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荷包牡丹碱通过抑制核因子-κB通路和减少脂质积累来改善代谢功能障碍相关的脂肪性肝病。

Bicuculline ameliorates metabolic dysfunction-associated steatotic liver disease by inhibiting the nuclear factor-kappa B pathway and reducing lipid accumulation.

作者信息

Wang Xiao-Mei, Dai Ze, Lu Dai-Jun, Bao Chao-Qun, Yang Nai-Bin, Zhou Yu-Ping

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, Ningbo 315020, Zhejiang Province, China.

Health Science Center, Ningbo University, Ningbo 315211, Zhejiang Province, China.

出版信息

World J Gastroenterol. 2025 May 7;31(17):105438. doi: 10.3748/wjg.v31.i17.105438.

DOI:10.3748/wjg.v31.i17.105438
PMID:40521270
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12159988/
Abstract

BACKGROUND

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a prominent and pervasive global health challenge. Bicuculline (BIC), which is a key active component of the anti-MASLD prescription "Eight Zhes Decoction", has been preliminarily shown by our research team to have significant potential in treating MASLD.

AIM

To determine BIC's efficacy in treating MASLD by regulating lipid metabolism and suppressing hepatic inflammation nuclear factor-kappa B (NF-κB) pathway, identifying it as a therapeutic candidate.

METHODS

This study explored the potential of BIC in preventing and treating MASLD using zebrafish, cellular (HepG2 and AML12), and mouse models.

RESULTS

Our results indicate that BIC significantly reduces lipid accumulation and inflammation both and . Transcriptomic analysis suggested that the anti-MASLD effects of BIC are linked to the inhibition of the NF-κB pathway, which plays a critical role in mitigating inflammation and lipid deposition.

CONCLUSION

This study is the first to demonstrate that BIC specifically alleviates lipid accumulation and hepatic steatosis in MASLD models the NF-κB signaling pathway. Overall, BIC has emerged as a promising candidate for treating MASLD.

摘要

背景

代谢功能障碍相关脂肪性肝病(MASLD)已成为一个突出且普遍的全球健康挑战。荷包牡丹碱(BIC)是抗MASLD方剂“八折汤”的关键活性成分,我们的研究团队初步表明其在治疗MASLD方面具有显著潜力。

目的

通过调节脂质代谢和抑制肝脏炎症核因子-κB(NF-κB)途径来确定BIC治疗MASLD的疗效,将其确定为一种治疗候选药物。

方法

本研究使用斑马鱼、细胞(HepG2和AML12)和小鼠模型探索BIC预防和治疗MASLD的潜力。

结果

我们的结果表明,BIC显著降低脂质积累和炎症。转录组分析表明,BIC的抗MASLD作用与抑制NF-κB途径有关,该途径在减轻炎症和脂质沉积中起关键作用。

结论

本研究首次证明BIC通过NF-κB信号通路特异性减轻MASLD模型中的脂质积累和肝脂肪变性。总体而言,BIC已成为治疗MASLD的有希望的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/dbbf6a4d6e0d/105438-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/a2dc12765301/105438-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/fd669e56d9a2/105438-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/100e3d4f634c/105438-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/bb997e143120/105438-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/fb54c96ab783/105438-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/b6bc250f394e/105438-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/dbbf6a4d6e0d/105438-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/a2dc12765301/105438-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/fd669e56d9a2/105438-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/100e3d4f634c/105438-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/bb997e143120/105438-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/fb54c96ab783/105438-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/b6bc250f394e/105438-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a41c/12159988/dbbf6a4d6e0d/105438-g007.jpg

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