As one of the ligands of aryl hydrocarbon receptor (AhR), baicalein, isolated from Scutellaria baicalensis Georgi, has been proved to exert potential therapeutic effects on ulcerative colitis (UC), but its therapeutic mechanism remains obscure. Authentically, ulcerative colitis can be alleviated by regulating the differentiation of naïve CD4⁺ T cells via AhR activation. So, our study planned to prove the hypothesis that baicalein protected mice against UC by regulating the balance of Th17/Treg cells via AhR activation. Immunofluorescence and western blot results showed that baicalein could promote AhR activation and induce it to transfer to the nucleus. We further determined the effect of baicalein on naïve CD4⁺ T cell differentiation in vitro by magnetic cell separation and drug intervention. The results showed that baicalein could promote Treg cell differentiation by activating AhR. In vivo study, UC mice were established by free drinking of dextran sulfate sodium (DSS) for 7 days and then were orally administrated by baicalein (10, 20, and 40 mg/kg), TCDD (AhR agonist), and CH223191 (antagonist). The results demonstrated that baicalein improved the symptoms of UC mice, regulated the balance of Th17/Treg cells, and restored the balance of proinflammatory cytokines such as IL-17, IL-6, and TNF-α; anti-inflammatory cytokines such as IL-10 and TGF-β; and epithelial protective cytokine IL-22 in UC mice, and these effects were related to AhR. Taken together, our research found that baicalein might be a potential drug for UC via regulating Treg cell differentiation and maintaining immune homeostasis and attempted to shed a light on the pivotal role of AhR in these effects.

中文翻译：

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黄芩素通过芳烃受体恢复Th17/Treg细胞平衡以减轻结肠炎

作为芳烃受体（AhR）的配体之一，从黄芩中分离得到的黄芩素已被证明对溃疡性结肠炎（UC）具有潜在的治疗作用，但其治疗机制尚不清楚。诚然，溃疡性结肠炎可以通过 AhR 激活调节幼稚 CD4 ⁺ T 细胞的分化来缓解。因此，我们的研究计划证明黄芩素通过通过 AhR 激活调节 Th17/Treg 细胞的平衡来保护小鼠免受 UC 的假设。免疫荧光和蛋白质印迹结果表明黄芩素可以促进AhR活化并诱导其转移到细胞核。我们进一步确定了黄芩素对体外CD4 ⁺ T 细胞分化的影响通过磁性细胞分离和药物干预。结果表明黄芩素可通过激活AhR促进Treg细胞分化。在体内研究中，UC 小鼠通过自由饮用葡聚糖硫酸钠 (DSS) 7 天建立，然后口服黄芩素（10、20 和 40 mg/kg）、TCDD（AhR 激动剂）和 CH223191（拮抗剂） ）。结果表明黄芩素改善了UC小鼠的症状，调节了Th17/Treg细胞的平衡，恢复了IL-17、IL-6、TNF- α等促炎细胞因子的平衡；抗炎细胞因子，如 IL-10 和 TGF- β; 和上皮保护性细胞因子 IL-22 在 UC 小鼠中，这些作用与 AhR 相关。总之，我们的研究发现，黄芩素可能通过调节 Treg 细胞分化和维持免疫稳态而成为治疗 UC 的潜在药物，并试图阐明 AhR 在这些作用中的关键作用。