Anti-inflammatory effects of tectroside on UVB-induced HaCaT cells

Ultraviolet B (UVB) irradiation causes skin damage and inflammation by inducing the secretion of various cytokines, which are immune regulators produced by cells. To prevent skin inflammation, keratinocytes that have been irreversibly damaged by UVB must be eliminated through apoptosis. Ixeris denta...

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Bibliographic Details
Published in:International journal of molecular medicine 2013-06, Vol.31 (6), p.1471-1476
Main Authors: KIM, SUNG-BAE, KANG, OK-HWA, JOUNG, DAE-KI, MUN, SU-HYUN, SEO, YUN-SOO, CHA, MI-RAN, RYU, SHI-YONG, SHIN, DONG-WON, KWON, DONG-YEUL
Format: Article
Language:English
Subjects:
Apoptosis
Binding sites
Cytokines
Enzymes
Folk medicine
Hepatitis
Herbal medicine
human keratinocyte
Immunoglobulins
Inflammation
Inflammatory diseases
Ixeris dentata
Kinases
Medicine
Penicillin
Phosphorylation
Pneumonia
Proteins
Rodents
Skin
Studies
tectroside
Tumors
ultraviolet B
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Summary:Ultraviolet B (UVB) irradiation causes skin damage and inflammation by inducing the secretion of various cytokines, which are immune regulators produced by cells. To prevent skin inflammation, keratinocytes that have been irreversibly damaged by UVB must be eliminated through apoptosis. Ixeris dentata (I. dentata) (family Asteraceae) is a perennial medicinal herb indigenous to Korea. It is used in Korea, China and Japan to treat indigestion, pneumonia, diabetes, hepatitis, contusions and tumors. Guaiane-type sesquiterpene lactones were isolated from the whole extract of I. dentata. This led to the isolation of the anti-inflammatory sesquiterpene lactone compound tectroside (TES), which was tested on a human keratinocyte cell line. To determine the anti-inflammatory effects of TES, we examined its influence on UVB-induced pro-inflammatory cytokine production in human keratinocytes (HaCaT cells) by observing these cells in the presence or absence of TES. In the present study, pro-inflammatory cytokine production was determined by performing enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction and western blot analysis to evaluate the activation of mitogen-activated protein kinases (MAPKs). TES inhibited UVB-induced production of the pro-inflammatory cytokines interleukin (IL)-6 and IL-8 in a dose-dependent manner. In addition, TES inhibited the expression of cyclooxygenase (COX)-2 and the phosphorylation of c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) MAPKs, suggesting that it inhibits the secretion of the pro-inflammatory cytokines IL-6 and IL-8 and COX-2 expression by blocking MAPK phosphorylation. These results suggest that TES can potentially protect against UVB-induced skin inflammation.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2013.1343