cypress
Active member
- Joined
- Nov 6, 2012
- Messages
- 46
- Reason
- PALS
- Diagnosis
- 08/2012
- Country
- US
- State
- Alabama
- City
- Newton
Do any of you have knowledge or experience with TB4, it is available. RegenRx is testing it
Neuroprotective effects of thymosin beta4 in experimental models of excitotoxicity.
Patrizia Popoli, Rita Pepponi, Alberto Martire, Monica Armida, Antonella Pèzzola, Mariangela Galluzzo, M Rosaria Domenici, Rosa Luisa Potenza, M Teresa Tebano, Cristiana Mollinari, Daniela Merlo, Enrico Garaci
Istituto Superiore di Sanità, Viale Regina Elena, 299 Rome, Italy.
Annals of the New York Academy of Sciences (impact factor: 3.15). 10/2007; 1112:219-24. DOI:10.1196/annals.1415.033
Source: PubMed
ABSTRACT The aim of this study was to evaluate the possible neuroprotective effects of thymosin beta(4) in different models of excitotoxicity. The application of thymosin beta(4) significantly attenuated glutamate-induced toxicity both in primary cultures of cortical neurons and in rat hippocampal slices. In in vivo experiments, the intracerebroventricular administration of thymosin beta(4) significantly reduced hippocampal neuronal loss induced by kainic acid. These results show that thymosin beta(4) induced a protective effect in models of excitotoxicity. The mechanisms underlying such an effect, as well as the real neuroprotective potential of thymosin beta(4), are worthy of further investigations.
Neuroprotective effects of thymosin beta4 in experimental models of excitotoxicity.
Patrizia Popoli, Rita Pepponi, Alberto Martire, Monica Armida, Antonella Pèzzola, Mariangela Galluzzo, M Rosaria Domenici, Rosa Luisa Potenza, M Teresa Tebano, Cristiana Mollinari, Daniela Merlo, Enrico Garaci
Istituto Superiore di Sanità, Viale Regina Elena, 299 Rome, Italy.
Annals of the New York Academy of Sciences (impact factor: 3.15). 10/2007; 1112:219-24. DOI:10.1196/annals.1415.033
Source: PubMed
ABSTRACT The aim of this study was to evaluate the possible neuroprotective effects of thymosin beta(4) in different models of excitotoxicity. The application of thymosin beta(4) significantly attenuated glutamate-induced toxicity both in primary cultures of cortical neurons and in rat hippocampal slices. In in vivo experiments, the intracerebroventricular administration of thymosin beta(4) significantly reduced hippocampal neuronal loss induced by kainic acid. These results show that thymosin beta(4) induced a protective effect in models of excitotoxicity. The mechanisms underlying such an effect, as well as the real neuroprotective potential of thymosin beta(4), are worthy of further investigations.