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目的血管紧张素原是血管活性多肽－血管紧张素Ⅱ的唯一前体，又是急期蛋白之一。因此，研究ＩＬ－６调节血管紧张素原基因表达对阐明人体感染时血浆血管紧张素Ⅱ水平增加致高血压有重要意义。方法应用Ｎｏｒｔｈｅｒｎ印迹杂交技术检测了ＩＬ－６刺激的肝癌细胞Ｈｅｐ３Ｂ中血管紧张素原ｍＲＮＡ，并且进一步通过ＤＮＡ－蛋白质电泳泳动漂移、ＤＮＡ重组和瞬时转染技术分析了人血管紧张素原基因５′端侧翼序列－５６８位置的一个ＩＬ－６反应元件同源序列（ＨＡＧＩＬ－６ＲＥ）。结果ＩＬ－６使血管紧张素原ｍＲＮＡ明显提高，位于血管紧张素原基因启动子中的ＨＡＧＩＬ－６ＲＥ结合于转录因子ＣＡＡＴ／增强子结合蛋白（Ｃ／ＥＢＰ）；将多拷贝的ＨＡＧＩＬ－６同ＴＫ核心启动子连接，再与氯霉素乙酰转移酶（ＣＡＴ）基因融合，构成异源表达载体，转染ＨｅｐＧ２细胞，发现ＩＬ－６增强Ｃ／ＥＢＰα的作用活性。结论Ｃ／ＥＢＰ在ＩＬ－６诱导血管紧张素原基因表达中具有调节作用。
Purpose Angiotensinogen is the only precursor of vasoactive peptide-angiotensin II and one of the proteins of the acute phase. Therefore, to study the regulation of angiotensinogen gene expression by IL-6 is of great significance to elucidate the increase of plasma angiotensin Ⅱ level in patients with human-induced hypertension. Methods Northern blot hybridization was used to detect the mRNA of angiotensinogen in Hep3B cells stimulated by IL-6. The mRNA of human angiotensinogen gene 5 was further analyzed by electrophoretic mobility shift, DNA recombination and transient transfection. One flanking sequence of the IL-6 response element (HAGIL-6RE) at position -568. Results IL-6 markedly increased angiotensinogen mRNA. HAGIL-6RE located in the promoter of angiotensinogen gene binds to the transcription factor CAAT / enhancer binding protein (C / EBP); multiple copies of HAGIL-6 TK core promoter, and then fused with chloramphenicol acetyltransferase (CAT) gene to construct a heterologous expression vector. Transfection of HepG2 cells revealed that IL-6 enhances the activity of C / EBPα. Conclusion C / EBP regulates the expression of angiotensinogen gene by IL-6.