Empagliflozin promotes skin flap survival by activating AMPK signaling pathway
Abstract
Flaps are widely used in surgical wound repair, yet distal necrosis poses a significant postoperative challenge, stemming from potential factors such as inadequate blood perfusion, inflammation, ischemia/reperfusion (I/R) injury, mitochondrial impairment, and subsequent ferroptosis. Empagliflozin (EMPA), a sodium-glucose cotransporter 2 inhibitor, has pharmacological activities that promote angiogenesis, mitophagy, and inhibit inflammation, I/R injury, and ferroptosis. However, it is unclear whether EMPA can enhance flap survival. Here, we established a modified McFarlane flap model and applied EMPA to demonstrate its mechanism of action. 24 rats were evenly divided into four groups: the control, low-dose EMPA (10 mg/kg), high-dose EMPA (30 mg/kg), and inhibitor groups. Molecular biology experiments demonstrated that EMPA promoted the expression of angiogenesis-related factors vascular endothelial growth factor (VEGF) and CD34. Additionally, it also increased superoxide dismutase (SOD) activity and reduced malondialdehyde (MDA) levels, thus suppressing oxidative stress. EMPA further alleviated inflammation by downregulating the expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In vitro experiments showed that EMPA promoted the proliferation of human umbilical vein endothelial cells (HUVECs) and reduce their reactive oxygen species (ROS) production. Further investigation demonstrated that EMPA improves flap prognosis by inducing the expression of the…
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