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Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate.
Toxicol Appl Pharmacol 2001; 176(2):110-7TA

Abstract

Exposure of normal human epidermal keratinocytes (NHEK) to UVB radiation induces intracellular release of hydrogen peroxide (oxidative stress) and phosphorylation of mitogen-activated protein kinase cell signaling pathways. Here, we demonstrate that pretreatment of NHEK with (-)-epigallocatechin-3-gallate (EGCG), an antioxidant from green tea, inhibits UVB-induced hydrogen peroxide (H(2)O(2)) production and H(2)O(2)-mediated phosphorylation of MAPK signaling pathways. We found that treatment of EGCG (20 microg/ml of media) to NHEK before UVB (30 mJ/cm(2)) exposure inhibited UVB-induced H(2)O(2) production (66-80%) concomitant with the inhibition of UVB-induced phosphorylation of ERK1/2 (57-80%), JNK (53-83%), and p38 (50-77%) proteins. To demonstrate whether UVB-induced phosphorylation of MAPK occurs via UVB-induced H(2)O(2) (oxidative stress) production, NHEK were treated with the oxidant H(2)O(2). Treatment of H(2)O(2) to NHEK resulted in phosphorylation of ERK1/2, JNK, and p38. Using the same in vitro system, when these cells were pretreated with EGCG or with the known antioxidant ascorbic acid (as positive control), H(2)O(2)-induced phosphorylation of ERK1/2, JNK, and p38 was found to be significantly inhibited. These findings demonstrate that EGCG has the potential to inhibit UVB-induced oxidative stress-mediated phosphorylation of MAPK signaling pathways, suggesting that EGCG could be useful in attenuation of oxidative stress-mediated and MAPK-caused skin disorders in humans.

Authors+Show Affiliations

Department of Dermatology, Case Western Reserve University, Cleveland, Ohio 44106, USA. shatiyar@uab.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11601887

Citation

Katiyar, S K., et al. "Inhibition of UVB-induced Oxidative Stress-mediated Phosphorylation of Mitogen-activated Protein Kinase Signaling Pathways in Cultured Human Epidermal Keratinocytes By Green Tea Polyphenol (-)-epigallocatechin-3-gallate." Toxicology and Applied Pharmacology, vol. 176, no. 2, 2001, pp. 110-7.
Katiyar SK, Afaq F, Azizuddin K, et al. Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate. Toxicol Appl Pharmacol. 2001;176(2):110-7.
Katiyar, S. K., Afaq, F., Azizuddin, K., & Mukhtar, H. (2001). Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate. Toxicology and Applied Pharmacology, 176(2), pp. 110-7.
Katiyar SK, et al. Inhibition of UVB-induced Oxidative Stress-mediated Phosphorylation of Mitogen-activated Protein Kinase Signaling Pathways in Cultured Human Epidermal Keratinocytes By Green Tea Polyphenol (-)-epigallocatechin-3-gallate. Toxicol Appl Pharmacol. 2001 Oct 15;176(2):110-7. PubMed PMID: 11601887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate. AU - Katiyar,S K, AU - Afaq,F, AU - Azizuddin,K, AU - Mukhtar,H, PY - 2001/10/17/pubmed PY - 2002/1/5/medline PY - 2001/10/17/entrez SP - 110 EP - 7 JF - Toxicology and applied pharmacology JO - Toxicol. Appl. Pharmacol. VL - 176 IS - 2 N2 - Exposure of normal human epidermal keratinocytes (NHEK) to UVB radiation induces intracellular release of hydrogen peroxide (oxidative stress) and phosphorylation of mitogen-activated protein kinase cell signaling pathways. Here, we demonstrate that pretreatment of NHEK with (-)-epigallocatechin-3-gallate (EGCG), an antioxidant from green tea, inhibits UVB-induced hydrogen peroxide (H(2)O(2)) production and H(2)O(2)-mediated phosphorylation of MAPK signaling pathways. We found that treatment of EGCG (20 microg/ml of media) to NHEK before UVB (30 mJ/cm(2)) exposure inhibited UVB-induced H(2)O(2) production (66-80%) concomitant with the inhibition of UVB-induced phosphorylation of ERK1/2 (57-80%), JNK (53-83%), and p38 (50-77%) proteins. To demonstrate whether UVB-induced phosphorylation of MAPK occurs via UVB-induced H(2)O(2) (oxidative stress) production, NHEK were treated with the oxidant H(2)O(2). Treatment of H(2)O(2) to NHEK resulted in phosphorylation of ERK1/2, JNK, and p38. Using the same in vitro system, when these cells were pretreated with EGCG or with the known antioxidant ascorbic acid (as positive control), H(2)O(2)-induced phosphorylation of ERK1/2, JNK, and p38 was found to be significantly inhibited. These findings demonstrate that EGCG has the potential to inhibit UVB-induced oxidative stress-mediated phosphorylation of MAPK signaling pathways, suggesting that EGCG could be useful in attenuation of oxidative stress-mediated and MAPK-caused skin disorders in humans. SN - 0041-008X UR - https://www.unboundmedicine.com/medline/citation/11601887/Inhibition_of_UVB_induced_oxidative_stress_mediated_phosphorylation_of_mitogen_activated_protein_kinase_signaling_pathways_in_cultured_human_epidermal_keratinocytes_by_green_tea_polyphenol_____epigallocatechin_3_gallate_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-008X(01)99276-2 DB - PRIME DP - Unbound Medicine ER -