Yinzhilan Formula Ameliorates Healing Delay in Diabetic Ulcer by Inhibiting PARP1 Activation and Regulating Macrophage Polarization.

IF 2.8 4区医学 Q2 PHARMACOLOGY & PHARMACY

Current pharmaceutical design Pub Date : 2026-05-04 DOI:10.2174/0113816128437855260214193425

Jiawei Feng, Yiming Ni, Wei Zhang, Min Tang, Shiyu Wang, Jijia Sun, Xiaozhou Han, Mingmei Zhou, Cheng Zhao

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引用次数: 0

Abstract

Introduction: Yinzhilan formula (YZL) is an effective prescription for diabetic ulcers (DU) with clinical efficacy. This study aimed to explore the mechanism of YZL in ameliorating the healing delay of DU through network pharmacology and experimental validation.

Methods: Network pharmacology integrated with bioinformatics to screen the chemical composition of YZL, as well as its protein targets and disease targets. A mouse model of DU was established, and the efficacy of YZL was evaluated according to ulcer size and histopathological examination. The levels of inflammatory factors were detected by ELISA, and the changes in macrophage polarization were detected by immunofluorescence and flow cytometry.

Results: Network pharmacology identified 291 potential targets in YZL, which synergistically targeted PARP1 and STAT3 to exert their role in promoting wound healing. In vivo experiments showed that YZL accelerated wound closure, regulated the levels of inflammatory factors and macrophage polarization, and suppressed the mRNA and protein expression levels of PARP1 and STAT3.

Discussion: Bioinformatics studies suggested that HSP90AA1, IL6, PARP1, and STAT3 may be potential targets of YZL in the treatment of DU. Immune infiltration analysis suggested that macrophages may be related to the mechanism of action.

Conclusion: YZL may accelerate DU healing by inhibiting PARP1 and STAT3 and reprogramming macrophage polarization towards the M2 phenotype.

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茵栀兰方通过抑制PARP1激活和调节巨噬细胞极化改善糖尿病溃疡愈合延迟。

简介：银栀兰方是治疗糖尿病溃疡的有效方剂，临床疗效显著。本研究旨在通过网络药理学和实验验证，探讨YZL改善DU愈合延迟的机制。方法：采用网络药理学与生物信息学相结合的方法，筛选YZL的化学成分、蛋白靶点和疾病靶点。建立小鼠DU模型，根据溃疡大小和组织病理学检查评价中药复方合剂的疗效。ELISA检测炎性因子水平，免疫荧光和流式细胞术检测巨噬细胞极化变化。结果：网络药理学鉴定出YZL中291个潜在靶点，协同靶向PARP1和STAT3，发挥其促进创面愈合的作用。体内实验表明，YZL加速创面愈合，调节炎症因子水平和巨噬细胞极化，抑制PARP1和STAT3 mRNA和蛋白表达水平。讨论：生物信息学研究提示HSP90AA1、IL6、PARP1和STAT3可能是YZL治疗DU的潜在靶点。免疫浸润分析提示可能与巨噬细胞的作用机制有关。结论：YZL可能通过抑制PARP1和STAT3以及重编程巨噬细胞向M2型极化来加速DU愈合。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Current pharmaceutical design 医学-药学

CiteScore

6.30

自引率

0.00%

发文量

302

审稿时长

2 months

期刊介绍： Current Pharmaceutical Design publishes timely in-depth reviews and research articles from leading pharmaceutical researchers in the field, covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area guest edited by an acknowledged authority in the field. Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design including: medicinal chemistry, pharmacology, drug targets and disease mechanism.