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Article

Sympathetic Regulation of Hematopoiesis and the Mobilization of Inflammatory Cells in ICR Mice with Traumatic Brain Injury: A Novel Approach to Targeting Neuroinflammation and Degenerative Processes

Institute of General Pathology and Pathophysiology, Moscow 125315, Russia
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Author to whom correspondence should be addressed.
Biomedicines 2025, 13(12), 3080; https://doi.org/10.3390/biomedicines13123080
Submission received: 27 October 2025 / Revised: 10 December 2025 / Accepted: 12 December 2025 / Published: 13 December 2025
(This article belongs to the Section Neurobiology and Clinical Neuroscience)

Abstract

Background/Objectives: Neuroinflammation is a leading factor in secondary brain damage following a traumatic brain injury (TBI). Existing therapeutic approaches have limited efficacy against neuroinflammation. The bone marrow, the primary hematopoietic organ, is also a source of inflammatory cells. We propose that targeting the sympathetic regulation of inflammatory cell mobilization could reduce neuroinflammation after TBI. Methods: In ICR mice, we investigated the immune cell response in the blood, bone marrow, motor cortex, and the subventricular zone after TBI modeling and treatment with the sympatholytic agent reserpine. Results: TBI induced neutrophilia and lymphocytosis in the peripheral blood, activated hematopoiesis in the bone marrow, and triggered neuroinflammation and degenerative changes in the cerebral cortex (CC) and the subventricular zone (SVZ) of mice. Reserpine reduced leukocytosis in the blood and hematopoietic activity in the bone marrow of mice with TBI compared to untreated TBI mice. Furthermore, reserpine decreased neutrophilic and lymphocytic infiltration, as well as the number of Iba1+ microglial cells, including M1-polarized microglia, Caspase-3+ cells, and cells expressing myeloperoxidase (MPO) in the CC and SVZ of treated mice. The activity of degenerative processes was also reduced. Additionally, reserpine reduced the number of M2-polarized microglial cells in the SVZ. Conclusions: The sympatholytic drug reserpine may hold promise for the development of a novel approach to treating neuroinflammation and degeneration following a TBI. This is based on its ability to reduce hematopoiesis and mobilize inflammatory cells from the bone marrow into the bloodstream.
Keywords: traumatic brain injury; neuroinflammation; degenerative processes; reserpine; hematopoiesis; mobilization; inflammatory cells traumatic brain injury; neuroinflammation; degenerative processes; reserpine; hematopoiesis; mobilization; inflammatory cells

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MDPI and ACS Style

Ermakova, N.; Skurikhina, V.; Pan, E.; Zhukova, M.; Zharkikh, I.; Pan, V.; Dygai, A. Sympathetic Regulation of Hematopoiesis and the Mobilization of Inflammatory Cells in ICR Mice with Traumatic Brain Injury: A Novel Approach to Targeting Neuroinflammation and Degenerative Processes. Biomedicines 2025, 13, 3080. https://doi.org/10.3390/biomedicines13123080

AMA Style

Ermakova N, Skurikhina V, Pan E, Zhukova M, Zharkikh I, Pan V, Dygai A. Sympathetic Regulation of Hematopoiesis and the Mobilization of Inflammatory Cells in ICR Mice with Traumatic Brain Injury: A Novel Approach to Targeting Neuroinflammation and Degenerative Processes. Biomedicines. 2025; 13(12):3080. https://doi.org/10.3390/biomedicines13123080

Chicago/Turabian Style

Ermakova, Natalia, Victoria Skurikhina, Edgar Pan, Mariia Zhukova, Irina Zharkikh, Valentina Pan, and Alexander Dygai. 2025. "Sympathetic Regulation of Hematopoiesis and the Mobilization of Inflammatory Cells in ICR Mice with Traumatic Brain Injury: A Novel Approach to Targeting Neuroinflammation and Degenerative Processes" Biomedicines 13, no. 12: 3080. https://doi.org/10.3390/biomedicines13123080

APA Style

Ermakova, N., Skurikhina, V., Pan, E., Zhukova, M., Zharkikh, I., Pan, V., & Dygai, A. (2025). Sympathetic Regulation of Hematopoiesis and the Mobilization of Inflammatory Cells in ICR Mice with Traumatic Brain Injury: A Novel Approach to Targeting Neuroinflammation and Degenerative Processes. Biomedicines, 13(12), 3080. https://doi.org/10.3390/biomedicines13123080

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