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HaCaT 세포주에서 Epigallocatechin-3-Gallate (EGCG)가 자외선 및 LPS에 의한 iNOS mRNA 발현 및 NO 생성에 미치는 영향
탁우정 ( Tag U Jeong ),이창균 ( Lee Chang Gyun ),서성준 ( Seo Seong Jun ),김명남 ( Kim Myeong Nam ),노병인 ( No Byeong In ),홍창권 ( Hong Chang Gwon ) 대한피부과학회 2004 대한피부과학회지 Vol.42 No.1
N/A Background: Nitric oxide (NO) plays an important role in inflammation and multiple stages of carcinogenesis. Green tea (Camellia sinensis polyphenols are potent antiinflammatory agents and have been shown to inhibit NO production in tumor cell lines. In the present study, we examined the effect of epigallocatechinp-3-gallate (EGCG), a generation of NO in HaCaT cells. Methods: HaCaT cells were treated with 10μM EGCG and 100μM NAC for 1 hour. 1 hour later, they were irradiated with 50mJ/cm^2 UVB and treated with 200 u㎍/ml LPS for 12 hours, respectively. The iNOS mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR) and NO production was assessed by spectrophotometric method based on Griess reaction. Nuclear factor κB (NF-κB) binding activity was determined by electophoretic mobility shift assay (EMSA). Results: The results were as follows 1. EGCG inhibited UVB and LPS induced expression of inducible nitric oxide synthase. 2. HaCaT cells cotreated with EGCG produced significantly less iNOS mRNA and NO compared with HaCaT cells stimulated with UVB irradiation of LPS. 3. The inhibition of iNOS mRNA and NO production correlated with the suppression of expression of NF-κB dependent gene iNOS. 4. EGCG inhibited the activation and translocation of NF-κB to the nucleus Conclusion: inhibited the activation and translocation of NF-κB to the nucleus in HaCaT cells by interfering with the activation of NF-κB through a novel mechanism. Our results further suggest that EGCG may be therapeutically effective in UVB and cytokine induced cutaneous inflammation. (Korean J Dermatol 2004;42(1):37~46)
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