Apolipoprotein A-I (ApoA-I) concentrations are decreased during inflammation, which may reduce high-density lipoprotein (HDL) functionality. Thus, rescuing ApoA-I concentrations during inflammation might help to prevent atherosclerosis. Recent studies have shown that butyric acid (C4) has anti-inflammatory effects and rescues ApoA-I production. However, whether intestinal short chain fatty acids (SCFAs) are able to influence hepatic processes is unknown. Therefore, we investigated C4 anti-inflammatory effects on ApoA-I transcription in the intestine-liver co-culture model. C4 dose-response experiments in the presence or absence of cytokines were performed in a co-culture system including Caco-2 cells, HepG2 cells, or both. Changes in ApoA-I transcription in Caco-2 cells and HepG2 cells were analyzed using qPCR. C4 increased ApoA-I expression in HepG2 cells that cultured alone. When both cells were cultured together, C4 decreased ApoA-I expression in Caco-2 cells and increased ApoA-I expression in HepG2 cells. However, adding C4 to apical Caco-2 cells resulted in a smaller effect in HepG2 cells compared with adding C4 directly to the hepatocytes. Moreover, C4 rescued ApoA-I expression in inflamed HepG2 cells. These findings suggests that intestinal SCFAs can affect hepatic processes. However, the smaller effect in the co-culture experiment indicates cross-talk between intestine and liver.

中文翻译：

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向肠Caco-2细胞中添加丁酸可提高肝脏ApoA-I的转录水平，并拯救在基底外侧隔室共同培养的发炎的HepG2细胞中较低的ApoA-I表达

炎症过程中载脂蛋白AI（ApoA-I）的浓度降低，这可能会降低高密度脂蛋白（HDL）的功能。因此，在炎症过程中抢救ApoA-I浓度可能有助于预防动脉粥样硬化。最近的研究表明，丁酸（C4）具有抗炎作用，可以挽救ApoA-I的产生。但是，肠短链脂肪酸（SCFAs）是否能够影响肝过程尚不清楚。因此，我们在肠肝共培养模型中研究了C4对ApoA-I转录的抗炎作用。在存在或不存在细胞因子的情况下，在包括Caco-2细胞，HepG2细胞或两者的共培养系统中进行C4剂量反应实验。使用qPCR分析Caco-2细胞和HepG2细胞中ApoA-I转录的变化。C4增加了单独培养的HepG2细胞中ApoA-1的表达。当两个细胞一起培养时，C4降低了Caco-2细胞中ApoA-1的表达，并增加了HepG2细胞中ApoA-1的表达。但是，与直接将C4添加到肝细胞相比，将C4添加到顶端Caco-2细胞对HepG2细胞的作用较小。此外，C4拯救了发炎的HepG2细胞中的ApoA-I表达。这些发现表明肠道SCFA可以影响肝过程。但是，共培养实验中较小的影响表明肠与肝之间存在串扰。与将C4直接添加到肝细胞相比，向顶部Caco-2细胞添加C4对HepG2细胞的作用较小。此外，C4拯救了发炎的HepG2细胞中的ApoA-I表达。这些发现表明肠道SCFA可能影响肝过程。但是，共培养实验中较小的影响表明肠与肝之间存在串扰。与将C4直接添加到肝细胞相比，向顶部Caco-2细胞添加C4对HepG2细胞的作用较小。此外，C4拯救了发炎的HepG2细胞中的ApoA-I表达。这些发现表明肠道SCFA可能影响肝过程。但是，共培养实验中较小的影响表明肠与肝之间存在串扰。