首页> 外文期刊>International Journal of Pharmacology >Synergic Effect of Ligusticum chuanxiong Hort Extract and Borneol in Protecting Brain Microvascular Endothelial Cells against Oxygen-Glucose Deprivation/Reperfusion Injury
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Synergic Effect of Ligusticum chuanxiong Hort Extract and Borneol in Protecting Brain Microvascular Endothelial Cells against Oxygen-Glucose Deprivation/Reperfusion Injury

机译:Ligusticum川芎霍尔提取物和冰酚在保护脑微血管内皮细胞对氧葡萄糖剥夺/再灌注损伤中的协同作用

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Background and Objective: Ligusticum chuanxiong Hort (LC) and borneol (BO) are usually prescribed as a combination of ischemic stroke patients for a better therapeutic effect in China. However, their synergic mechanism is unclear. Considering the critical role of Brain Microvascular Endothelial Cells (BMECs) in this disorder, the present study was designed to explore their synergic mechanism in protecting BMECs against Oxygen-Glucose Deprivation/Reperfusion (OGD/R) injury. Materials and Methods: The primary cultured BMECs were identified and divided into 5 groups of control, model, ELC (50 mg LG1 ), BO (50 :g LG1 ) and ELC BO. Then their synergic treatment was evaluated via measuring oxidative stress, [Ca2 ]i, apoptosis ratio, levels of apoptosis-related genes and angiogenesis-related proteins. Results: After a comparison between the combined group and their monotherapies, it was shown that the superiority of ELC was in inhibiting oxidative stress and apoptosis, regulating [Ca2 ]i and levels of apoptosis-related genes, while that of BO was in promoting angiogenesis. Interestingly, the combined therapy even reduced VEGFR1 expression which was unaffected in both of their monotherapies. Conclusion: ELC and BO might play different roles in protecting BMECs against oxygen-glucose deprivation/reperfusion injury and their synergic effect was displayed in the present study.
机译:背景和目的:Ligusticum Chuanxiong Hort(LC)和冰片(BO)通常被规定为缺血性卒中患者的组合,在中国进行更好的治疗效果。然而,他们的协同机制尚不清楚。考虑到脑微血管内皮细胞(BMEC)在该疾病中的关键作用,本研究旨在探讨它们在保护BMECS免受氧葡萄糖剥夺/再灌注(OGD / R)损伤的协同机制。材料和方法:鉴定了初级培养的BMEC,并分为5组对照,模型,ELC(50mg LG1),BO(50:G LG1)和ELC Bo。然后通过测量氧化应激,[CA2] I,凋亡率,凋亡相关基因水平和血管生成相关蛋白质评估其协同治疗。结果:在组合组及其单极之间进行比较后,表明ELC的优越性是抑制氧化应激和凋亡,调节[CA2] I和细胞凋亡相关基因的水平,而BO的水平是促进血管生成。有趣的是,联合治疗甚至还减少了VEGFR1表达,这些表达不受它们两种单疗法的影响。结论:ELC和BO可能在保护BMEC免受氧血糖剥夺/再灌注损伤的不同作用,并且在本研究中显示了它们的协同效应。

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