Delayed treatment with TGF-β1 associated neuroprotection in trimethyltin-induced hippocampal neurodegeneration.

In experiments conducted on Wistar rats, the effects of the multifunctional cytokine TGF-β1 were investigated using a neurodegeneration model induced by a single injection of the neurotoxicant trimethyltin chloride (TMT). Animals in the experimental group received intranasal administration of TGF-β1 on days 7 and 9 following TMT injection. Behavioral tests were performed to assess cognitive function, and three weeks after TMT administration, hippocampal morphology was analyzed using Nissl staining. Additionally, the state of microglia was evaluated through immunohistochemical labeling of IBA1. The results revealed that exogenous TGF-β1 significantly modulated the progression of hippocampal neurodegeneration. In the passive avoidance test, TGF-β1 ameliorated TMT-induced long-term memory impairment and promoted neuronal preservation in the CA1 region of the hippocampus, although no such effect was observed in the CA3 and CA4 regions. Furthermore, TGF-β1 treatment reduced microglial activation levels in the hippocampal CA1 region compared to animals treated with TMT alone. These findings suggest that the multifunctional cytokine TGF-β1 exerts a neuroprotective effect in the context of ongoing neurodegeneration when delivered intranasally to the brain. The cytokine's ability to regulate microglial activity appears to contribute, at least in part, to its protective properties.