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一种由尿苷和吡喹酮组成的新型联合疗法通过促进脂肪生成分化有效减轻血吸虫病诱导的肝纤维化。

A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation.

作者信息

Zhou Xiangyu, Xue Qingkai, Wu Chengwei, Li Xiaojing, Wang Yuyan, Dai Yang, Xiong Chunrong, Zhang Ying, Xu Yongliang, Liu Xinjian, Huang Yuzheng

机构信息

National Health Commission Key Laboratory of Parasitic Disease Control and Prevention, Jiangsu Provincial Key Laboratory on Parasite and Vector Control Technology, Jiangsu Institute of Parasitic Diseases, Wuxi, Jiangsu, PR China.

Tropical Diseases Research Center, Nanjing Medical University, Wuxi, Jiangsu, PR China.

出版信息

PLoS Pathog. 2025 Aug 6;21(8):e1013403. doi: 10.1371/journal.ppat.1013403. eCollection 2025 Aug.

DOI:10.1371/journal.ppat.1013403
PMID:40768528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12349724/
Abstract

Schistosomiasis-induced hepatic fibrosis, a consequence of egg-induced granulomatous lesions, remains untreated by current drugs. Therefore, the development of novel antifibrosis drugs is of paramount importance. Our previous study indicated that aberrant uridine concentrations play a pivotal role in schistosomiasis-induced hepatic fibrosis. This study aimed to explore the inhibitory role of uridine in schistosomiasis-induced liver fibrosis and the regulatory mechanism of uridine on hepatic stellate cell (HSC) activation. The results indicated that uridine could inhibit schistosomiasis-induced liver fibrosis in vivo and TGF-β-induced HSC activation in vitro. Molecular docking revealed a strong interaction between uridine and the adenosine receptor A1 (ADORA1) receptor. Subsequent in vitro investigations demonstrated that uridine modulated the cAMP/PKA/CREB pathway, influencing HSC adipogenic differentiation and exerting an antifibrotic effect. In addition, compared with praziquantel (PZQ) alone, combined uridine and PZQ therapy resulted in a reduced fibrotic area and improved hepatic parameters in vivo. Our study reveals the antifibrosis mechanism of the uridine molecule, which may be a promising drug for the treatment of schistosomiasis-induced liver fibrosis.

摘要

血吸虫病诱导的肝纤维化是虫卵诱导的肉芽肿性病变的结果，目前的药物对此仍无法治疗。因此，开发新型抗纤维化药物至关重要。我们之前的研究表明，异常的尿苷浓度在血吸虫病诱导的肝纤维化中起关键作用。本研究旨在探讨尿苷对血吸虫病诱导的肝纤维化的抑制作用以及尿苷对肝星状细胞（HSC）激活的调节机制。结果表明，尿苷在体内可抑制血吸虫病诱导的肝纤维化，在体外可抑制转化生长因子-β（TGF-β）诱导的HSC激活。分子对接显示尿苷与腺苷受体A1（ADORA1）之间存在强烈相互作用。随后的体外研究表明，尿苷调节cAMP/PKA/CREB通路，影响HSC脂肪生成分化并发挥抗纤维化作用。此外，与单独使用吡喹酮（PZQ）相比，尿苷与PZQ联合治疗在体内可减少纤维化面积并改善肝脏参数。我们的研究揭示了尿苷分子的抗纤维化机制，它可能是治疗血吸虫病诱导的肝纤维化的一种有前景的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/ebcd20c2cd13/ppat.1013403.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/f348ed8b6962/ppat.1013403.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/553abbc8d004/ppat.1013403.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/91fb33892563/ppat.1013403.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/92bf9af4c2b3/ppat.1013403.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/964cadb679b2/ppat.1013403.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/666ba8a0b100/ppat.1013403.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/ed00df58f2c8/ppat.1013403.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/ebcd20c2cd13/ppat.1013403.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/f348ed8b6962/ppat.1013403.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/553abbc8d004/ppat.1013403.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/91fb33892563/ppat.1013403.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/92bf9af4c2b3/ppat.1013403.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/964cadb679b2/ppat.1013403.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/666ba8a0b100/ppat.1013403.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/ed00df58f2c8/ppat.1013403.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2d/12349724/ebcd20c2cd13/ppat.1013403.g008.jpg

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本文引用的文献

1
Mass spectrometry imaging reveals spatial metabolic variation and the crucial role of uridine metabolism in liver injury caused by Schistosoma japonicum.质谱成像揭示了日本血吸虫所致肝损伤中的空间代谢变化及尿苷代谢的关键作用。
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Uridine Administration Promotes Normalization of Heart Mitochondrial Function in Dystrophin-Deficient Mice and Decreases Tissue Fibrosis.尿苷给药可促进肌营养不良症小鼠心脏线粒体功能正常化并减少组织纤维化。
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Uridine Alleviates Sepsis-Induced Acute Lung Injury by Inhibiting Ferroptosis of Macrophage.尿苷通过抑制巨噬细胞铁死亡缓解脓毒症诱导的急性肺损伤。
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