氧化苦参碱对脑出血大鼠神经元细胞凋亡的保护作用。
The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain.
机构信息
Department of Intensive Care Unit, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, 3 Qingchun East Road, Hangzhou 310000, China.
出版信息
J Ethnopharmacol. 2012 Aug 30;143(1):228-35. doi: 10.1016/j.jep.2012.06.028. Epub 2012 Jun 28.
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.
民族药理学相关性
氧化苦参碱从传统中药苦参中提取，具有抗炎、抗氧化和抗凋亡作用，已用于治疗慢性病毒性肝炎和许多其他疾病。
研究目的
本研究旨在探讨氧化苦参碱对 Toll 样受体 4（TLR4）和核因子 kappa-B（NF-κB）介导的炎症反应、12/15 脂氧合酶（12/15-LOX）诱导的氧化损伤、磷酸化 p38 丝裂原活化蛋白激酶（磷酸化 p38 MAPK）和胞质型磷脂酶 A2（cPLA2）以及脑出血（ICH）大鼠脑细胞凋亡的影响。
材料和方法
ICH 后，Wistar 大鼠每天腹腔注射 60 或 120mg/kg 氧化苦参碱，连续 5 天。ICH 后 2、6、12、24、48、72 和 120 小时处死大鼠。测定 TLR-4 和 NF-κB 的基因表达、TNF-α、白细胞介素-1β、白细胞介素-6、12/15-LOX、磷酸化 p38 MAPK 和 cPLA2 的水平，以及大鼠脑组织中凋亡神经元细胞的数量。
结果
120mg/kg 氧化苦参碱显著抑制 TLR-4 和 NF-κB 的基因表达，降低 TNF-α、白细胞介素-1β 和白细胞介素-6 的水平，抑制 12/15-LOX、磷酸化 p38 MAPK 和 cPLA2 蛋白的合成，减轻 ICH 后大鼠的凋亡神经元变化。
结论
ICH 后 120mg/kg 氧化苦参碱抑制大鼠炎症反应、氧化损伤和神经元细胞凋亡。
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