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矢车菊素通过抑制 ROS 介导的 DNA 损伤和调节 ERK 和 AKT 通路逆转顺铂诱导的 HK-2 近端肾小管细胞凋亡。

Cyanidin reverses cisplatin-induced apoptosis in HK-2 proximal tubular cells through inhibition of ROS-mediated DNA damage and modulation of the ERK and AKT pathways.

机构信息

School of Life Sciences and State Key Laboratory of Agrobiotechnology, The Chinse University of Hong Kong, Shatin, Hong Kong Special Administrative Region.

出版信息

Cancer Lett. 2013 Jun 1;333(1):36-46. doi: 10.1016/j.canlet.2012.12.029. Epub 2013 Jan 27.

DOI:10.1016/j.canlet.2012.12.029
PMID:23360684
Abstract

Cyanidin is an anthocyanin widely distributed in food diet with novel antioxidant activity. Herein, we investigated the protective effects of cyanidin on HK-2 proximal tubular cells against cisplatin-induced apoptosis and elucidated the underlying mechanisms. The results showed that cisplatin-induced apoptosis in HK-2 cells was significantly attenuated by cyanidin. The cleavage of caspases and PARP, activation of p53 and mitochondrial-mediated apoptosis pathways induced by cisplatin were effectively blocked by cyanidin. Moreover, cyanidin significantly suppressed the overproduction of ROS, and activation of ERK and AKT pathways triggered by cisplatin. Our results indicate that cyanidin exhibits therapeutic potential in prevention of cisplatin-induced nephrotoxicity.

摘要

矢车菊素是一种广泛存在于饮食中的花色苷,具有新颖的抗氧化活性。本研究旨在探讨矢车菊素对顺铂诱导的 HK-2 近端肾小管细胞凋亡的保护作用,并阐明其潜在机制。结果表明,矢车菊素可显著减轻顺铂诱导的 HK-2 细胞凋亡。同时,矢车菊素还能有效抑制顺铂诱导的半胱天冬酶和聚腺苷二磷酸核糖聚合酶的裂解、p53 和线粒体介导的细胞凋亡途径的激活。此外,矢车菊素还能显著抑制顺铂诱导的活性氧过度产生以及细胞外信号调节激酶和蛋白激酶 B 通路的激活。本研究结果表明,矢车菊素在预防顺铂诱导的肾毒性方面具有潜在的治疗作用。

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