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Lycium barbarum Polysaccharide Prevents Focal Cerebral Ischemic Injury by Inhibiting Neuronal Apoptosis in Mice
Author(s) -
Tengfei Wang,
YuXiang Li,
Yongsheng Wang,
Ru Zhou,
Lin Ma,
Yinju Hao,
Shaoju Jin,
Juan Du,
Chengjun Zhao,
Tao Sun,
Jianqiang Yu
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0090780
Subject(s) - apoptosis , tunel assay , neuroprotection , pharmacology , nimodipine , ischemia , medicine , western blot , h&e stain , poly adp ribose polymerase , pathology , reperfusion injury , staining , anesthesia , chemistry , immunohistochemistry , biochemistry , polymerase , gene , calcium
Aims of the Study To investigate the neuroprotective effect of Lycium barbarum polysaccharide (LBP) on focal cerebral ischemic injury in mice and to explore its possible mechanism. Materials and Methods Male 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. Results LBP (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. Conclusions Based on these findings we propose that LBP protects against focal cerebral ischemic injury by attenuating the mitochondrial apoptosis pathway.

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