哈卡特
促炎细胞因子
p38丝裂原活化蛋白激酶
肿瘤坏死因子α
MAPK/ERK通路
姜黄素
癌症研究
NF-κB
细胞周期蛋白D1
细胞周期蛋白D
化学
细胞生物学
生物
细胞凋亡
免疫学
信号转导
药理学
细胞周期
炎症
生物化学
体外
作者
Jae-We Cho,Kyu-Suk Lee,Chang-Wook Kim
标识
DOI:10.3892/ijmm.19.3.469
摘要
TNF-α induces some proinflammatory cytokines including IL-1β, IL-6, IL-8, and itself by activation of NF-κB 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-α treatment. However, it was unknown whether curcumin, showing inhibitory effects on NF-κB and MAPKs, attenuates the expression of TNF-α-induced IL-1β, IL-6, IL-8, and TNF-α 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-α-treated HaCaT cells. We found that curcumin inhibited the expression of TNF-α-induced IL-1β, IL-6, and TNF-α, but not IL-8, in TNF-α-treated HaCaT cells as well as the TNF-α-induced cyclin E expression. In addition, curcumin inhibited the activation of MAPKs (JNK, p38 MAPK, and ERK) and NF-κB in TNF-α-treated HaCaT cells. Taken together, curcumin exerts anti-inflammatory and growth inhibitory effects in TNF-α-treated HaCaT cells through inhibition of NF-κB and MAPK pathways.
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