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紫薯花色苷通过抑制 caspase-3 的激活和增强 PI3K/Akt 通路来保护小鼠肝脏免受半乳糖诱导的细胞凋亡。

Purple sweet potato color protects mouse liver against d-galactose-induced apoptosis via inhibiting caspase-3 activation and enhancing PI3K/Akt pathway.

机构信息

Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Xuzhou Normal University, Xuzhou 221116, Jiangsu Province, PR China.

出版信息

Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2500-7. doi: 10.1016/j.fct.2010.06.023. Epub 2010 Jun 18.

Abstract

Purple sweet potato color (PSPC) has been shown to possess hepatoprotective effects in our previous study. To clarify the detailed mechanism of hepatoprotective effects of PSPC, we investigated the potential protective effect of PSPC against caspase-3 activation induced by d-gal, as well as its influence on Bcl-2 levels and PI3K/Akt cell survival pathway. The results of TUNEL assay showed that PSPC effectively suppressed the d-gal-induced hepatocytes apoptosis, suggesting that anti-apoptosis mechanism was involved in PSPC-mediated protection against d-gal-induced liver injury in mouse. PSPC significantly increased GSH levels and promoted a marked increase in the activities of GSH related enzymes including GR, GST in d-gal-treated mice. The activation and activity of caspase-3 were markedly inhibited by the treatment of PSPC in the livers of d-gal-treated mice. Furthermore, the level of Bcl-2 was significantly raised, and the levels of PI3K p110 and phosphorylated Akt were also largely enhanced by the treatment of PSPC in the livers of d-gal-treated mice. In conclusion, these results suggested that PSPC could protect mouse liver against d-gal-induced hepatocyte apoptosis via attenuating oxidative stress, inhibiting the activation of caspase-3 and enhancing cell survival signaling (enhancing the level of anti-apoptotic protein Bcl-2 and the activation of PI3K/Akt pathway).

摘要

在我们之前的研究中已经表明,紫薯花色苷(PSPC)具有保肝作用。为了阐明 PSPC 保肝作用的详细机制,我们研究了 PSPC 对 d-gal 诱导的 caspase-3 激活的潜在保护作用,以及其对 Bcl-2 水平和 PI3K/Akt 细胞存活途径的影响。TUNEL 检测结果表明,PSPC 能有效抑制 d-gal 诱导的肝细胞凋亡,提示抗凋亡机制参与了 PSPC 介导的对 d-gal 诱导的小鼠肝损伤的保护作用。PSPC 显著增加了 GSH 水平,并促进了 GSH 相关酶(包括 GR、GST)的活性在 d-gal 处理的小鼠中明显增加。PSPC 处理显著抑制了 d-gal 处理小鼠肝脏中 caspase-3 的激活和活性。此外,PSPC 处理还显著提高了 Bcl-2 的水平,并且还大大增强了 d-gal 处理小鼠肝脏中 PI3K p110 和磷酸化 Akt 的水平。综上所述,这些结果表明 PSPC 可以通过减轻氧化应激、抑制 caspase-3 的激活和增强细胞存活信号(提高抗凋亡蛋白 Bcl-2 的水平和激活 PI3K/Akt 途径)来保护小鼠肝脏免受 d-gal 诱导的肝细胞凋亡。

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