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

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 pat...

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Bibliographic Details
Published in:Nature communications 2024-02, Vol.15 (1), p.1327-1327, Article 1327
Main Authors: Bao, Rong, Wang, Shuiyuan, Liu, Xiaoxian, Tu, Kejun, Liu, Jingquan, Huang, Xiaohe, Liu, Chunsen, Zhou, Peng, Liu, Shen
Format: Article
Language:English
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Summary: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.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-024-45590-8