Cerebrolysin is the only drug available for clinical use containing active fragments of some important neurotrophic factors obtained from purified porcine brain proteins, which has long been used for the treatment of dementia and stroke sequels. Cerebrolysin has growth factor-like activities and promotes neuronal survival and sprouting, however its molecular mechanism still needs to be determined. It has been shown that Cerebrolysin may interact with proteolytic pathways linked to apoptosis. Administration of Cerebrolysin significantly reduces the number of apoptotic neurons after glutamate exposure. Furthermore, it has been reported that Cerebrolysin inhibits free radicals formation and lipid peroxidation. We in vitro evaluated the protective effects of Cerebrolysin towards spontaneous and induced apoptotic death in cells from human healthy subjects. Peripheral blood lymphocytes (PBLs) from 10 subjects were used as cell model; 2-deoxy-D-ribose (dRib), a highly reducing sugar, was used as paradigm pro-apoptotic stimulus. Apoptosis was analyzed by flow cytometry and fluorescence microscopy. Our results showed that Cerebrolysin significantly reduced the number of apoptotic PBLs after dRib treatment, while it had no significative effects on cells cultured in standard conditions. Our work showed a protective effect of Cerebrolysin on oxidative stress-induced apoptosis and suggested that PBLs can be used as an easy obtainable and handy cell model to verify Cerebrolysin effects in neurodegenerative pathologies. © 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

Formichi, P., Radi, E., Battisti, C., Maio, G.d., Muresanu, D., Federico, A. (2012). Cerebrolysin administration reduces oxidative-stress induced apoptosis in limphocytes from healthy subjects. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 16(11), 2840-2843 [10.1111/j.1582-4934.2012.01615.x].

Cerebrolysin administration reduces oxidative-stress induced apoptosis in limphocytes from healthy subjects

FORMICHI, PATRIZIA;RADI, ELENA;BATTISTI, CARLA;FEDERICO, ANTONIO
2012-01-01

Abstract

Cerebrolysin is the only drug available for clinical use containing active fragments of some important neurotrophic factors obtained from purified porcine brain proteins, which has long been used for the treatment of dementia and stroke sequels. Cerebrolysin has growth factor-like activities and promotes neuronal survival and sprouting, however its molecular mechanism still needs to be determined. It has been shown that Cerebrolysin may interact with proteolytic pathways linked to apoptosis. Administration of Cerebrolysin significantly reduces the number of apoptotic neurons after glutamate exposure. Furthermore, it has been reported that Cerebrolysin inhibits free radicals formation and lipid peroxidation. We in vitro evaluated the protective effects of Cerebrolysin towards spontaneous and induced apoptotic death in cells from human healthy subjects. Peripheral blood lymphocytes (PBLs) from 10 subjects were used as cell model; 2-deoxy-D-ribose (dRib), a highly reducing sugar, was used as paradigm pro-apoptotic stimulus. Apoptosis was analyzed by flow cytometry and fluorescence microscopy. Our results showed that Cerebrolysin significantly reduced the number of apoptotic PBLs after dRib treatment, while it had no significative effects on cells cultured in standard conditions. Our work showed a protective effect of Cerebrolysin on oxidative stress-induced apoptosis and suggested that PBLs can be used as an easy obtainable and handy cell model to verify Cerebrolysin effects in neurodegenerative pathologies. © 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Formichi, P., Radi, E., Battisti, C., Maio, G.d., Muresanu, D., Federico, A. (2012). Cerebrolysin administration reduces oxidative-stress induced apoptosis in limphocytes from healthy subjects. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 16(11), 2840-2843 [10.1111/j.1582-4934.2012.01615.x].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/38857
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