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柏柏林通过促进NLRP3/Caspase-1/GSDMD途径在乳腺状甲状腺癌中的乳腺状甲状腺癌中诱导热致死

Xiaoyan Huang¹, Yanhong Lu², Shicheng Li³

¹Department of Endocrinology and Metabolism, Central Theatre General Hospital, Wuhan, 430070, China; Department of Geriatrics, Guangzhou Dongsheng Hospital, Guangzhou, 510663, China; The First School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, China.

Biochemical and biophysical research communications

|February 25, 2026

概括

柏柏林 (BBR) 通过触发细胞灭亡,一种编程细胞死亡途径来抑制乳头甲状腺癌 (PTC). 这项研究表明BBR是BBR.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

乳头甲状腺癌 (PTC) 是一种复杂的恶性瘤.
来自Coptis的柏柏林 (BBR) 对PTC表现出抑制作用.
精确的BBR作用机制可能涉及到由NLRP3炎症酶调节的热致死.

研究的目的:

为了研究 pyroptosis 在 Berberine (BBR) 治疗乳头甲状腺癌 (PTC) 中的作用.
阐明BBR在PTC中的抗癌作用背后的分子机制.

主要方法:

使用BRAF (V600E) 突变和野生型PTC细胞系进行体外研究.
通过Hoechst 33342和PI染色,西部涂抹,qRT-PCR,ELISA和ATP/LDH释放测试来评估热.
在小鼠异种移植模型中使用殖民地形成试验和瘤生长来评估细胞增殖.

主要成果:

在BRAF (V600E) 突变细胞和野生类型细胞中,BBR抑制了PTC细胞的增殖,并诱导了热.
在BBR上调节了NLRP3,caspase-1,GSDMD,IL-1β和IL-18,激活了NLRP3/caspase-1/GSDMD通路.
在体内,BBR显著抑制了PTC瘤的形成,NLRP3和GSDMD knockdown减弱了BBR诱导的热.

结论:

柏柏林 (BBR) 通过诱导 pyroptosis 抑制乳头甲状腺癌 (PTC) 的瘤发生.
这些发现表明BBR是PTC的潜在治疗剂.
BBR的机制涉及NLRP3炎症酶通路的激活,导致热亡.

关键词:

柏柏林蛋白是一种柏柏林蛋白.GSDMDMD的总体发展目标在NLRP3中,NLRP3是NLRP3中的一个.乳头甲状腺癌是一种乳头甲状腺癌.热灭菌的发生.

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