lomerizine神经保护的预防性治疗偏头痛的药物,对氢peroxide-induced海马神经毒性。

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Mori Ishii M, Iizuka R,登Y, Y,清水

lomerizine神经保护的预防性治疗偏头痛的药物,对氢peroxide-induced海马神经毒性。

摩尔细胞生物化学。2011年12月,358 (2):1 - 11。doi: 10.1007 / s11010 - 011 - 0913 - 3。Epub 2011 6月9。

PubMed ID
21656126 (在PubMed
]
文摘

偏头痛是缺血性中风的危险因素之一。本研究的目的是检查lomerizine的影响,预防性治疗偏头痛的药物,在H (2) O(2)全身的海马神经元的细胞死亡。胞质钙(2 +)浓度测定用fura-2 Ca(2 +)指标。细胞死亡被台盼蓝排斥估计。在rat-cultured海马神经元,添加H (2) O(2)诱导两相的Ca(2 +)海拔和细胞死亡。全身的H (2) O(2)两相的Ca(2 +)海拔和细胞死亡只发生在细胞外钙(2 +)。两相的Ca(2 +)高程由Ca通过质膜(2 +)流入,但不是Ca(2 +)释放胞内钙(2 +)存储。H的早期和晚期阶段(2)O(2)全身的Ca(2 +)流入减少了T -或l型压敏电阻器Ca(2 +)通道(VDCC)拦截器,lomerizine。事实上,l型VDCC(α(1 c)亚基)和衣架VDCC(α(1 g)亚基)mRNA表达鼠海马神经元。虽然一个l型VDCC杀杀杀,硝苯地平,部分抑制Ca的后期阶段(2 +)涌入针对H (2) O(2),一个衣架VDCC杀杀杀,mibefradil,减少Ca的两个阶段(2 +)涌入。 Moreover, lomerizine and mibefradil strongly reduced H(2)O(2)-induced cell death, and nifedipine weakly reduced it. These findings suggest that the inhibition of H(2)O(2)-induced Ca(2+) influx through T-type VDCC seems to be important in the protective effect of lomerizine against oxidative stress. It is possible that lomerizine may be a useful drug for prophylactic treatment of migraine, because migraine is a risk factor for ischemic stroke.

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