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应激诱导早衰细胞体系下矢车菊素的抗衰老作用。

Anti-aging effects of cyanidin under a stress-induced premature senescence cellular system.

机构信息

Department of Food Science and Nutrition, Research Institute of Ecology for the Elderly, Pusan National University, Jangjeon-dong, Geumjeong-gu, Busan 609-735, Korea.

出版信息

Biol Pharm Bull. 2010;33(3):421-6. doi: 10.1248/bpb.33.421.

Abstract

The anti-aging effects of cyanidin were investigated under stress-induced premature senescence (SIPS) using WI-38 human diploid fibroblasts. WI-38 cells that were treated with 300 microM H(2)O(2) showed losses of cell viability, increased lipid peroxidation, and shortened cell lifespans. However, treatment with cyanidin attenuated cellular oxidative stress through increase of cell viability and the inhibition of lipid peroxidation. In addition, the life spans of young-, middle-, and old-aged WI-38 cells were prolonged by cyanidin treatment. Furthermore, H(2)O(2)-treated WI-38 cells significantly increased mRNA and protein expressions of nuclear factor-kappaB, cyclooxygenase-2, and inducible nitric oxide synthase, while those treated with cyanidin had significantly decreased expressions. These results suggest that cyanidin may delay the aging process by attenuating oxidative stress under the SIPS cellular model.

摘要

研究了矢车菊素在应激诱导早衰(SIPS)下对 WI-38 人二倍体成纤维细胞的抗衰老作用。用 300μM H2O2处理的 WI-38 细胞表现出细胞活力丧失、脂质过氧化增加和细胞寿命缩短。然而,矢车菊素处理可通过增加细胞活力和抑制脂质过氧化来减轻细胞氧化应激。此外,用矢车菊素处理可延长年轻、中年和老年 WI-38 细胞的寿命。此外,H2O2 处理的 WI-38 细胞显著增加了核因子-κB、环氧化酶-2 和诱导型一氧化氮合酶的 mRNA 和蛋白表达,而用矢车菊素处理的细胞表达则显著降低。这些结果表明,矢车菊素可能通过减轻 SIPS 细胞模型中的氧化应激来延缓衰老过程。

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