Pretreatment is not mandatory for neuroprotection with 1alpha,25-dihydroxyvitamin D3 in perinatal hypoxic-ischemic rat brain damage in vivo and in excitotoxic injury of primary neuronal cell cultures

• Autorzy: Makarewicz D. , Kajta M. , Zieminska E. , Jantas D. , Domin H. , Lason W. , Kutner A. , Lazarewicz J.W.
• Języki publikacji: EN

Abstrakty

EN

Previous in vivo and in vitro studies demonstrated neuroprotective potential of pretreatment with 1α, 25-dihydroxyvitamin D3 (calcitriol). The aim of present study was to determine effectiveness of calcitriol administered in vivo after brain ischemic episode in the rat model of perinatal asphyxia, or co-applied with some delay during 24 h exposure to glutamate of the mice hippocampal, cortical and cerebellar neuronal cultures at 7th and 12th day in vitro. In some experiments calcitriol was given after acute exposure to glutamate of the rat cerebellar neurons. Our results demonstrated, that in the 7 day old rat pups submitted to hypoxia ñ ischemia acute application of calcitriol in one dose of 2 μg/kg 30 min after termination of the insult or sub-chronic, 7-day post-treatment with calcitriol effectively diminished brain damage. The rate of such accomplished neuroprotection exceeded that achieved by hypoxic preconditioning, used as the reference neuroprotective method. Moreover the results of our in vitro experiments revealed the ability of calcitriol to reduce excitotoxicity in a way dependent on origin of neuronal cells, stage of their development and duration of excitotoxic insult. Calcitriol was neuroprotective when it was applied together with glutamate or even with up to 6 h delay during 24-h excitotoxic challenge to the hippocampal and neocortical, but not cerebellar neuronal cultures. In addition calcitriol inhibited glutamate-induced caspase-3 activity in hippocampal cultures. We ascribe these protective effects of calcitriol to a rapid, possibly non-genomic modulation by this compound of the mechanisms that are instrumental in its direct neuroprotective action. The study was supported by Polish MNSW Scientifi c Network Fund no 26/E-40/SN-0023/2007

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2009
• Tom: 69
• Numer: 1
• Opis fizyczny: p.85

Twórcy

autor

Makarewicz D.

• Laboratory of Pharmaconeurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Kajta M.

• Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Zieminska E.

• Laboratory of Pharmaconeurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Jantas D.

• Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Domin H.

• Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Lason W.

• Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Kutner A.

• Pharmaceutical Research Institute, Warsaw, Poland

autor

Lazarewicz J.W.

• Laboratory of Pharmaconeurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland