Glucose-Powered Bioabsorbable Bandage Restores the Body's Own Electric Signals to Heal Diabetic Wounds

Data:2026-07-10  |  【 A  A  A 】  |  【Print】 【Close

In a study published in Science Advances, a research team led by Prof. CHEN Chunying from the National Center for Nanoscience and Technology (NCNST) of the Chinese Academy of Sciences, working with researchers from Tsinghua University and the University of Chinese Academy of Sciences, developed a glucose-powered, fully bioabsorbable electronic bandage that heals diabetic wounds by restoring the body's own electrical signals.

Nearly 800 million people worldwide live with diabetes, and chronic nonhealing wounds, particularly diabetic foot ulcers, rank among its most serious complications. Healthy skin runs on a quiet kind of electricity: when the barrier breaks, a natural voltage gradient appears at the wound edge, steering cell migration, immune activation, and tissue regeneration. Persistent hyperglycemia weakens these endogenous electric fields (EFs), leaving diabetic wounds trapped in a pro-inflammatory state. External electrical stimulation can compensate, but conventional devices rely on bulky power sources and wired connections, making them impractical for routine wound care.

The team's answer is a glucose-powered electronic bandage (GEB) that is thin, soft, breathable, and entirely biodegradable. Built on an electrospun polycaprolactone (PCL) fiber mat, it carries two MXene (Ti₃C₂)-based electrodes: a glucose oxidase (GOx) anode and a platinum (Pt) cathode. When the bandage touches wound exudate, GOx oxidizes the excess glucose and releases electrons, which travel through the MXene nanosheets to the Pt cathode and drive an oxygen reduction reaction. The result is a stable bioelectric field with no external power input—while the wound's surplus glucose is consumed in the process. Simulations showed that MXene's nanoscale interlayer channels confine and accelerate these catalytic reactions, and a mask-assisted spraying process allows the electrodes to be customized in shape and scaled up in production.

The bandage delivers. It generated an open-circuit voltage of up to ~350 mV at diabetic glucose levels and operated stably for at least six days under physiological conditions. Reactive oxygen species produced during glucose oxidation killed 86.7% of Escherichia coli and 90.7% of Staphylococcus aureus. In infected diabetic mouse wounds, the GEB rebuilt an "outer-positive, inner-negative" electric field averaging ~140 mV, resembling the physiological one. By day 9, only 29.9% of the wound area remained open, compared with more than half in control groups. The restored field guided cell migration, drove pro-inflammatory M1 macrophages down from 62% to 34.7% while raising regenerative M2 macrophages from 7.6% to 36.6%, and boosted angiogenesis. Transcriptomic analysis confirmed a coordinated regenerative program, with 709 genes up-regulated along the PI3K-Akt/MAPK/VEGF signaling axis.

The same strategy held up across species and organs. In diabetic pigs—whose skin closely resembles human skin—GEB-treated wounds were nearly closed by day 20, while about one-third of the wound area remained in control groups. In a diabetic mouse intestinal injury model, a serpentine-electrode version of the bandage, coated with an adhesive hydrogel, attached to the wound within 10 seconds, cut local glucose from ~22 mM to ~7 mM within 90 minutes, and sustained its electrical output for two weeks. Treated intestines regained orderly villi and goblet cells, and their gut microbiota shifted back toward a healthy composition. Throughout all models, the bandage showed no detectable local or systemic toxicity.

By turning a pathological excess of glucose into the very energy that drives repair, this work establishes an "endogenous glucose-powered symbiotic bioelectronics" paradigm: the device lives off the wound's chemistry, corrects it, and then disappears. Beyond diabetic ulcers, the researchers envision applications wherever disrupted bioelectric signaling is a pathological hallmark, such as peripheral nerve injury and bone defects. Future work will map the long-term fate of the inorganic components and the device's operational lifetime under clinically complex conditions.


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