本文選題：亞硝酸鹽暴露　切入點(diǎn)：炎癥反應(yīng)　出處：《解剖學(xué)報(bào)》2017年06期 　論文類型：期刊論文

【摘要】：目的觀察慢性亞硝酸鹽暴露對(duì)小鼠大腦皮質(zhì)炎癥損傷的影響及其探討DNA甲基化和組蛋白去乙酰化等相關(guān)機(jī)制。方法選取8周齡健康雄性C57BL/6J小鼠,隨機(jī)分為對(duì)照組(生理鹽水)、低劑量亞硝酸鹽組(3g/L)和高劑量亞硝酸鹽組(6 g/L),建立亞硝酸鹽暴露模型,收集各組小鼠大腦皮質(zhì),利用免疫熒光染色法和Western blotting法分析大腦皮質(zhì)炎癥損傷,組蛋白去乙酰化酶和DNA甲基化相關(guān)酶的表達(dá)情況。結(jié)果慢性亞硝酸鹽暴露后小鼠大腦皮質(zhì)炎癥損傷因子環(huán)氧化酶2(COX2)、白細(xì)胞介素-1β(IL-1β)、離子鈣接頭蛋白分子1(Iba1)、c-Fos、IL-6表達(dá)量明顯多于對(duì)照組(P0.01),同時(shí)高劑量暴露組DNA甲基化相關(guān)酶5-甲基胞嘧啶(5-m C)、DNA甲基轉(zhuǎn)移酶1(DNMT1)、DNMT3a、和組蛋白去乙�；�1(HDAC1)表達(dá)明顯低于對(duì)照組(P0.01)且都呈亞硝酸鹽劑量依賴性。結(jié)論亞硝酸鹽暴露可通過(guò)促進(jìn)細(xì)胞免疫炎癥對(duì)小鼠大腦皮質(zhì)造成損傷,并且DNA甲基化和組蛋白去乙�；赡軈⑴c了慢性亞硝酸鹽暴露過(guò)程中的應(yīng)答過(guò)程及其調(diào)控機(jī)制。
[Abstract]:Objective to observe the effects of chronic nitrite exposure on inflammatory injury of cerebral cortex in mice and to explore the mechanisms of DNA methylation and histone deacetylation. Methods healthy male C57BL / 6J mice aged 8 weeks were selected. The rats were randomly divided into control group (normal saline group, low dose nitrite group) and high dose nitrite group (6 g / L) to establish nitrite exposure model and collect cerebral cortex of each group. The inflammatory injury of cerebral cortex was analyzed by immunofluorescence staining and Western blotting method. The expression of histone deacetylase and DNA methylation related enzymes. Results after chronic nitrite exposure, the expression of cyclooxygenase 2 (COX2), interleukin-1 尾 (IL 1 尾), ion calcium junction protein molecule 1 (IBA 1) and c-Fossin-6 (IL-6) in the cerebral cortex of mice exposed to chronic nitrite were detected. The expression of 5-methylcytosine 5-methylcytosine 5-methylcytosine (5-methylcytosine 5-methylcytosine 5-methylcytosine) and histone deacetylase (1HDAC1) in high dose exposure group was significantly lower than that in control group (P 0.01) and the expression of DNMT3a and histone deacetylase 1HDAC1 was significantly lower than that in control group (P 0.01) and the expression of DNMT3a and histone deacetylase 1HDAC1 was significantly lower than that in control group (P 0.01). It is suggested that nitrite exposure may damage the cerebral cortex of mice by promoting cellular immune inflammation. DNA methylation and histone deacetylation may be involved in the response process and its regulatory mechanism during chronic nitrite exposure.
【作者單位】： 河南大學(xué)護(hù)理學(xué)院河南大學(xué)神經(jīng)生物研究所;
【基金】：河南省高等學(xué)校重點(diǎn)科研項(xiàng)目(15A180031,16A330001)
【分類號(hào)】：R99
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本文編號(hào)：1625558