【摘要】：目的：黃連素（BBR）是在中國(guó)傳統(tǒng)醫(yī)藥中廣泛應(yīng)用廣譜抗菌藥物。臨床上主要用于治療腸道細(xì)菌感染性疾病。它是否能影響人視網(wǎng)膜色素上皮細(xì)胞產(chǎn)生炎癥因子的尚不可知。因此，研究黃連素對(duì)ARPE-19細(xì)胞產(chǎn)生炎癥因子的影響作用及機(jī)制是本實(shí)驗(yàn)的目的。 方法：在不同時(shí)間點(diǎn)，用黃連素處理與TNF-α共培養(yǎng)的ARPE-19細(xì)胞。酶聯(lián)免疫吸附實(shí)驗(yàn)（ELISA）檢查細(xì)胞養(yǎng)上清中IL-6、IL-8和MCP-1的蛋白濃度。實(shí)時(shí)定量PCR（real-time PCR）檢測(cè)三種因子的mRNA水平。Western-Blot分析細(xì)胞內(nèi)p38絲裂原活化蛋白激酶、胞外信號(hào)調(diào)節(jié)激酶（ERK1/2）和c-Jun N-端激酶(JNK)的磷酸化水平。使用p38、ERK1/2和JNK特異性抑制劑探討三種因子的產(chǎn)生可能涉及的信號(hào)轉(zhuǎn)導(dǎo)通路。 結(jié)果：TNF-α能顯著的促進(jìn)ARPE-19細(xì)胞從蛋白水平以及mRNA水平產(chǎn)生IL-6、IL-8和MCP-1。也能提高p38、ERK1/2和JNK的磷酸化水平。而抑制劑實(shí)驗(yàn)表明IL-6的產(chǎn)生主要是通過(guò)p38路徑調(diào)節(jié)，，而IL-8和MCP-1的產(chǎn)生與p38、ERK1/2以及JNK三條路徑都有關(guān)系。黃連素則從蛋白和mRNA水平都能顯著抑制由TNF-α刺激產(chǎn)生的IL-6、IL-8和MCP-1,并且下調(diào)p38、ERK1/2和JNK的磷酸化水平。 結(jié)論：黃連素能顯著抑制ARPE-19細(xì)胞表達(dá)炎癥因子，并且該抑制作用是通過(guò)下調(diào)p38、ERK1/2和JNK信號(hào)通路來(lái)完成實(shí)現(xiàn)的。
[Abstract]:Objective: berberine (BBR) is widely used in traditional Chinese medicine. It is mainly used in the treatment of intestinal bacterial infectious diseases. It is unclear whether it can affect the production of inflammatory factors by human retinal pigment epithelial cells. Therefore, the aim of this study is to study the effect and mechanism of berberine on the production of inflammatory factors in ARPE-19 cells. Methods: ARPE-19 cells co-cultured with TNF- 偽 were treated with berberine at different time points. The protein concentrations of IL-6,IL-8 and MCP-1 in cell culture supernatant were detected by enzyme-linked immunosorbent assay (ELISA). The phosphorylation levels of p38 mitogen-activated protein kinase (p38 mitogen-activated protein kinase), extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) were measured by real-time quantitative PCR (real-time PCR). P38, ERK 1 / 2 and JNK specific inhibitors were used to investigate the possible signal transduction pathways involved in the production of the three factors. Results: TNF- 偽 significantly promoted the production of IL-6,IL-8 and MCP-1. from protein level and mRNA level in ARPE-19 cells. The phosphorylation levels of p38, ERK 1, 2 and JNK were also increased. The inhibition experiments showed that the production of IL-6 was mainly mediated by p38 pathway, while the production of IL-8 and MCP-1 was related to p38, ERK1 / 2 and JNK pathways. Berberine could significantly inhibit IL-6,IL-8 and MCP-1, induced by TNF- 偽 and down-regulate the phosphorylation levels of p38, ERK1-2 and JNK from both protein and mRNA levels. Conclusion: berberine can significantly inhibit the expression of inflammatory factors in ARPE-19 cells, and this inhibition is achieved by down-regulating the p38, ERK-1, and JNK signaling pathways.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類(lèi)號(hào)】：R285;R774

【共引文獻(xiàn)】

相關(guān)期刊論文 前6條

1 鄒節(jié)明,潘佐靜,王淑霖;腦脈泰膠囊藥效學(xué)及毒理研究[J];中國(guó)醫(yī)藥學(xué)報(bào);2003年07期

2 張瀅瑩;屈強(qiáng);唐顯玲;;神經(jīng)遞質(zhì)參與精神興奮藥物成癮的研究進(jìn)展[J];重慶醫(yī)學(xué);2011年04期

3 閔寒毅,劉熙樸;細(xì)胞因子和葡萄膜炎[J];國(guó)外醫(yī)學(xué).眼科學(xué)分冊(cè);2005年01期

4 巫玲玲;蔣偉哲;黃興振;施曉霞;呂聰;許崇搖;邱卓;;山烏龜中延胡索乙素的提取和含量測(cè)定[J];廣西醫(yī)學(xué);2011年01期

5 陸靜金;劉圣;;小檗堿對(duì)糖尿病及其并發(fā)癥作用的研究進(jìn)展[J];安徽醫(yī)藥;2012年11期

6 何莉;吳思宇;王廷龍;張萍;黃曦;;登革病毒誘導(dǎo)人單核細(xì)胞VEGF的表達(dá)及機(jī)制[J];病毒學(xué)報(bào);2012年06期

本文編號(hào)：2467035