Neuromorphic electro-stimulation based on atomically thin semiconductor for damage-free inflammation inhibition

• Published in: Nature communications Vol. 15; no. 1; p. 1327
• Main Authors: Bao, Rong, Wang, Shuiyuan, Liu, Xiaoxian, Tu, Kejun, Liu, Jingquan, Huang, Xiaohe, Liu, Chunsen, Zhou, Peng, Liu, Shen
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 13.02.2024; Nature Publishing Group; Nature Portfolio
• Subjects: 13; 13/21; 142/126; 639/301/1005/1007; 639/925/357/1018; Acupuncture; Adrenergic Agents; Animals; Bionics; Cell lineage; Cytokines; Cytokines - metabolism; Damage accumulation; Fire damage; Humanities and Social Sciences; Inflammation; Inflammation - metabolism; Leukocytes (granulocytic); Low currents; Macrophages; Mice; Mice, Transgenic; Monocytes; multidisciplinary; Neurons; Neurons - metabolism; Science; Science (multidisciplinary); Stimulation; Stimulators; Sympathetic nerves; Transgenic mice
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/s41467-024-45590-8

Inflammation, caused by accumulation of inflammatory cytokines from immunocytes, is prevalent in a variety of diseases. Electro-stimulation emerges as a promising candidate for inflammatory inhibition. Although electroacupuncture is free from surgical injury, it faces the challenges of imprecise pathways/current spikes, and insufficiently defined mechanisms, while non-optimal pathway or spike would require high current amplitude, which makes electro-stimulation usually accompanied by damage and complications. Here, we propose a neuromorphic electro-stimulation based on atomically thin semiconductor floating-gate memory interdigital circuit. Direct stimulation is achieved by wrapping sympathetic chain with flexible electrodes and floating-gate memory are programmable to fire bionic spikes, thus minimizing nerve damage. A substantial decrease (73.5%) in inflammatory cytokine IL-6 occurred, which also enabled better efficacy than commercial stimulator at record-low currents with damage-free to sympathetic neurons. Additionally, using transgenic mice, the anti-inflammation effect is determined by β2 adrenergic signaling from myeloid cell lineage (monocytes/macrophages and granulocytes). Bao et al. report a neuromorphic bionic electro-stimulation solution based on atomic-scale semiconductor floating-gate memory circuit, which enables efficient inhibition of acute inflammation with low stimulation currents that are damage-free to neurons.