The journal of trauma and acute care surgery · 2025
Transcutaneous auricular vagus nerve stimulation attenuates neuroinflammation in a mouse model of traumatic brain injury.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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El Baassiri Mahmoud G, Lawandos Leonard, Scheese Daniel, Tragesser Cody, Duess Johannes W, Fulton William B, Sodhi Chhinder P, Fridman Gene Y, Hackam David J, Nasr Isam W, Baltimore, Maryland
Аннотация
INTRODUCTION: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Although TBI pathophysiology has been thoroughly investigated, the effectivity of therapeutic approaches for TBI is still lacking. Our group has developed a novel approach of noninvasive transcutaneous auricular vagus nerve stimulation (taVNS) in a mouse model of TBI to investigate its impact on neuroinflammation.
METHODS: A murine-controlled cortical impact model was used, and results were analyzed on postinjury days (PIDs) 3 and 7. The experimental groups included (1) sham C57BL/6 wild type (WT), (2) TBI wild type, (3) sham-taVNS, and (4) TBI-taVNS. The animals underwent anesthesia, off-site stimulation, or taVNS for 30 minutes. The short- and long-term groups received two sessions of taVNS treatment and were tested on PIDs 3 and 7, respectively. A combination of real-time polymerase chain reaction and immunohistochemistry was used to validate the success of the model and to quantify gene expression associated with microglial and astrocyte activation. Student's t test and one-way analysis of variance were used for statistical analysis, with significance achieved when p < 0.05.
RESULTS: Transcutaneous auricular vagus nerve stimulation (VNS) activated the solitary tract nucleus and the dorsal motor nucleus of the vagus nerve as evidenced by a significant upregulation of the neuronal activation marker c-Fos, indicating vagus nerve activation. Transcutaneous auricular VNS treatment reduced the expression of pro-inflammatory microglial markers Tnf (1.69 ± 0.17 vs. 3.615 ± 0.86, p < 0.05) and Lcn2 (64.15 ± 14 vs. 337.7 ± 104.8, p < 0.01) in the ipsilateral injured cortex on PIDs 3 and 7, respectively. Transcutaneous auricular VNS also increased the expression of anti-inflammatory microglial marker Arg1 (55 ± 6.47 vs. 30.49 ± 3.94, p < 0.01) and astrocyte Gfap reactivity (8,582 ± 826 vs. 4,569 ± 554.3, p < 0.01) on PID 3. ( J Trauma Acute Care Surg . 2026;100: 707-713. Copyright © 2025 Wolters Kluwer Health, Inc. All rights reserved.).
METHODS: A murine-controlled cortical impact model was used, and results were analyzed on postinjury days (PIDs) 3 and 7. The experimental groups included (1) sham C57BL/6 wild type (WT), (2) TBI wild type, (3) sham-taVNS, and (4) TBI-taVNS. The animals underwent anesthesia, off-site stimulation, or taVNS for 30 minutes. The short- and long-term groups received two sessions of taVNS treatment and were tested on PIDs 3 and 7, respectively. A combination of real-time polymerase chain reaction and immunohistochemistry was used to validate the success of the model and to quantify gene expression associated with microglial and astrocyte activation. Student's t test and one-way analysis of variance were used for statistical analysis, with significance achieved when p < 0.05.
RESULTS: Transcutaneous auricular vagus nerve stimulation (VNS) activated the solitary tract nucleus and the dorsal motor nucleus of the vagus nerve as evidenced by a significant upregulation of the neuronal activation marker c-Fos, indicating vagus nerve activation. Transcutaneous auricular VNS treatment reduced the expression of pro-inflammatory microglial markers Tnf (1.69 ± 0.17 vs. 3.615 ± 0.86, p < 0.05) and Lcn2 (64.15 ± 14 vs. 337.7 ± 104.8, p < 0.01) in the ipsilateral injured cortex on PIDs 3 and 7, respectively. Transcutaneous auricular VNS also increased the expression of anti-inflammatory microglial marker Arg1 (55 ± 6.47 vs. 30.49 ± 3.94, p < 0.01) and astrocyte Gfap reactivity (8,582 ± 826 vs. 4,569 ± 554.3, p < 0.01) on PID 3. ( J Trauma Acute Care Surg . 2026;100: 707-713. Copyright © 2025 Wolters Kluwer Health, Inc. All rights reserved.).