Abstract
Aims of the StudyTo investigate the neuroprotective effect of Lycium barbarum polysaccharide (LBP) on focal cerebral ischemic injury in mice and to explore its possible mechanism.Materials and MethodsMale ICR mice were used to make the model of middle cerebral artery occlusion (MCAO) after intragastric administration with LBP (10, 20 and 40 mg/kg) and Nimodipine (0.4 mg/kg) for seven successive days. After 24 h of reperfusion, neurological scores were estimated and infarct volumes were measured by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. Morphological changes in ischemic brains were performed for hematoxylin-eosin (HE) staining. The number of apoptotic neurons was detected by TUNEL staining. The Bax, Bcl-2 protein expression and CytC, Caspase-3, -9 and cleaved PARP-1 activation were investigated by immunofluorescence and western-blot analysis.ResultsLBP (10, 20 and 40 mg/kg) treatment groups significantly reduced infract volume and neurological deficit scores. LBP also relieved neuronal morphological damage and attenuated the neuronal apoptosis. LBP at the dose of 40 mg/kg significantly suppressed overexpression of Bax, CytC, Caspase-3, -9 and cleaved PARP-1, and inhibited the reduction of Bcl-2 expression.ConclusionsBased on these findings we propose that LBP protects against focal cerebral ischemic injury by attenuating the mitochondrial apoptosis pathway.
Highlights
Ischemic stroke is a major cause of human death and disability worldwide [1]
Lycium barbarum polysaccharide (LBP) at the dose of 40 mg/kg significantly suppressed overexpression of Bax, CytC, Caspase-3, -9 and cleaved poly (ADP-ribose) polymerase (PARP)-1, and inhibited the reduction of Bcl-2 expression. Based on these findings we propose that LBP protects against focal cerebral ischemic injury by attenuating the mitochondrial apoptosis pathway
We examined the protective effects of LBP in a model of middle cerebral artery occlusion (MCAO) in mice
Summary
Determination of Infarct Volume The mice (n = 6, for each group) were decapitated to remove the brain after the evaluation of neurological deficit. C Representative Western blot band of Bcl-2 protein expression in the ischemic cortex at 24 h after reperfusion. D Effect of LBP (40 mg/kg) on the Bcl-2 expression in MCAO mice cortex at 24 h after reperfusion. B Effect of LBP (40 mg/kg) on the Caspase-9 activation in MCAO mice cortex at 24 h after reperfusion. Mean density of Bax, Bcl-2, CytC and Caspase-3 in mice brains per section (4006) was measured with microscope image-analysis software (Image-Pro plus, U.S.A.) by a single investigator who was blind to sample identity. Western blot Analysis After 24 h of reperfusion, the mice (n = 6, for each group) were decapitated and ischemic brains were collected.
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