Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Mai Guan Fu Kang tablet (MGFK) accelerates diabetic foot ulcer healing via antioxidant defense and inflammation suppression.
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Jiang Xiaowen, Han Ziyang, Jin Yue, Liu Jie, Zhao Yijia, Gu Yujia, Zhou Dapeng, Li Keqiang, Gao Huiyuan
Аннотация
BACKGROUND: Diabetic foot ulcer (DFU), a severe complication of diabetes characterized by impaired healing and high morbidity, demand novel therapeutic strategies. Mai Guan Fu Kang tablets (MGFK) and combined therapy have been used in the clinical treatment of DFU, showing potential in DFU management, but their mechanisms remain unclear.
PURPOSE: This study aimed to elucidate the molecular mechanisms of MGFK in DFU, focusing on oxidative stress, inflammation, and vascular-neural repair.
METHODS: Firstly, we performed a comprehensive pathological analysis of tissue samples obtained from patients with chronic diabetic wounds. Subsequently, we conducted in-depth investigations using DFU mouse model and diabetic lower limb ischemia rat model, as well as network pharmacology approaches. The efficacy and underlying mechanisms of MGFK were further elucidated through advanced analytical techniques, including liquid chromatography-mass spectrometry (LC-MS), molecular docking, qPCR, Western blotting, and immunohistochemistry (IHC).
RESULTS: Clinical pathological analysis of tissue samples demonstrated significantly elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines in patients with DFU. MGFK-treated DFU mice could significantly increase the wound healing rate, reduce inflammation and inhibit oxidative stress. In diabetic limb ischemia rat model, MGFK improved blood flow, reduced coagulation markers (FIB, PT), and restored sciatic nerve function, correlating with increased VEGF and NO levels. Network pharmacology and molecular docking highlighted key components suggesting that MGFK is related to inflammation-related pathways and targets. Finally, through the construction of LPS-induced Raw264.7 cell models and tert‑butyl hydroperoxide (TBHP)-induced L929 cell models, it was found that MGFK has significant anti-inflammatory and antioxidant stress effects in vitro. Finally, we formulated a compound prescription, whose anti-inflammatory effect in vitro is superior to that of MGFK.
CONCLUSIONS: These findings highlight the multi-target mechanism of MGFK, which integrates antioxidant, anti-inflammatory, and vascular repair properties. Specifically, MGFK promotes wound healing by restoring antioxidant capacity, inhibiting NF-κB-mediated inflammatory responses, and enhancing vascular function.
PURPOSE: This study aimed to elucidate the molecular mechanisms of MGFK in DFU, focusing on oxidative stress, inflammation, and vascular-neural repair.
METHODS: Firstly, we performed a comprehensive pathological analysis of tissue samples obtained from patients with chronic diabetic wounds. Subsequently, we conducted in-depth investigations using DFU mouse model and diabetic lower limb ischemia rat model, as well as network pharmacology approaches. The efficacy and underlying mechanisms of MGFK were further elucidated through advanced analytical techniques, including liquid chromatography-mass spectrometry (LC-MS), molecular docking, qPCR, Western blotting, and immunohistochemistry (IHC).
RESULTS: Clinical pathological analysis of tissue samples demonstrated significantly elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines in patients with DFU. MGFK-treated DFU mice could significantly increase the wound healing rate, reduce inflammation and inhibit oxidative stress. In diabetic limb ischemia rat model, MGFK improved blood flow, reduced coagulation markers (FIB, PT), and restored sciatic nerve function, correlating with increased VEGF and NO levels. Network pharmacology and molecular docking highlighted key components suggesting that MGFK is related to inflammation-related pathways and targets. Finally, through the construction of LPS-induced Raw264.7 cell models and tert‑butyl hydroperoxide (TBHP)-induced L929 cell models, it was found that MGFK has significant anti-inflammatory and antioxidant stress effects in vitro. Finally, we formulated a compound prescription, whose anti-inflammatory effect in vitro is superior to that of MGFK.
CONCLUSIONS: These findings highlight the multi-target mechanism of MGFK, which integrates antioxidant, anti-inflammatory, and vascular repair properties. Specifically, MGFK promotes wound healing by restoring antioxidant capacity, inhibiting NF-κB-mediated inflammatory responses, and enhancing vascular function.