Lei Bo,Xie Zongyi,Ma Ying,Cheng Yuan.Correlation between VDAC1 expression and neuronal apoptosis in cerebral cortex of rats in early brain injury after subarachnoid hemorrhage[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(16):1705-1709.
Lei Bo,Xie Zongyi,Ma Ying,Cheng Yuan.Correlation between VDAC1 expression and neuronal apoptosis in cerebral cortex of rats in early brain injury after subarachnoid hemorrhage[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(16):1705-1709.DOI:
Correlation between VDAC1 expression and neuronal apoptosis in cerebral cortex of rats in early brain injury after subarachnoid hemorrhage
Objective To study the correlation between voltage-dependent anion channel 1 (VDAC1) expression and neuronal apoptosis in the cerebral cortex of rats after subarachnoid hemorrhage (SAH)
and to investigate the mechanism of VDAC1 involved in the early brain injury after SAH. Methods A total of 108 SD rats were randomly divided into a sham operation group (n=18) and an SAH group (n=90). The SAH group was subdivided into 6-
12-
36-
48-
and 72-h subgroups (n=18 for each subgroup; 6
12
36
48
and 72 hours after SAH
respectively). An SAH model was induced by injecting blood (300 μl) into the pre-chiasmatic cistern. VDAC1 expression in the cerebral cortex at both mRNA and protein levels were examined by RT-PCR as well as immunohistochemistry and Western blotting at 6
12
36
48 and 72 h after SAH. Neuronal apoptosis in the cerebral cortex was evaluated by TUNEL at 6
12
36
48 and 72 h after SAH. Results VDAC1 expression increased significantly at 12 h after SAH [mRNA (2.40±0.19)
protein (1.14±0.08)]
peaked at 36 h [mRNA (3.40±0.65)
protein (1.72±0.22)]
decreased at 48 h [mRNA (1.94±0.30)
protein (0.97±0.07)]
and fell to a normal level at 72 h (P0.05). The number of apoptotic neurons in the cerebral cortex
as measured by TUNEL
increased at 12 h after SAH
reached the peak level at 36 h
then began to decrease (P0.05)
and fell to a normal level at 72 h (P0.05). Conclusion There is a positive correlation between VDAC1 expression level and neuron apoptosis degree in the cerebral cortex of rats at different time points after SAH
implying that VDAC1 may be involved in the pathologic process of early brain injury after SAH through apoptotic pathways.