Lycium barbarum polysaccharide prevents focal cerebral ischemic injury by inhibiting neuronal apoptosis in mice

• Published in: PloS one 2014-03, Vol.9 (3), p.e90780
• Main Authors: Wang, Tengfei, Li, Yuxiang, Wang, Yongsheng, Zhou, Ru, Ma, Lin, Hao, Yinju, Jin, Shaoju, Du, Juan, Zhao, Chengjun, Sun, Tao, Yu, Jianqiang
• Format: Article
• Language: English
• Subjects: Analysis; Analysis of Variance; Animals; Apoptosis; Apoptosis - drug effects; BAX protein; Bcl-2 protein; Biology; Blotting, Western; Brain; Brain injury; Brain Ischemia - prevention & control; Caspase; Caspase-3; Cerebral blood flow; Chemistry; Chlorides; Dose-Response Relationship, Drug; Drugs, Chinese Herbal - administration & dosage; Drugs, Chinese Herbal - pharmacology; Fluorescent Antibody Technique; Immunofluorescence; In Situ Nick-End Labeling; Infarction, Middle Cerebral Artery; Injury prevention; Ischemia; Kinases; Lycium barbarum; Lymphoma; Male; Medicine; Metabolism; Mice; Mice, Inbred ICR; Mitochondria; Neurons; Neurons - drug effects; Neuroprotection; Nimodipine; Occlusion; Pharmacology; Poly (ADP-Ribose) Polymerase-1; Poly(ADP-ribose) polymerase; Poly(ADP-ribose) Polymerases - metabolism; Polysaccharides; Proteins; Reperfusion; Rodents; Staining; Triphenyltetrazolium chloride; Veins & arteries
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0090780

To investigate the neuroprotective effect of Lycium barbarum polysaccharide (LBP) on focal cerebral ischemic injury in mice and to explore its possible mechanism. 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. 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. Based on these findings we propose that LBP protects against focal cerebral ischemic injury by attenuating the mitochondrial apoptosis pathway.