¼º¼÷ GerbilÀÇ ÀÏ°ú¼º Àü³ú ÇãÇ÷¸ðµ¨¿¡¼ Çظ¶ÀÇ Áö¿¬¼º ½Å°æ¼¼Æ÷ ¼Õ»ó¿¡ ´ëÇÑ CalcitriolÀÇ ¿µÇâ
Effects of Calcitriol on Delayed Neuronal Damage of Hippocampus in Transient Global Ischemia Model of Mature Gerbil
¹ÚÇýÁø, ±¸Çý¼ö, ÇÑ¿î¼·, ÃÖ°æ±Ô,
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¹ÚÇýÁø ( Park Hye-Jin )
ÀÌÈ¿©ÀÚ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
±¸Çý¼ö ( Koo Hea-Soo )
ÀÌÈ¿©ÀÚ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
ÇÑ¿î¼· ( Han Woon-Sup )
ÀÌÈ¿©ÀÚ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
ÃÖ°æ±Ô ( Choi Kyoung-Kyu )
ÀÌÈ¿©ÀÚ´ëÇб³ ÀÇ°ú´ëÇÐ ½Å°æ°úÇб³½Ç
KMID : 0357920030370050307
Abstract
Background: It is well documented that calcium ions perform a major role in neuronal degeneration in cerebrovascular disease and the other degenerative diseases, and that 1.25-dihydroxyvitamin D3 (D3) has the dose-dependent protective effects. This study was performed to examine the effects of different D3 dosages against delayed neuronal damage of the hippocampus.
Methods: Mature mongolian gerbils were injected with either 0.8 ¥ìg/kg/day (group 2) for 5 days of 1.0 ¥ìg/kg/day for 8 days (group 3) prior to the 10 min ligation of the bilateral common carotid arteries. Immunohistochemical expression for the glial cell line-derived neurotrophic factor (GDNF), the basic fibroblast growth factor (bFGF) and the platelet-drived neurotrophic factor (PDNF) was observed in the D3-injected (0.8 ¥ìg/kg/day for 5 days) group.
Results: Group 2 showed a highly significant attenuation of delayed neuronal damage in the lateral CA1 region at 7 days after reperfusion. Group 3 showed unilateral or bilateral hemispheric infarcts 24 h after the onset of reperfusion. The D3-injected group showed a markedly increased bFGF expression level.
Conclusions: The dose-dependent effect of D3 suggests the importance of determining the appropriate D3 dose for clinical applications. Although the mechanism(s) of neuroprotection by D3 remains unclear, D3 may facilitate a reduction in ischemia-induced oxidative stress via the activation of the neurotrophic factors, including bFGF and GDNF.
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Calcitiriol;Cerebrovascular Disorders;Hypoxic;Ischemic Brain Injury
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