Work

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

Year: 2026

Type: article

Abstract: Traumatic brain injury (TBI) represents a severe neurological disorder characterized by a complex interplay of pathological mechanisms, including inflammation, oxidative stress, and cellular apoptosis. Transforming growth factor-β2 (TGF-β2) is a multifunctional cytokine that plays a pivotal role in various cellular processes, such as neuroinflammation and apoptosis. Despite extensive research on TGF-β2's involvement in neuroinflammation and fibrosis, its precise mechanisms and protective effects on neuronal apoptosis following TBI remain inadequately understood. In this study, we conducted in vitro experiments to evaluate the impact of TGF-β2 on neuronal apoptosis. Utilizing qRT-PCR, Western blot, and immunofluorescence techniques, we observed a significant increase in TGF-β2 expression following TBI, with levels peaking on the seventh day post-injury. Furthermore, through qRT-PCR, Western blot, and ELISA assays, we determined that TGF-β2 effectively reduced the expression of inflammatory factors TNF-α, IL-1β, and IL-6 following LPS stimulation. Additionally, overexpression of TGF-β2 significantly mitigated LPS-induced neuronal apoptosis, as evidenced by CCK8, qRT-PCR, Western blot, and TUNEL assays. Subsequent research has identified that the Smad3 signaling pathway mediates the anti-inflammatory and anti-apoptotic effects of TGF-β2 in TBI. Behavioral assessments indicated a significant improvement in motor function impairment and a marked reduction in neuronal apoptosis in the TGF-β2 overexpression group. In conclusion, this study elucidates the role and mechanism of TGF-β2 in neuronal apoptosis following TBI, thereby offering novel targets and strategies for TBI treatment.

Source: BMC Neuroscience

DOI: 10.1186/s12868-026-01025-2