Electroacupuncture Ameliorates Traumatic Brain Injury in Mice via Suppression of Neuroinflammation and Regulation of Adiponectin Receptor 1–TRPV1 Pathways

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Authors: I‐Han Hsiao, Younbyoung Chae, Ming-Chia Lin, Chien-Yi Ho, Hsin-Cheng Hsu, Yi-Wen Lin
Cited by: 1

Abstract

Traumatic brain injury (TBI) refers to a brain injury caused by a traumatic impact. Depending on severity, TBI can be classified as mild, which may temporarily affect brain function, or severe, which can cause long-term complications such as headaches, speech disorders, mood changes, anxiety, and depression. At present, common treatments for TBI include anti-anxiety drugs, anticonvulsants, antidepressants, and muscle relaxants. However, the use of electroacupuncture (EA) for TBI and its molecular mechanisms remain poorly studied. To address this research gap, this study examined the influence of EA on neuroinflammation, adiponectin, and transient receptor potential vanilloid 1 (TRPV1) pathways in a mouse model of TBI. TBI was induced using automatic gravity impact. Molecular analyses confirmed that TBI causes a neuroinflammatory response in the medial prefrontal cortex. TBI model mice showed decreases in the adiponectin receptor 1 (AdipoR1) and TRPV1 signaling pathways, leading to comorbid depression. Next, we demonstrated that EA or Trpv1−/− reduced levels of astrocytes, microglia, and their signaling mediators high mobility group box 1 and s100 calcium-binding protein B. Notably, EA or Trpv1−/− further increased AdipoR1–APPL1 and these effects were downstream to the AMPK/PPAR/SIRT1 pathway. Similar results were observed in the TRPV1 signaling pathway. Taken together, these findings indicate that EA effectively treats TBI by reducing neuroinflammation and activating the AdipoR1 and TRPV1 pathways, providing important directions and applications for future clinical research.

Fields of Study & Subjects

Acupuncture Treatment Research Studies Traumatic Brain Injury Research Pain Mechanisms and Treatments

Publication details

Journal / source
Preprints.org
Publisher
MDPI AG
Publication date
28 January 2026
Document type
Preprint