Ginsenoside Rg1 promotes skin flap survival by alleviating mitochondrial oxidative stress and apoptosis via the JNK/ERK/p38 pathway

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Background: Meyer, has demonstrated protective effects against ischemia in various tissues. This study endeavors to explore whether Rg1 mitigates mitochondrial oxidative stress and apoptosis to enhance flap survival, and investigates the underlying mechanisms. Materials and methods: Male rats' McFarlane flap models were established and randomly divided into sham, control, low-dose Rg1, medium-dose Rg1, and high-dose Rg1 groups. On the seventh day postoperative, flap necrosis rate and blood perfusion were evaluated. Western blotting was used to detect mitochondrial stress proteins, apoptosis and inflammation-related molecules, and angiogenesis pathway activity. In vitro, human umbilical vein endothelial cells (HUVECs) were used to simulate ischemia-reperfusion injury for analyzing oxidative stress, mitochondrial function and apoptosis rate. Results: Rg1 treatment dose-dependently enhanced flap survival, attenuated neutrophil infiltration and promoted angiogenesis. At the cellular level, Rg1 promoted viability and migration capacity of HUVECs while diminishing the accumulation of ROS. Furthermore, Rg1 regulated mitochondrial dynamics by upregulating fusion protein Mfn2 and downregulating fission protein Drp1, thereby inhibiting apoptosis. Western blot analysis revealed that Rg1 bidirectionally modulated the JNK/ERK/p38 pathway, suppressing pro-apoptotic signals (p-JNK, p-p38) and activating pro-survival signals (p-ERK). Additionally, Rg1 promoted angiogenesis by upregulating VEGF, Ang-1, and PDGFR-β, and reduced inflammation by suppressing IL-1β, IL-6, and TNF-α. Conclusion: Ginsenoside Rg1 regulates the JNK/ERK/p38 signaling pathway, mitigates mitochondrial oxidative stress and suppresses apoptosis, establishing a novel therapeutic target for flap necrosis prevention.

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