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• W3028211103 abstract "Transforming growth factor-beta (TGF-β) is ubiquitously expressed in various tissues and functions in pathologic processes, including hyperoxia. In the present study, we investigated the expression and functional role of TGF-β in brain tissue during hyperoxia-induced brain damage. Three days old neonatal rats were treated with hyperoxic conditions (80% O2) for 7 days, followed by TGF-β, Smad, and MAPK detection by western blotting and immunohistochemical staining. The functional role of TGF-β was assessed by treating hyperoxic neonatal rats with neutralizing antibody against TGF-β and caffeine, followed by histological and myelin basic protein (MBP) staining. Our results demonstrated upregulation of TGF-β and activation of the Smad/MAPK signaling pathway in brain tissue of neonatal rats under hyperoxic conditions. Injection of neutralizing antibody against TGF-β efficiently blocked TGF-β expression, accompanied by inactivation of the Smad/MAPK signaling pathway. Further evidence confirmed the attenuation of hyperoxia-induced brain damage by a neutralizing antibody against TGF-β in neonatal rats. Similar attenuation was also observed for caffeine. Collectively, our results indicate that TGF-β is a therapy target for hyperoxia-induced brain damage in neonates." @default.
• W3028211103 created "2020-05-29" @default.
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• W3028211103 date "2019-01-01" @default.
• W3028211103 modified "2023-10-16" @default.
• W3028211103 title "Inhibition of TGF-β-Smad signaling attenuates hyperoxia-induced brain damage in newborn rats." @default.
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• W3028211103 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6949745" @default.
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