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丙酮酸对 HaCaT 人角质形成细胞中 UVB 诱导损伤的保护作用。

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

机构信息

The Institute of Livestock and Grassland Science, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.

出版信息

J Biosci Bioeng. 2013 Apr;115(4):442-8. doi: 10.1016/j.jbiosc.2012.11.004. Epub 2012 Dec 6.

Abstract

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)-1α, IL-1β, IL-6 and cyclooxygenase-2 (Cox-2). This decrease was associated with the reduced secretion of IL-1α, IL-1β, IL-6 and prostaglandin E2 (PGE2) 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.

摘要

研究了丙酮酸对中波紫外线(UVB)诱导损伤的保护作用在人永生化角质形成细胞(HaCaT 细胞)中。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,丙酮酸抑制了炎性介质如白细胞介素(IL)-1α、IL-1β、IL-6 和环加氧酶-2(Cox-2)的 UVB 诱导的 mRNA 表达。这种减少与细胞培养液中 IL-1α、IL-1β、IL-6 和前列腺素 E2(PGE2)分泌减少有关。此外,丙酮酸逆转了 UVB 照射诱导的 HaCaT 细胞中 p38 丝裂原活化蛋白激酶(MAPK)的磷酸化,但增加了假照射细胞中 p38 MAPK 的磷酸化。p38 MAPK 抑制剂 SB203580 抑制了 UVB 诱导的 IL-6 产生。这些结果表明,丙酮酸通过抑制 p38 MAPK 的激活来抑制 UVB 介导的炎症反应。

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