黄芩苷通过SOCS1驱动的巨噬细胞重编程减轻酒精相关性肝病。
Baicalin mitigates alcoholic-associated liver disease via SOCS1-driven reprogramming of macrophages.
作者信息
Huang Sha, Wang Yuhua, Wen Jinjie, Ji Wenjuan, Zeng Qiuxiang, Deng Kaili, Li Min, Kuang Shanshan, Zhang Wen, Chan Mo, Zhou Chuying, Lv Zhiping, Huang Shaohui
机构信息
School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Guangdong Provincial Key Laboratory of Chinese Medicine Pharmaceutics, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
出版信息
Chin Med. 2025 May 13;20(1):63. doi: 10.1186/s13020-025-01110-4.
BACKGROUNDS
Alcoholic liver disease (ALD), a consequence of excessive alcohol consumption, is characterized by high incidence and mortality rates. Presently, there are no effective pharmacological interventions available for the treatment of ALD. Baicalin (BA), a natural flavonoid derived from the root of Scutellaria baicalensis, has exhibited notable hepatoprotective effects. Nevertheless, the mechanisms through which BA influences the interaction between suppressor of cytokine signaling 1 (SOCS1) and macrophages during hepatic immune development remain insufficiently understood.
MATERIALS AND METHODS
This study seeks to examine the regulatory effects of BA on ALD and to elucidate the relationship between SOCS1 and macrophage differentiation. Our experimental methodology involves the novel application of zebrafish as an in vivo model for ALD. To further investigate the underlying mechanisms, we employed gene knockout and overexpression techniques.
RESULTS
The study demonstrates that BA substantially alleviates ALD in both in vivo and in vitro settings by upregulating SOCS1 expression in macrophages. Furthermore, we elucidated the association between SOCS1 and macrophage reprogramming. Specifically, SOCS1 knockdown led to the downregulation of CD86, CD80, and iNOS expression, whereas SOCS1 overexpression enhanced the expression of CD206, CD163, IL-4, and IL-10.
CONCLUSION
In conclusion, our findings suggest that BA attenuates ALD via the modulation of SOCS1-mediated macrophage reprogramming.
背景
酒精性肝病（ALD）是过度饮酒的后果，具有高发病率和死亡率的特点。目前，尚无有效的药物干预措施可用于治疗ALD。黄芩苷（BA）是一种从黄芩根中提取的天然黄酮类化合物，已显示出显著的肝脏保护作用。然而，BA在肝脏免疫发育过程中影响细胞因子信号转导抑制因子1（SOCS1）与巨噬细胞之间相互作用的机制仍未得到充分了解。
材料与方法
本研究旨在探讨BA对ALD的调节作用，并阐明SOCS1与巨噬细胞分化之间的关系。我们的实验方法涉及将斑马鱼作为ALD的体内模型的新应用。为了进一步研究潜在机制，我们采用了基因敲除和过表达技术。
结果
研究表明，BA通过上调巨噬细胞中SOCS1的表达，在体内和体外环境中均能显著减轻ALD。此外，我们阐明了SOCS1与巨噬细胞重编程之间的关联。具体而言，SOCS1基因敲低导致CD86、CD80和诱导型一氧化氮合酶（iNOS）表达下调，而SOCS1过表达则增强了CD206、CD163、白细胞介素-4（IL-4）和白细胞介素-10（IL-10）的表达。
结论
总之，我们的研究结果表明，BA通过调节SOCS1介导的巨噬细胞重编程来减轻ALD。
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