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首页> 外文期刊>Cellular Physiology and Biochemistry >Cytoprotective Effect of Eriodictyol in UV-irradiated Keratinocytes via Phosphatase-dependent Modulation of both the p38 MAPK and Akt Signaling Pathways
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Cytoprotective Effect of Eriodictyol in UV-irradiated Keratinocytes via Phosphatase-dependent Modulation of both the p38 MAPK and Akt Signaling Pathways

机译：通过磷酸酶依赖性调节p38 MAPK和Akt信号通路对紫dict醇在紫外线照射的角质形成细胞中的细胞保护作用

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Although flavonoids exhibit a variety of beneficial biological activities, the exact molecular mechanism of the cellular effects is still not fully explained. In this study, we investigated the molecular mechanism of cytoprotective effect of eriodictyol in UV-irradiated keratinocytes. We found that treatment with eriodictyol effectively suppressed the UV-induced cell death of the keratinocytes, concomitant with the inhibition of pro-caspase-3 or pro-caspase-9 cleavage and the suppression of cytochrome C release. The phosphorylation of p38 MAPK was suppressed during UV-induced apoptosis of the keratinocytes and eriodictyol could reverse the down-regulation of p38 MAPK upon UV irradiation. Inhibition of p38 MAPK activity by SB202190, or over-expression of dominant-negative mutant form of p38 MAPK resulted in suppression of cytoprotective effect of the flavonoid. PP2A appeared to participate in the regulation of both p38 MAPK and Akt activities by directly associating with the kinases. UV treatment stimulated not only the phosphatase activity, but also its association with p38 MAPK or Akt. Interestingly, eriodictyol reversed the increase in PP2A activity and the association between the proteins. Taken together, these findings suggest that eriodictyol may lead to protection of keratinocytes from UV-induced cytotoxicity by modulating both the p38 MAPK and Akt signaling pathways in a phosphatase-dependent manner.
机译：尽管类黄酮表现出多种有益的生物活性，但仍未完全解释细胞作用的确切分子机制。在这项研究中，我们研究了紫dict醇在紫外线照射的角质形成细胞中的细胞保护作用的分子机制。我们发现，用二十碳三烯酚处理可有效抑制紫外线诱导的角质形成细胞死亡，并同时抑制caspase-3或caspase-9的裂解和细胞色素C的释放。在紫外线诱导的角质形成细胞凋亡期间，p38 MAPK的磷酸化受到抑制，而雌黄醇可以逆转紫外线照射下p38 MAPK的下调。 SB202190对p38 MAPK活性的抑制或p38 MAPK显性负突变体形式的过表达导致类黄酮的细胞保护作用受到抑制。 PP2A似乎通过直接与激酶相关联而参与p38 MAPK和Akt活性的调节。紫外线处理不仅刺激了磷酸酶活性，而且刺激了其与p38 MAPK或Akt的结合。有趣的是，雌黄醇逆转了PP2A活性的增加以及蛋白质之间的缔合。综上所述，这些发现表明，通过以磷酸酶依赖的方式调节p38 MAPK和Akt信号传导途径，Eriodictyol可能导致角质形成细胞免受紫外线诱导的细胞毒性的影响。

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