Chinese Journal of Tissue Engineering Research ›› 2026, Vol. 30 ›› Issue (35): 9206-9216.doi: 10.12307/2026.281

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MicroRNA-23a-3p improves neurological function in mice with traumatic brain injury by regulating microglial polarization

Li Xiaoyan1, Li Jinglin1, Zhang Qiujuan1, Zhang Xiaolina2, Yang Li1   

  1. 1Department of Emergency Medicine, ²Department of Pain Management, First Affiliated Hospital of Kunming Medical University, Kunming 650000, Yunnan Province, China
  • Received:2025-09-17 Revised:2026-01-26 Online:2026-12-18 Published:2026-04-28
  • Contact: Yang Li, MD, Department of Emergency Medicine, First Affiliated Hospital of Kunming Medical University, Kunming 650000, Yunnan Province, China
  • About author:Li Xiaoyan, MS, Department of Emergency Medicine, First Affiliated Hospital of Kunming Medical University, Kunming 650000, Yunnan Province, China Li Jinglin, MS, Department of Emergency Medicine, First Affiliated Hospital of Kunming Medical University, Kunming 650000, Yunnan Province, China Li Xiaoyan and Li Jinglin contributed equally to this article.
  • Supported by:
    Young Scientists Fund of Basic Research Special Program of Yunnan Provincial Science and Technology Department, No. 202301AU070164 (to YL); Basic Research Special Program of Yunnan Provincial Science and Technology Department (General Program), No. 202401AT070067 (to ZXLN) 

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Abstract: BACKGROUND: Previous studies have demonstrated neuroprotective potential of microRNA-23a-3p in traumatic brain injury. However, direct evidence is still lacking regarding whether this protective effect stems from its precise regulation of the M1/M2 polarization balance of microglia.
OBJECTIVE: To clarify the expression changes of microRNA-23a-3p in mouse brain tissue after traumatic brain injury and to explore the specific mechanism by which it affects neurological function through regulating microglial polarization.
METHODS: Eighty C57BL/6J mice were randomly assigned to four groups: a sham operation group (sham group), a traumatic brain injury group, a traumatic brain injury + agomir-NC group, and a traumatic brain injury + agomir-microRNA-23a-3p group. The traumatic brain injury group used the cortical impact method to establish the severe traumatic brain injury model. The sham group did not undergo cortical impact treatment. The intervention groups were given intraventricular injection of agomir-NC or agomir-microRNA-23a-3p after modeling. For the sham and traumatic brain injury groups, six rats were sampled at 1, 3, 7, and 14 days post-modeling, respectively; six rats from each of the remaining two groups were sampled at 14 days post-modeling. The neurological deficits were evaluated by modified neurological severity score. Hematoxylin-eosin staining and Nissl staining were used to observe the pathological damage of brain tissue and neurons. qRT-PCR and western blot assay were performed to detect the levels of microRNA-23a-3p, the expression of M1 (CD16, CD86) and M2 (CD206, Arginase-1) phenotypic markers in microglia, as well as the mRNA and protein expression of the inflammatory factors tumor necrosis factor-alpha and interleukin-10 in mouse brain tissue. Immunohistochemical staining was used to further assess the M1/M2 polarization status of microglia and to observe the aggregation of F4/80 positive cells in the damaged area.
RESULTS AND CONCLUSION: Compared with the sham group, the expression of microRNA-23a-3p in the brain tissue of the traumatic brain injury group showed a “V” shaped curve change, with downregulation in the early stage of injury and upregulation starting 7 days after the injury. Upregulation of microRNA-23a-3p could reduce the modified neurological severity score of traumatic brain injury mice. Morphological results showed that upregulation of microRNA-23a-3p alleviated brain tissue edema and neuronal damage. Molecular biology detection results showed that upregulation of microRNA-23a-3p promoted microglia polarization from M1 type to M2 type. These findings indicate that microRNA-23a-3p promotes the recovery of neurological function in mice after traumatic brain injury by regulating microglial polarization.


Key words: traumatic brain injury, microRNA-23a-3p, microglial polarization, neural repair, immune regulation

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