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Reduction in ischemic brain injury following the administration of pentoxifylline
after transient global ischemia/ reperfusion in a rat model
#MMPMID26157711
Nadia Sharifi Z
; Movassaghi S
; Mohamadzadeh F
; Soleimani Asl S
; Pourheydar B
; Mehdizadeh M
Med J Islam Repub Iran
2015[]; 29
(?): 193
PMID26157711
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BACKGROUND: It is well known that the hippocampus, the CA1 Pyramidal cells in
particular, is selectively vulnerable during global cerebral ischemia. Recently,
it is observed that pentoxifylline has a neuroprotective effect. This study
explored the pharmacological relationship between ischemiainduced cell death of
the hippocampus and the efficacy of a vasodilator agent (pentoxifylline) in the
prevention of delayed neuronal death. METHODS: This experimental study was
performed on 4 groups: control, ischemia, experimental (200mg/kg pentoxifylline
injection one hour prior to and one hour following ischemia) and vehicle (normal
saline). Transient global ischemia was induced by bilateral common carotid
arteries occlusion. To investigate the apoptotic bodies and caspase-3 activities
as a central role in the execution phase of apoptosis, the brains were prepared
for the TUNEL technique. RESULTS: Pentoxifylline administration limited apoptosis
and caspase-3 activities in rats' hippocampi. Our data showed no significant
difference between the number of apoptotic bodies in the CA1 region of the
hippocampus in the control and pentoxifylline -treated groups (p= 0.994). The
results of one- way ANOVA revealed that that ischemia significantly increased
caspase-3 levels in the hippocampus (p< 0.05); however, the level of caspase-3 in
pentoxifylline -treated rats was less than the ischemic group. CONCLUSION: These
results suggest that the neuroprotective effect of pentoxifylline (200mg/kg) may
be accompanied by a reduction in ischemic damage within the CA1 region of the
hippocampus in rats subjected to transient global cerebral ischemia.
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