Humanin improves impaired metabolic activity and prolongs survival of serum-deprived human lymphocytes
Humanin improves impaired metabolic activity and prolongs survival of serum-deprived human lymphocytes
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DOI：
10.1023/a:1027372519726
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发表时间：
2003-12-01
影响因子：
4.3
通讯作者：
Ueno, S
中科院分区：
文献类型：
--
作者：
Kariya, S;Takahashi, N;Ueno, S
据报道，Humanin （HN）是一种内源性肽，对各种阿尔茨海默病相关损伤诱导的细胞死亡具有高度选择性的神经保护作用。我们先前从HN抑制血清剥夺诱导的大鼠嗜铬细胞瘤细胞死亡的结果中提出了HN更广泛的细胞保护潜力。在本研究中，我们发现HN也能抑制血清剥夺条件下培养的人淋巴细胞的死亡。此外，通过分析代谢活性和存活率，我们发现HN是一个能够增加个体血清剥夺淋巴细胞代谢活性的有效因素。据我们所知，没有报道描述了一种拯救因子可以增加个体血清剥夺细胞的代谢活性并延长其生存时间。HN的这种新特征可能使我们能够将这种肽应用于代谢活性差的疾病的治疗，如线粒体相关疾病和脑缺血。
Humanin (HN) has been reported to be an endogenous peptide that exerts highly selective neuroprotection against cell death induced by various types of Alzheimer's disease-related insults. We previously proposed the much broader cytoprotective potential of HN from the result that HN suppressed serum-deprivation-induced death of rat pheochromocytoma cells. In this study, we showed that HN also suppressed death of human lymphocytes cultured under serum-deprived condition. Further, we revealed, by assaying metabolic activity and survival rate, that HN was a potent factor capable of increasing the metabolic activity of individual serum-deprived lymphocytes. To our knowledge, there is no report described about a rescue factor that increases the metabolic activity of individual serum-deprived cells and prolongs their survival. This novel feature of HN may enable us to apply this peptide for the management of diseases involving poor metabolic activity, such as mitochondria-related disorders and brain ischemia.