Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment

Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment

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Apolipoprotein A-I (ApoA-I) concentrations are decreased during inflammation, which may reduce high-density lipoprotein (HDL) functionality.Thus, angilina white 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 mohair torquay 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.