Protective effect of pyruvate against UVB-induced damage in HaCaT human keratinocytes

Protective effect of pyruvate against UVB-induced damage in HaCaT human keratinocytes
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DOI:
10.1016/j.jbiosc.2012.11.004
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发表时间:
2013-04-01
影响因子:
2.8
通讯作者:
Takayama, Yoshiharu
Takayama, Yoshiharu
中科院分区:
工程技术3区
文献类型:
--
作者:
Aoki-Yoshida, Ayako;Aoki, Reiji;Takayama, Yoshiharu

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在人永生化角质形成细胞(HaCaT细胞)中研究丙酮酸盐对紫外线B(UVB)诱导的损伤的保护作用。虽然丙酮酸不能抑制UVB诱导的细胞内活性氧(ROS)水平的刺激,但它确实提高了UVB照射的HaCaT细胞的存活率。此外,丙酮酸抑制UVB诱导的炎症介质如白细胞介素(IL)-1 α、IL-1 β、IL-6和环氧合酶-2(考克斯-2)的mRNA表达。这种减少与IL-1 α、IL-1 β、IL-6和前列腺素E2(PGE(2))分泌到培养基中的减少有关。此外,丙酮酸逆转p38丝裂原活化蛋白激酶(MAPK)的磷酸化,诱导UVB照射,在HaCaT细胞,但增加p38 MAPK磷酸化假照射细胞。p38 MAPK抑制剂SB 203580可抑制UVB诱导的IL-6产生。这些结果表明,丙酮酸通过抑制p38 MAPK激活来抑制UVB介导的炎症反应。(C)2012年,生物技术学会,日本。All rights reserved.
The protective effect of pyruvate against ultraviolet B (UVB)-induced damage was investigated in human immortalized keratinocytes (HaCaT cells). Although pyruvate did not inhibit UVB-induced stimulation of intracellular reactive oxygen species (ROS) levels, it did improve the survival rate of UVB-irradiated HaCaT cells. Furthermore, pyruvate suppressed the UVB-induced mRNA expression of inflammatory mediators such as interleukin (IL)-1 alpha IL-1 beta, IL-6 and cyclooxygenase-2 (Cox-2). This decrease was associated with the reduced secretion of IL-1 alpha, IL-1 beta, IL-6 and prostaglandin E2 (PGE(2)) into culture media. In addition, pyruvate reversed the phosphorylation of p38 mitogen-activated protein kinase (MAPK), induced by UVB-irradiation, in HaCaT cells but increased p38 MAPK phosphorylation in sham-irradiated cells. UVB-induced production of IL-6 was inhibited by SB203580, a p38 MAPK inhibitor. These results suggested that pyruvate inhibits UVB-mediated inflammatory response by inhibiting the p38 MAPK activation. (C) 2012, The Society for Biotechnology, Japan. All rights reserved.