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黄芩汤可增加SLC6A4表达，并阻断NFκB介导的NLRP3/Caspase1/GSDMD通路，从而抑制结肠炎相关致癌作用。

Huang Qin decoction increases SLC6A4 expression and blocks the NFκB-mediated NLRP3/Caspase1/GSDMD pathway to disrupt colitis-associated carcinogenesis.

作者信息

Tao Yili, Wang Lai, Ye Xiaofeng, Qian Xin, Pan Danye, Dong Xiaoyu, Jiang Qian, Hu Po

机构信息

Department of Gastroenterology, Changzhou Hospital of Traditional Chinese Medicine, Changzhou, 213000, Jiangsu, P.R. China.

Digestive Disease Diagnosis and Treatment Center of Integrated Traditional Chinese and Western Medicine, Changzhou Hospital of Traditional Chinese Medicine, Changzhou, 213000, Jiangsu, P.R. China.

出版信息

Funct Integr Genomics. 2024 Mar 12;24(2):55. doi: 10.1007/s10142-024-01334-x.

DOI:10.1007/s10142-024-01334-x
PMID:38467948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10927794/
Abstract

Huang Qin decoction (HQD) is a traditional Chinese medicine formula for treating colitis, but the effects and molecular mechanism of action of HQD in colitis-associated carcinogenesis (CAC) are still unclear. Therefore, we aimed to determine the beneficial effects of HQD on CAC in mice and to reveal the underlying mechanism involved. AOM/DSS was used to induce CAC in mice, and the effects of HQD on tumorigenesis in mice were examined (with mesalazine serving as a positive control). Mesalazine or HQD treatment alleviated body weight loss and decreased the disease activity index in mice induced by AOM/DSS. Mesalazine or HQD treatment also suppressed the shortening of colon tissue length, the number of tumors, and the infiltration of inflammatory cells. The genes targeted by HQD were predicted and verified, followed by knockout experiments. Elevated SLC6A4 and inhibited serotonin production and inflammation were observed in HQD-treated mice. HQD inhibited the NFκB and NLRP3/caspase1/GSDMD pathways. The therapeutic effect of HQD was diminished in SLC6A4-deficient AOM/DSS mice. Additionally, the downregulation of SLC6A4 mitigated the inhibitory effect of HQD-containing serum on MODE-K cell pyroptosis. Our findings suggest that SLC6A4 is a pivotal regulator of HQD-alleviated CAC via its modulation of the NLRP3/caspase1/GSDMD pathway.

摘要

黄芩汤（HQD）是一种治疗结肠炎的中药方剂，但HQD在结肠炎相关癌（CAC）中的作用效果及分子作用机制仍不清楚。因此，我们旨在确定HQD对小鼠CAC的有益作用，并揭示其潜在机制。采用氧化偶氮甲烷/葡聚糖硫酸钠（AOM/DSS）诱导小鼠发生CAC，并检测HQD对小鼠肿瘤发生的影响（以美沙拉嗪作为阳性对照）。美沙拉嗪或HQD治疗可减轻AOM/DSS诱导的小鼠体重减轻，并降低疾病活动指数。美沙拉嗪或HQD治疗还可抑制结肠组织长度缩短、肿瘤数量及炎性细胞浸润。对HQD作用靶点基因进行预测和验证，随后进行基因敲除实验。在HQD治疗的小鼠中观察到溶质载体家族6成员4（SLC6A4）升高、5-羟色胺生成受抑制及炎症减轻。HQD抑制核因子κB（NFκB）和NLRP3/半胱天冬酶1/ Gasdermin D（GSDMD）通路。在SLC6A4基因缺陷的AOM/DSS小鼠中，HQD的治疗效果减弱。此外，SLC6A4的下调减轻了含HQD血清对MODE-K细胞焦亡的抑制作用。我们的研究结果表明，SLC6A4是HQD通过调节NLRP3/半胱天冬酶1/GSDMD通路减轻CAC的关键调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/b51e0f3bda42/10142_2024_1334_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/18fe6475f361/10142_2024_1334_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/4f8826b20f17/10142_2024_1334_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/74584140af1b/10142_2024_1334_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/940ca80434c1/10142_2024_1334_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/217f2bf28489/10142_2024_1334_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/b51e0f3bda42/10142_2024_1334_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/18fe6475f361/10142_2024_1334_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/4f8826b20f17/10142_2024_1334_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/74584140af1b/10142_2024_1334_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/940ca80434c1/10142_2024_1334_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/217f2bf28489/10142_2024_1334_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4739/10927794/b51e0f3bda42/10142_2024_1334_Fig6_HTML.jpg

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