Recently, several drugs have been developed
to treat psoriasis through inhibiting TNF-a [15,16]. One of the
TNF-a targets is ERK, which has recently been shown to upregulate
the expression of cyclin E and also results in accumulation
of cyclin D1 [17]. In addition, p38 MAPK and c-Jun NH2-
terminal kinase (JNK) are highly activated by TNF-a treatment
in keratinocytes [18], and activation of p38, and JNK are associated
with the expression of proinflammatory cytokines such
as IL-6 and IL-8 [19–21]. Psoriasis is also characterized by
hyperproliferation and abnormal differentiation of keratinocytes.
Curcumin is a selective phosphorylase kinase inhibitor,
which has been shown to have anti-inflammatory and antiproliferative
properties and decrease the expression of proinflammatory
cytokines in psoriatic keratinocytes [22]. In addition,
Grandjean-Laquerriere et al. reported that curcumin attenuates
the expression of ultraviolet B (UVB)-induced IL-6 and IL-
8 in keratinocytes partially through the inhibition of NF-jB
activation [23]. Curcumin is known to exert its anti-inflammatory
action in various cell lines through the inhibition of NFjB,
AP-1, and MAPK pathways [24–27]. Cho et al. also showed
that curcumin inhibited NF-jB and MAPK pathway to decrease
cell proliferation as well as reduce the expression of IL-6 and
IL-8 in TNF-a-treated keratinocytes [28]. Hence, it may be a
good strategy to achieve broad anti-inflammatory effects
through the inhibition of TNF-a, NF-jB, and MAPK by
curcumin.