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首页> 外文期刊>Journal of natural medicines >Hydroxyobtustyrene protects neuronal cells from chemical hypoxia-induced cell death
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Hydroxyobtustyrene protects neuronal cells from chemical hypoxia-induced cell death

机译:羟基氟钛烯保护来自化学缺氧诱导的细胞死亡的神经元细胞

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Hydroxyobtustyrene is a derivative of cinnamyl phenol isolated from Dalbergia odorifera T. Chen. The heartwood, known as ‘JiangXiang’, is a traditional Chinese medicine. Previous studies showed that hydroxyobtustyrene inhibited the biosynthesis of prostaglandins, which are mediators of neuronal cell death in ischemia. However, it currently remains unclear whether hydroxyobtustyrene protects neurons against ischemic stress. In the present study, we investigated the protective effects of hydroxyobtustyrene against sodium cyanide (NaCN)-induced chemical ischemia. Hippocampal neurons were cultured from the cerebral cortices of E18 Wistar rats. The effects of hydroxyobtustyrene on neuronal survival and trophic effects were estimated under lower and higher cell density conditions. After the treatment of 1?mM NaCN with or without hydroxyobtustyrene, an MTT assay, Hoechst staining, and immunocytochemistry for cyclooxygenase (COX)-2 were performed. Hydroxyobtustyrene increased cell viability under lower, but not normal density conditions. Neither the neurite number nor the length was influenced by hydroxyobtustyrene. NaCN significantly decreased viability and increased fragmentation in cell nuclei, and these changes were prevented by hydroxyobtustyrene. Moreover, NaCN increased the number of COX-2-positive neurons, and this was significantly prevented by the co-treatment with hydroxyobtustyrene. Therefore, hydroxyobtustyrene protected cultured hippocampal neurons against NaCN-induced chemical ischemia, which may be mediated by the inhibition of COX-2 production.
机译:羟基比铜汀是从达伯利亚odorifera t.陈氏蛋白分离的肉桂酚的衍生物。作为“江乡”的心材是一种中医。以往的研究表明,羟基氟苯醚抑制了前列腺素的生物合成,这是缺血中神经元细胞死亡的介质。然而,它目前尚不清楚羟基氟乙烯是否保护神经元免受缺血应激。在本研究中,我们研究了羟基氟乙烯对氰化钠(NaCN)诱导的化学缺血的保​​护作用。从E18 Wistar大鼠的大脑皮质培养海马神经元。在较低且较高细胞密度条件下估计羟基氟乙烯对神经元存活和营养效应的影响。在用或不含羟基氟乙烯的1℃下处理1?mm NaCn后,进行MTT测定,Hoechst染色和用于环氧化酶(COX)-2的免疫细胞化学。羟基氟苯醚在较低但不是正常密度条件下增加细胞活力。无论是神经突数还是长度都不受羟基氟乙烯的影响。 NACN显着降低了细胞核的活力和增加的碎片,并且通过羟基氟烯预防这些变化。此外,NACN增加了COX-2阳性神经元的数量,并且通过用羟基氟乙烯的共同处理显着防止了这一点。因此,羟基氟乙烯保护培养的海马神经元针对NACN诱导的化学缺血,其可以通过抑制COX-2生产来介导。

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