TY - JOUR
T1 - Green tea extract protects human skin fibroblasts from reactive oxygen species induced necrosis
AU - Silverberg, Jonathan I.
AU - Jagdeo, Jared
AU - Patel, Mital
AU - Siegel, Daniel
AU - Brody, Neil
PY - 2011/10/1
Y1 - 2011/10/1
N2 - Oxidative damage by reactive oxygen species (ROS) plays a major role in skin aging, carcinogenesis and inflammation. Little is known about the protective effects of green tea extract (GTE) on toxic ROS-induced skin death. We use an in vitro model of normal human skin fibroblasts (AG13145) to study the effects of green tea extract (GTE) on hydrogen peroxide (H 2O 2) induced necrosis. Cell morphology, numbers, apoptosis, necrosis, and ROS were assessed by epifluorescence microscopy and flow cytometry. This study demonstrates that GTE protected from H 2O 2-induced necrosis in a dose-dependent manner, with highest dose GTE (100 ng/mL) resulting in the most protection from necrosis, as assessed by improved cell morphology, increased cell numbers, and decreased necrosis. The protective effects of GTE on H 2O 2-induced necrosis appear to be mediated directly by decreasing intracellular ROS. The present study suggests that pretreatment with high doses of GTE could protect from toxic ROS-induced injury of skin in the clinical setting. However, additional studies are necessary to determine the clinical utility of GTE for decreasing skin cell ROS, necrosis and inflammation.
AB - Oxidative damage by reactive oxygen species (ROS) plays a major role in skin aging, carcinogenesis and inflammation. Little is known about the protective effects of green tea extract (GTE) on toxic ROS-induced skin death. We use an in vitro model of normal human skin fibroblasts (AG13145) to study the effects of green tea extract (GTE) on hydrogen peroxide (H 2O 2) induced necrosis. Cell morphology, numbers, apoptosis, necrosis, and ROS were assessed by epifluorescence microscopy and flow cytometry. This study demonstrates that GTE protected from H 2O 2-induced necrosis in a dose-dependent manner, with highest dose GTE (100 ng/mL) resulting in the most protection from necrosis, as assessed by improved cell morphology, increased cell numbers, and decreased necrosis. The protective effects of GTE on H 2O 2-induced necrosis appear to be mediated directly by decreasing intracellular ROS. The present study suggests that pretreatment with high doses of GTE could protect from toxic ROS-induced injury of skin in the clinical setting. However, additional studies are necessary to determine the clinical utility of GTE for decreasing skin cell ROS, necrosis and inflammation.
UR - http://www.scopus.com/inward/record.url?scp=80054761750&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80054761750&partnerID=8YFLogxK
M3 - Article
C2 - 21968658
AN - SCOPUS:80054761750
SN - 1545-9616
VL - 10
SP - 1096
EP - 1101
JO - Journal of Drugs in Dermatology
JF - Journal of Drugs in Dermatology
IS - 10
ER -