Objective This study aimed to examine the metabolising effect of chrysin by investigating the mRNA expression levels of PPARα and its related cellular mechanisms in HCT116 cells. Results The mRNA expression of PPARα was significantly induced in HCT116 cells following treatment with chrysin for 36 h, but the mRNA expression of PPARα was inhibited, when the cells were treated with a combination of chrysin and MK886 (PPARα inhibitor). This phenomenon proved that the incorporation of MK886 lowers the expression levels of PPARα, thus enabling us to study the function of PPARα. The cell population of the G0/G1 phase significantly increased in chrysin-treated cells, which was accompanied by a decrease in the percentage of S phase cell population after 12 h of treatment. However, treatments of HCT116 cells with chrysin only or a combination of chrysin and MK886 did not show the opposite situation in the G0/G1 and S phase cell populations, indicating that the expression of PPARα may not be associated with the cell cycle in the treated cells. The migration rate in chrysin-treated HCT116 cells was reduced significantly after 24 and 36 h of treatments. However, the activity was revived, when the expression of PPARα was inhibited, indicating that the migration activity of chrysin-treated cells is likely correlated with the expression of PPARα. Comparison of the CYP2S1 and CYP1B1 mRNA expression in chrysin only treated, and a combination of chrysin and MK886-treated HCT116 cells for 24 and 36 h showed a significant difference in the expression levels, indicating that PPARα inhibitor could also modify the expression of CYP2S1 and CYP1B1. Conclusion The study indicates that PPARα may play an essential role in regulating the migration activity, and the expression of CYP2S1 and CYP1B1 in chrysin-treated colorectal cancer cells.

中文翻译：

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PPARα在迁移活性中起重要作用，白杨素处理的HCT116细胞中CYP2S1和CYP1B1的表达

目的本研究旨在通过研究HCT116细胞中PPARα的mRNA表达水平及其相关细胞机制，探讨白杨素的代谢作用。结果白杨素处理36 h后HCT116细胞中PPARα的mRNA表达显着上调，而白杨素与MK886（PPARα抑制剂）联合处理后，PPARα的mRNA表达受到抑制。这一现象证明MK886的掺入降低了PPARα的表达水平，从而使我们能够研究PPARα的功能。在白杨素处理的细胞中，G0/G1 期细胞数量显着增加，同时处理 12 小时后 S 期细胞数量百分比下降。然而，仅用白杨素或白杨素和 MK886 的组合处理 HCT116 细胞在 G0/G1 和 S 期细胞群中没有表现出相反的情况，表明 PPARα 的表达可能与处理细胞中的细胞周期无关。白杨素处理的 HCT116 细胞的迁移率在处理 24 和 36 小时后显着降低。然而，当 PPARα 的表达被抑制时，活性又恢复了，表明白杨素处理的细胞的迁移活性可能与 PPARα 的表达相关。CYP2S1 和 CYP1B1 mRNA 在仅处理白杨素和联合白杨素和 MK886 处理的 HCT116 细胞中 24 和 36 小时的表达水平的比较显示表达水平有显着差异，表明 PPARα 抑制剂也可以改变 CYP2S1 和 CYP1B1 的表达。结论 研究表明，PPARα可能在调节白杨素处理的结直肠癌细胞迁移活性、CYP2S1和CYP1B1的表达中起重要作用。