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<p>Traumatic brain injury (TBI) is a severe neurological condition associated with complex pathological cascades. Transforming growth factor-β2 (TGF-β2) is a pleiotropic cytokine that participates in multiple cellular events in the central nervous system; however, its potential protective role and molecular mechanisms in the context of TBI-induced neuronal injury have not been fully elucidated. In this study, we observed that TGF-β2 expression was markedly increased following TBI, with peak expression at day 7 post-injury. Using an in vitro LPS-induced inflammatory model, we found that exogenous TGF-β2 treatment significantly reduced the expression of pro-inflammatory factors TNF-α, IL-1β, and IL-6, as assessed by qRT-PCR, Western blot, and ELISA. Co-culture of neurons with conditioned medium from LPS-stimulated astrocytes revealed that TGF-β2 overexpression indirectly attenuated neuronal apoptosis and enhanced neuronal viability, as demonstrated by CCK-8, TUNEL staining, and molecular analyses. Mechanistic investigations suggested that the anti-inflammatory and anti-apoptotic effects of TGF-β2 may be mediated through activation of the Smad3 signaling pathway. Consistently, in vivo experiments indicated that TGF-β2 overexpression alleviated motor dysfunction and reduced neuronal apoptosis in a TBI mouse model. Collectively, these findings provide evidence for a protective role of TGF-β2 in inflammatory neuronal injury and offer insights into potential molecular targets for TBI therapeutic development.</p>

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TGF-β2 exerts neuroprotective effects via inhibition of astrocyte-mediated inflammatory responses

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月22日

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  • Wen Li,
  • Qiannan Zhang,
  • Jiajia Shao,
  • Qiao Jiang,
  • Jiale Gu,
  • Ruoxin Shi,
  • Fangyixiao Xu,
  • Youming Lu,
  • Chuanyu Cang,
  • Chen Liang,
  • Xiao Han,
  • Xinhua Zhang

摘要

Traumatic brain injury (TBI) is a severe neurological condition associated with complex pathological cascades. Transforming growth factor-β2 (TGF-β2) is a pleiotropic cytokine that participates in multiple cellular events in the central nervous system; however, its potential protective role and molecular mechanisms in the context of TBI-induced neuronal injury have not been fully elucidated. In this study, we observed that TGF-β2 expression was markedly increased following TBI, with peak expression at day 7 post-injury. Using an in vitro LPS-induced inflammatory model, we found that exogenous TGF-β2 treatment significantly reduced the expression of pro-inflammatory factors TNF-α, IL-1β, and IL-6, as assessed by qRT-PCR, Western blot, and ELISA. Co-culture of neurons with conditioned medium from LPS-stimulated astrocytes revealed that TGF-β2 overexpression indirectly attenuated neuronal apoptosis and enhanced neuronal viability, as demonstrated by CCK-8, TUNEL staining, and molecular analyses. Mechanistic investigations suggested that the anti-inflammatory and anti-apoptotic effects of TGF-β2 may be mediated through activation of the Smad3 signaling pathway. Consistently, in vivo experiments indicated that TGF-β2 overexpression alleviated motor dysfunction and reduced neuronal apoptosis in a TBI mouse model. Collectively, these findings provide evidence for a protective role of TGF-β2 in inflammatory neuronal injury and offer insights into potential molecular targets for TBI therapeutic development.