本文選題：山姜素 + IL-��； 參考：《免疫學(xué)雜志》2017年06期

【摘要】：目的通過檢測鼠巨噬細(xì)胞(RAW246.7)IL-6啟動子部位H3K9乙酰化修飾狀態(tài)以及轉(zhuǎn)錄因子P40和CREB含量,初步揭示H3K9去乙�；谏浇卣{(diào)節(jié)RAW246.7炎癥因子表達(dá)過程中的分子機制。方法 RAW246.7按照不同干預(yù)分為對照組、山姜素組(終質(zhì)量濃度分別為50、100、200μg/ml),山姜素+GW9662組,山姜素+HDAC1(組蛋白去乙酰化酶1)或Pgene(對照質(zhì)粒)Si RNA組,培養(yǎng)完成后ELISA法檢測培基中IL-6水平,Western blot檢測胞核PPAR、P40和CREB表達(dá)水平,并采用染色質(zhì)免疫共沉淀(Chip-q PCR)檢測RAW246.7 IL-6啟動子部位結(jié)合的去乙�；疕3K9、P40以及CREB的相對表達(dá)水平。結(jié)果與對照組相比,山姜素呈劑量依賴性促進(jìn)RAW246.7核內(nèi)PPAR表達(dá)并遏制IL-6合成,可促進(jìn)去乙�；疕3K9表達(dá),并下調(diào)核內(nèi)以及IL-6啟動子結(jié)合的轉(zhuǎn)錄因子水平;GW9662遏制山姜素誘導(dǎo)的核內(nèi)PPAR表達(dá),逆轉(zhuǎn)山姜素誘導(dǎo)的去乙�；疕3K9表達(dá),同時恢復(fù)啟動子部位、核內(nèi)P40和CREB含量以及IL-6合成;HDAC1干擾對山姜素誘導(dǎo)的PPAR表達(dá)以及核內(nèi)P40和CREB合成下降無顯著影響,但可遏制山姜素誘導(dǎo)的去乙�；疕3K9表達(dá),從而恢復(fù)IL-6啟動子結(jié)合P40和CREB含量以及IL-6合成,但表達(dá)水平低于GW9662組。結(jié)論 PPAR激動劑山姜素通過激活去乙酰化酶促進(jìn)IL-6啟動子部位H3K9去乙�；�,以上改變可能干擾轉(zhuǎn)錄因子P40和CREB結(jié)合于啟動子部位,從而干預(yù)IL-6表達(dá),而H3K9去乙�；挥绊慞40和CREB合成。
[Abstract]:Objective to explore the molecular mechanism of H3K9 deacetylation in the regulation of the expression of RAW246.7 inflammatory factors by detecting the H3K9 acetylation modification state and the contents of transcription factors P40 and CREB in the IL-6 promoter of rat macrophage RAW246.7. Methods according to different interventions, RAW246.7 was divided into control group (final concentration of 50100200 渭 g / ml), GW9662 group, histone deacetylase 1 (histone deacetylase 1) group or control plasmid RNA group. ELISA assay was used to detect the level of IL-6 and the expression of PPARN P40 and CREB were detected by Western blot, and the relative expression levels of deacetylated H3K9P40 and CREB in RAW246.7 IL-6 promoter were detected by chromatin immunoprecipitation (Chip-q PCR). Results compared with the control group, curcumin enhanced the expression of PPAR in RAW246.7 nucleus and inhibited the synthesis of IL-6 in a dose-dependent manner, and promoted the expression of deacetylated H3K9 in a dose-dependent manner. GW9662 inhibited the expression of PPAR, reversed the expression of deacetylated H3K9 induced by curcumin, and restored the site of promoter. The content of P40 and CREB in nucleus and the interference of IL-6 synthesis with HDAC1 had no significant effect on the expression of PPAR induced by curcumin and the decrease of synthesis of P40 and CREB in nucleus, but it could inhibit the expression of deacetylated H3K9 induced by curcumin. Thus, the levels of P40 and CREB binding and IL-6 synthesis of IL-6 promoter were restored, but the expression level was lower than that of GW9662 group. Conclusion the PPAR agonist curcumin promotes H3K9 deacetylation in the IL-6 promoter by activating deacetylase. These changes may interfere with the binding of transcription factor P40 and CREB to the promoter site and thus interfere with the expression of IL-6. However, H3K9 deacetylation did not affect the synthesis of P40 and CREB.
【作者單位】： 湖南醫(yī)藥學(xué)院臨床醫(yī)學(xué)院;
【基金】：湖南省自然科學(xué)基金(2010FJ3161)
【分類號】：R392

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