Curcumin attenuates the expression of IL-1beta, IL-6, and TNF-alpha as well as cyclin E in TNF-alpha-treated HaCaT cells; NF-kappaB and MAPKs as potential upstream targets.
Curcumin attenuates the expression of IL-1beta, IL-6, and TNF-alpha as well as cyclin E in TNF-alpha-treated HaCaT cells; NF-kappaB and MAPKs as potential upstream targets.
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发表时间：
2007
影响因子：
5.4
通讯作者：
Jae‐We Cho;K. Lee;Chang-Wook Kim
中科院分区：
文献类型：
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作者：
Jae‐We Cho;K. Lee;Chang-Wook Kim
TNF-α通过激活NF-κ B或MAPK（p38、JNK、ERK）诱导一些促炎细胞因子，包括IL-1 β、IL-6、IL-8及其本身。这些细胞因子在各种炎症性皮肤病如银屑病中起重要作用。最近也有报道，细胞周期蛋白E的表达在TNF-α处理后通过ERK途径上调。然而，姜黄素对NF-κ B和MAPK的抑制作用是否减弱TNF-α诱导的IL-1 β、IL-6、IL-8和TNF-α的表达以及HaCaT细胞中细胞周期蛋白E的表达尚不清楚。在这项研究中，我们研究了姜黄素对TNF-α处理的HaCaT细胞中促炎细胞因子和细胞周期蛋白E表达的抑制作用。我们发现，姜黄素抑制TNF-α诱导的IL-1 β，IL-6和TNF-α的表达，但不IL-8，在TNF-α处理的HaCaT细胞以及TNF-α诱导的细胞周期蛋白E的表达。此外，姜黄素抑制TNF-α处理的HaCaT细胞中MAPK（JNK，p38 MAPK和ERK）和NF-κ B的活化。总之，姜黄素通过抑制NF-κ B和MAPK途径在TNF-α处理的HaCaT细胞中发挥抗炎和生长抑制作用。
TNF-alpha induces some proinflammatory cytokines including IL-1beta, IL-6, IL-8, and itself by activation of NF-kappaB or MAPKs (p38, JNK, ERK). These cytokines play important roles in various inflammatory skin diseases, such as psoriasis. Recently it was also reported that expression of cyclin E is up-regulated by ERK pathway after TNF-alpha treatment. However, it was unknown whether curcumin, showing inhibitory effects on NF-kappaB and MAPKs, attenuates the expression of TNF-alpha-induced IL-1beta, IL-6, IL-8, and TNF-alpha as well as cyclin E expression in HaCaT cells. In this study, we investigated the inhibitory effect of curcumin on expression of proinflammatory cytokines and cyclin E in TNF-alpha-treated HaCaT cells. We found that curcumin inhibited the expression of TNF-alpha-induced IL-1beta, IL-6, and TNF-alpha, but not IL-8, in TNF-alpha-treated HaCaT cells as well as the TNF-alpha-induced cyclin E expression. In addition, curcumin inhibited the activation of MAPKs (JNK, p38 MAPK, and ERK) and NF-kappaB in TNF-alpha-treated HaCaT cells. Taken together, curcumin exerts anti-inflammatory and growth inhibitory effects in TNF-alpha-treated HaCaT cells through inhibition of NF-kappaB and MAPK pathways.