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Updated: Jun 21, 2025
A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
X-Paste improves wound healing in diabetes via NF-E2-related factor/HO-1 signaling pathway
Ming-Wei Du1,2, Xin-Lin Zhu2, Dong-Xing Zhang3
1Institute of Cardiovascular Disease, Shanghai Key Laboratory of Traditional Chinese Clinical Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200120, China.
Background:
Diabetic foot ulcers (DFU), as severe complications of diabetes mellitus (DM), significantly compromise patient health and carry risks of amputation and mortality.
Aim:
To offer new insights into the occurrence and development of DFU, focusing on the therapeutic mechanisms of X-Paste (XP) of wound healing in diabetic mice.
Methods:
Employing traditional Chinese medicine ointment preparation methods, XP combines various medicinal ingredients. High-performance liquid chromatography (HPLC) identified XP's main components. Using streptozotocin (STZ)-induced diabetic, we aimed to investigate whether XP participated in the process of diabetic wound healing. RNA-sequencing analyzed gene expression differences between XP-treated and control groups. Molecular docking clarified XP's treatment mechanisms for diabetic wound healing. Human umbilical vein endothelial cells (HUVECs) were used to investigate the effects of Andrographolide (Andro) on cell viability, reactive oxygen species generation, apoptosis, proliferation, and metastasis in vitro following exposure to high glucose (HG), while NF-E2-related factor-2 (Nrf2) knockdown elucidated Andro's molecular mechanisms.
Results:
XP notably enhanced wound healing in mice, expediting the healing process. RNA-sequencing revealed Nrf2 upregulation in DM tissues following XP treatment. HPLC identified 21 primary XP components, with Andro exhibiting strong Nrf2 binding. Andro mitigated HG-induced HUVECs proliferation, metastasis, angiogenic injury, and inflammation inhibition. Andro alleviates HG-induced HUVECs damage through Nrf2/HO-1 pathway activation, with Nrf2 knockdown reducing Andro's proliferative and endothelial protective effects.
Conclusion:
XP significantly promotes wound healing in STZ-induced diabetic models. As XP's key component, Andro activates the Nrf2/HO-1 signaling pathway, enhancing cell proliferation, tubule formation, and inflammation reduction.
Insights
X-Paste (XP) significantly improves diabetic wound healing by activating the Nrf2/HO-1 pathway. Its key component, Andrographolide, protects endothelial cells and reduces inflammation, offering a promising treatment for diabetic foot ulcers.
Area of Science:
- Biomedical Science
- Pharmacology
- Wound Healing Research
Background:
- Diabetic foot ulcers (DFU) are severe diabetes mellitus (DM) complications, increasing risks of amputation and mortality.
- Effective therapeutic strategies for DFU remain a critical unmet need.
Purpose of the Study:
- To investigate the therapeutic mechanisms of X-Paste (XP) for diabetic wound healing.
- To elucidate the role of XP's key component, Andrographolide (Andro), in regulating cellular processes relevant to DFU.
Main Methods:
- XP preparation using traditional Chinese medicine methods, component analysis via HPLC.
- Assessment of XP's efficacy in streptozotocin (STZ)-induced diabetic mouse models.
- RNA-sequencing for gene expression analysis and molecular docking to identify mechanisms.
- In vitro studies on human umbilical vein endothelial cells (HUVECs) exposed to high glucose (HG), including Nrf2 knockdown experiments.
Main Results:
- XP significantly accelerated wound healing in diabetic mice.
- RNA-sequencing identified Nrf2 upregulation in XP-treated tissues; Andro showed strong Nrf2 binding.
- Andro mitigated HG-induced HUVEC damage, including reduced proliferation, metastasis, and inflammation, via Nrf2/HO-1 pathway activation.
Conclusions:
- XP effectively promotes wound healing in diabetic models.
- Andrographolide is a key active component in XP, activating the Nrf2/HO-1 pathway.
- Andro enhances endothelial cell proliferation, tubule formation, and reduces inflammation, suggesting therapeutic potential for DFU.
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