TY - JOUR
T1 - Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus
AU - Yousuf, Seema
AU - Atif, Fahim
AU - Ahmad, Muzamil
AU - Nasrul Hoda, Md
AU - Badruzzaman Khan, M.
AU - Ishrat, Tauheed
AU - Islam, Fakhrul
PY - 2007/5/25
Y1 - 2007/5/25
N2 - During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.
AB - During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.
KW - ATP
KW - Calcium
KW - Caspase
KW - Hsp
KW - Ischemia
KW - Selenium
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U2 - 10.1016/j.brainres.2007.01.143
DO - 10.1016/j.brainres.2007.01.143
M3 - Article
C2 - 17376411
AN - SCOPUS:34147152673
SN - 0006-8993
VL - 1147
SP - 218
EP - 225
JO - Brain Research
JF - Brain Research
IS - 1
ER -