Vitexin protects brain against ischemia/reperfusion injury via modulating mitogen-activated protein kinase and apoptosis signaling in mice

• Published in: Phytomedicine (Stuttgart) Vol. 22; no. 3; pp. 379 - 384
• Main Authors: Wang, Yanan, Zhen, Yilan, Wu, Xian, Jiang, Qin, Li, Xiaoliang, Chen, Zhiwu, Zhang, Gongliang, Dong, Liuyi
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 15.03.2015; Urban & Fischer Verlag
• Subjects: Animals; Apigenin - pharmacology; Apoptosis; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; Bioflavonoids; Brain Ischemia - drug therapy; Care and treatment; Cellular signal transduction; Extracellular Signal-Regulated MAP Kinases - metabolism; Flavones; Flavonoids; Flavonoids - pharmacology; Hawthorns; Health aspects; Infarction, Middle Cerebral Artery; Ischemia/reperfusion injury; JNK Mitogen-Activated Protein Kinases - metabolism; Male; MAP Kinase Signaling System - drug effects; Mice; Mitogen-activated protein kinase; Neuroprotective Agents - pharmacology; p38 Mitogen-Activated Protein Kinases - metabolism; Phosphorylation; Proto-Oncogene Proteins c-bcl-2 - metabolism; Reperfusion injury; Reperfusion Injury - drug therapy; Vitexin; Mitogen-activated protein kinase; Mice; Ischemia/reperfusion injury; Vitexin; Apoptosis
• ISSN: 0944-7113; 1618-095X
• DOI: 10.1016/j.phymed.2015.01.009

Vitexin is a major bioactive flavonoid compound derived from the dried leaf of hawthorn (Crataegus pinnatifida), a widely used conventional folk medicine in China. Recent studies have shown that vitexin presents neuroprotective effects in vitro. Whether this protective effect applies to the cerebral ischemia/reperfusion (I/R) injury remains elusive. In the present study, we examined the potential neuroprotective effect of vitexin against cerebral I/R injury and underlying mechanisms. A focal cerebral I/R model in male Kunming mice was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 22 h. The neurological function and infarct volume were assessed by using Long's five-point scale system and triphenyl-tetrazolium chloride (TTC) staining technique, respectively. Neuronal damage was evaluated by histological staining. Extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 phosphorylation, and apoptosis were measured via Western blot at 24 h after reperfusion. As a result, systemic vitexin treatment significantly reduced neurological deficit, cerebral infarct volume and neuronal damage when compared with the I/R group. Western blot analyses revealed that vitexin markedly upregulated p-ERK1/2 and downregulated p-JNK and p-p38. Meanwhile, vitexin increased Bcl-2 expression and suppressed the overexpression of Bax in the I/R injury mice. In conclusion, the results indicate that vitexin protects brain against cerebral I/R injury, and this effect may be regulated by mitogen-activated protein kinase (MAPK) and apoptosis signaling pathways.