Stimulation of Sympathetic Nerve Using Ultraflexible Cuff Electrodes Inhibits Inflammation Caused by Tendon Rupture

Inflammation is a serious symptom of tendon rupture, that leads to peritendinous adhesion and damages the recovery of motor function. Although it is commonly treated using medical therapy, side effects occur in the cardiovascular and genitourinary systems. Electrical stimulation (ES) is a novel alternative to neural modulation. However, its inflammatory inhibitory effect around the tendon has rarely been investigated. Here, an ultraflexible cuff electrode with a thickness of only 3.3 mu m is constructed to conformally wrap around the sympathetic chain ganglia for both stimulation and recording. The superior pliancy of the electrode causes less damage to the surrounding tissues and enhances the efficiency of stimulation and recording. ES reduces inflammation-related factors of IL-6 and IL-1 beta by 51.6% and 19.8%, respectively, and increases the sympathetic nerve neurotransmitter of norepinephrine (NE) by almost an order of magnitude in the ruptured tendon. Sympathetic recordings have also demonstrated that more neural activity is evoked after ES. To the best of the knowledge, this study is the first to verify that the ES of the sympathetic nerve can inhibit inflammation around the tendon, bringing new inspiration for the tendon rupture treatment. Acute inflammation after tendon rupture is a representative disease that leads to peritendinous adhesion and hinders recovery. An ultraflexible cuff electrode is fabricated, combined with advanced minimally invasive surgery in a rodent model, demonstrating for the first time the inhibition of inflammation in injured tendons through electrical stimualtion (ES) of the sympathetic nerve, thus facilitating the treatment of tendon rupture. image