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姜黄素类似物J7通过调节TGF-β/Smad和NF-κB/BCL-2/BAX信号通路减轻2型糖尿病大鼠模型的肝纤维化和代谢失调。

Curcumin Analog J7 Attenuates Liver Fibrosis and Metabolic Dysregulation in a Rat Model of Type 2 Diabetes via Modulation of TGF-β/Smad and NF-κB/BCL-2/BAX Pathways.

作者信息

Ma Jun, Chen Wei, Vaishnani Deep K, Wang Congying, Xue Shuman, Yang Qiuqin, Tong Yuheng, Lei Ningjia, Zhao Zhichao, Ying Furong

机构信息

Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.

Renji College, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, People's Republic of China.

出版信息

Drug Des Devel Ther. 2025 Apr 1;19:2411-2432. doi: 10.2147/DDDT.S511372. eCollection 2025.

DOI:10.2147/DDDT.S511372
PMID:40190815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11971964/
Abstract

OBJECTIVE: To evaluate the therapeutic potential of the curcumin analog J7 in protecting the liver and regulating glucose and lipid metabolism in rats with type 2 diabetes. METHODS: Bioinformatics methods were used to identify signaling pathways linked to diabetic liver disease. Diabetic rats were treated with curcumin, low-dose J7, or high-dose J7, and liver function and fibrosis were assessed through biochemical analyses, histopathology, immunohistochemistry, and ELISA. RESULTS: J7 administration significantly improved lisver function, reduced fibrosis, and regulated metabolic profiles in diabetic rats. J7 downregulated TGF-β1, NF-κB p65, and BAX, while upregulating BCL-2, showing superior effects to traditional curcumin in reducing TGF-β1 and inhibiting α-SMA expression. CONCLUSION: J7 demonstrates potential as a therapeutic agent for managing liver complications in type 2 diabetes, effectively attenuating liver fibrosis and regulating metabolism through the modulation of key signaling pathways and proteins.

摘要

目的：评估姜黄素类似物J7在保护2型糖尿病大鼠肝脏及调节糖脂代谢方面的治疗潜力。 方法：运用生物信息学方法识别与糖尿病肝病相关的信号通路。给糖尿病大鼠分别用姜黄素、低剂量J7或高剂量J7进行治疗，并通过生化分析、组织病理学、免疫组织化学和酶联免疫吸附测定法评估肝功能和纤维化情况。 结果：给予J7可显著改善糖尿病大鼠的肝功能，减轻纤维化，并调节代谢谱。J7下调转化生长因子-β1（TGF-β1）、核因子-κB p65（NF-κB p65）和Bax，同时上调Bcl-2，在降低TGF-β1和抑制α-平滑肌肌动蛋白（α-SMA）表达方面显示出优于传统姜黄素的效果。 结论：J7显示出作为治疗2型糖尿病肝脏并发症药物的潜力，可通过调节关键信号通路和蛋白质有效减轻肝纤维化并调节代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/29abc73f411a/DDDT-19-2411-g0008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/49a2bc34751e/DDDT-19-2411-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/29abc73f411a/DDDT-19-2411-g0008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/2625ae40ce32/DDDT-19-2411-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/25863abda9c9/DDDT-19-2411-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/912956956f72/DDDT-19-2411-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/f31d3ef6cec5/DDDT-19-2411-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/0b8ade8397b8/DDDT-19-2411-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/49a2bc34751e/DDDT-19-2411-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95de/11971964/29abc73f411a/DDDT-19-2411-g0008.jpg

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[8]
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[10]
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