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The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain

Authors :
Huang, Man
Hu, Yue-Yu
Dong, Xiao-Qiao
Xu, Qiu-Ping
Yu, Wen-Hua
Zhang, Zu-Yong
Source :
Journal of Ethnopharmacology. Aug2012, Vol. 143 Issue 1, p228-235. 8p.
Publication Year :
2012

Abstract

Abstract: Ethnopharmacological relevance: Oxymatrine is extracted from the traditional Chinese herb Sophora flavescens Ait, possesses anti-inflammatory, anti-oxidative and anti-apoptotic properties, and has been used for the treatment of chronic viral hepatitis and many other diseases. Aims of the study: This study aimed to investigate the effects of oxymatrine on inflammatory response mediated by Toll-like receptor4 (TLR4) and nuclear factor kappa-B (NF-κB), oxidative injury induced by 12/15 lipoxygenase (12/15-LOX), phosphorylated p38 mitogen activated protein kinase (phosphor-p38 MAPK) and cytosolic phospholipase A2 (cPLA2), and neuronal cell apoptosis in rat brain with intracerebral hemorrhage (ICH). Materials and methods: Wistar rats were treated intraperitoneally with 60 or 120mg/kg of oxymatrine daily for 5 days following ICH. The rats were sacrificed at hour 2, 6, 12, 24, 48, 72, and 120 after ICH. The gene expressions of TLR-4 and NF-κB, the levels of TNF-alpha, interleukin-1beta, interleukin-6, 12/15-LOX, phospho-p38 MAPK and cPLA2, and the number of apoptotic neuronal cells in rat brain were determined. Results: Oxymatrine at 120mg/kg significantly suppressed gene expressions of TLR-4 and NF-κB, decreased levels of TNF-alpha, interleukin-1beta and interleukin-6, inhibited synthesis of 12/15-LOX, phospho-p38 MAPK and cPLA2 protein, and mitigated apoptotic neuronal changes following ICH in rat. Conclusion: Oxymatrine at 120mg/kg following ICH inhibits inflammatory responses, oxidative injury, and neuronal cell apoptosis in rats. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
03788741
Volume :
143
Issue :
1
Database :
Academic Search Index
Journal :
Journal of Ethnopharmacology
Publication Type :
Academic Journal
Accession number :
78432379
Full Text :
https://doi.org/10.1016/j.jep.2012.06.028