1 protein in human macrophages decreased significantly after exposure to CSE, and the expression of NF-kappa B protein was increased after incubation with erythromycin for 24 hours and 48 hours. Both of them increased the expression of SIRT1 protein and inhibited the expression of NF-kappa B protein in human macrophages, especially in 48h group. 2. The interaction between SIRT1 and NF-kappa B protein in human macrophages was detected by Co-IP. CSE stimulation could decrease the expression of SIRT1 protein and promote the expression of NF-kappa B protein. After incubation with erythromycin for 24h, 48 h, SIRT1 protein was increased. Conclusion: 1. Tobacco smoke may induce inflammation by inhibiting the expression of SIRT1 protein in human macrophages through oxidative stress, thereby promoting the expression of NF-kappa B protein, thereby promoting the release of inflammatory mediators IL-6, IL-8 and TNF-alpha. 2. Erythromycin inhibits oxidative stress-induced inflammation. The mechanism of inflammation may be that erythromycin increases the expression of SIRT1 protein and then inhibits the expression of NF-kappa B protein, thereby inhibiting the release of inflammatory mediators. The effect of erythromycin on the expression of SIRT1 and NF-kappa B protein in lung tissue of mice exposed to tobacco smoke was observed. Tobacco smoke exposure group, erythromycin treatment group. The expression of NF-kappa B and SIRT1 protein in lung tissue of mice in each group. Results: 1. Inflammation, aggregation of inflammatory cells around bronchi and emphysema appeared in lung tissue of mice exposed to tobacco smoke. The expression of SIRT1 protein in lung tissue of mice treated with erythromycin was lower than that of control group, but the expression of SIRT1 protein was higher than that of tobacco smoke exposure group. CONCLUSION: 1. Erythromycin can alleviate the inflammation of lung tissue induced by tobacco smoke exposure, which may be related to erythromycin up-regulating the expression of SIRT1 protein in lung tissue and inhibiting the expression of SIRT1 protein in lung tissue. The expression of NF-kappa B protein in tissues is correlated. 2. Erythromycin can alleviate emphysema in mice, which may be related to erythromycin promoting SIRT1 expression.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R563.9
本文編號(hào)：2218140
[Abstract]:Part I: Effects of erythromycin on the release of reactive oxygen species (ROS) and inflammatory factors from human macrophages exposed to tobacco smoke. Objective: 1. To observe the effects of tobacco smoke on the production of reactive oxygen species (ROS) in human macrophages and whether erythromycin can regulate the release of ROS from human macrophages mediated by tobacco smoke exposure. To observe the changes of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-A (TNF-a) released by human macrophages under tobacco smoke stimulation, and the effect of erythromycin on the release of inflammatory factors from human macrophages under tobacco smoke exposure. METHODS: Human lymphoma monocyte U937 was induced by 10 nM phorbol 12-myristate 13-acetate (PMA) for 24 hours. U937 was transformed into macrophages and stimulated by cigarette smoke extract (CSE). The optimum concentration of CSE and erythromycin on human lymphoma cells was determined by MTT assay. Cell groups: control group, CSE group (incubated with 1% CSE for 24 hours), CSE + erythromycin 24 hours group (incubated with 1 ug / ml erythromycin for 24 hours, added 1% CSE for 24 hours), CSE + erythromycin 48 hours group (incubated with 1 ugh / ml erythromycin for 48 hours, added 1% CSE for 24 hours). Cell groups were treated with Erythromycin (EM), CSE and 2', 7'-dichlorodihydrofluorescence. Optical diethyl ester (2', 7'-dichlorofluorescin-diacetate, DCFH-DA, 10mM) was used as a fluorescent probe to detect the ROS level in the cells of each group. The levels of IL-6, IL-8 and TNF-a in the supernatant of the cells of each experimental group were detected by enzyme-linked immunosorbent assay (ELISA). Results: CSE at 1% concentration could significantly up-regulate the release of ROS from human macrophages (P 0.01). Erythromycin (lug / ml) could inhibit the up-regulation of ROS by 1% CSE (p0.01), SIRT1 specific inhibitor (NAM) could significantly increase the release of ROS by human macrophages (p0.01), and 1% CSE could increase the release of IL-6, IL-8, TNF-a, and erythromycin (lug / ml) by 48 h after pre-incubation. Conclusion: 1. Tobacco smoke stimulates the release of reactive oxygen species from human macrophages. One of the mechanisms of erythromycin inhibiting oxidative stress is through inhibiting the release of reactive oxygen species. 2. Tobacco smoke stimulates the release of IL-6, IL-8, TNF-a from human macrophages, and erythromycin. One of the mechanisms of inhibiting inflammation is by inhibiting the release of IL-6, IL-8 and TNF-alpha from human macrophages. Part II: The effect of erythromycin on the expression of SIRT1, NF-kappa B protein in human macrophages stimulated by tobacco smoke and the interaction between the two proteins. To observe the interaction between SIRT1 and NF-kappa B protein in human macrophages and the interaction between SIRT1 and NF-kappa B protein in tobacco smoke exposure and erythromycin treatment. Methods: 1. Human lymphoma monocytes were incubated with 10 nmol/ml PMA for 24 hours. U937 cells were induced to differentiate into macrophages and stimulated with CSE to produce a model of oxidative stress induced by tobacco smoke exposure. The cells were divided into control group, CSE group, CSE + erythromycin 24 h group, CSE + erythromycin 48 h group, NF-kappa B protein specific inhibitor PDTC group (20nM PDTC pre-incubated for 24 h and added 1% CSE for 24 h), SIRT1 specific inhibitor NA. After U937 was induced to differentiate into macrophages, the cells were divided into control group, CSE group, CSE + erythromycin 24 h group and CSE + erythromycin 48 h group. The expression of NF-kappa B and SIRT1 protein was detected by Western blot (WB). Results: 1. The expression of SIRT1 protein in human macrophages was significantly decreased and the expression of NF-kappa B protein was increased after exposure to CSE. The expression of SIRT1 protein in human macrophages was stimulated by CSE 24 hours after incubation with erythromycin. After incubation with erythromycin for 48 hours, the expression of SIRT1 protein and the inhibition of NF-kappa B protein in human macrophages were increased. Results: 1. The expression of SIRT1 protein in human macrophages decreased significantly after exposure to CSE, and the expression of NF-kappa B protein was increased after incubation with erythromycin for 24 hours and 48 hours. Both of them increased the expression of SIRT1 protein and inhibited the expression of NF-kappa B protein in human macrophages, especially in 48h group. 2. The interaction between SIRT1 and NF-kappa B protein in human macrophages was detected by Co-IP. CSE stimulation could decrease the expression of SIRT1 protein and promote the expression of NF-kappa B protein. After incubation with erythromycin for 24h, 48 h, SIRT1 protein was increased. Conclusion: 1. Tobacco smoke may induce inflammation by inhibiting the expression of SIRT1 protein in human macrophages through oxidative stress, thereby promoting the expression of NF-kappa B protein, thereby promoting the release of inflammatory mediators IL-6, IL-8 and TNF-alpha. 2. Erythromycin inhibits oxidative stress-induced inflammation. The mechanism of inflammation may be that erythromycin increases the expression of SIRT1 protein and then inhibits the expression of NF-kappa B protein, thereby inhibiting the release of inflammatory mediators. The effect of erythromycin on the expression of SIRT1 and NF-kappa B protein in lung tissue of mice exposed to tobacco smoke was observed. Tobacco smoke exposure group, erythromycin treatment group. The expression of NF-kappa B and SIRT1 protein in lung tissue of mice in each group. Results: 1. Inflammation, aggregation of inflammatory cells around bronchi and emphysema appeared in lung tissue of mice exposed to tobacco smoke. The expression of SIRT1 protein in lung tissue of mice treated with erythromycin was lower than that of control group, but the expression of SIRT1 protein was higher than that of tobacco smoke exposure group. CONCLUSION: 1. Erythromycin can alleviate the inflammation of lung tissue induced by tobacco smoke exposure, which may be related to erythromycin up-regulating the expression of SIRT1 protein in lung tissue and inhibiting the expression of SIRT1 protein in lung tissue. The expression of NF-kappa B protein in tissues is correlated. 2. Erythromycin can alleviate emphysema in mice, which may be related to erythromycin promoting SIRT1 expression.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R563.9
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