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Sang-Han Lee,Hee Jeong Kim2,Hyo Jin Kang,이윤진,남해선,배인수 한국유방암학회 2009 Journal of breast cancer Vol.12 No.3
Purpose: Estrogen is known to act as both a growth factor and a survival factor for breast cancer. The responsible molecular mechanisms remain, however, to be fully elucidated. We hypothesize that the effect of estrogen relates to its ability to induce the cellular antioxidant defense enzymes. Methods: In the presence study, we examined the ability of 17β-estradiol (E2) to regulate the level of phospholipid hydroperoxide glutathione peroxidase (GPX4) protein, which is an anti-oxidative enzyme that can directly reduce both phospholipids and cholesterol-hydroperoxides located in the cell membranes and lipoproteins. Results: E2 elicited a dose- and time-dependent increase in the GPX4 expression in the MCF-7 breast cancer cells, and this up-regulation was blocked by the free radical scavenger N-acetylcysteine (NAC). Additionally, we confirmed that E2 triggered a rapid and transient increase in the intracellular reactive oxygen species (ROS) levels, and this E2-induced increase in the ROS levels was inhibited by pretreatment with NAC. Moreover, such ROS inducers as TGF-β, TNF-αand insulin induced an increase in the level of GPX4 protein. However, estrogen receptor (ER)αknockdown by transfection with ERα-siRNA did not significantly change the GPX4 protein level that was induced by E2. Furthermore, pre-incubation with the ER antagonist ICI 182,780 did not inhibit E2-mediated GPX4 induction. Conversely, pretreatment of cells with LY294002, a pharmacological inhibitor of phosphatidylinositol 3-kinase inhibitor, suppressed the E2-augmented GPX4 expression. Conclusion: Collectively, our data show that E2 may partly provide a survival advantage through the regulation of cellular oxidative homeostasis in MCF-7 breast cancer cells.
김진우 ( Jin Woo Kim ),김선빈 ( Seon Bin Gim ),오정민 ( Jeong Min2 Oh ),윤미영 ( Mi Young Yun ),이기무 ( Ki Moo Lee ),김동희 ( Dong Hee Kim ) 대전대학교 한의학연구소 2012 혜화의학회지 Vol.20 No.2
To investigate the clinical aspects of CHT in atopic dermatitis (AD) treatments, the effect of CHT in anti-oxidative and anti-inflammatory cytokines were tested. 100% or higher cell viability was observed in all tested groups from 25 to 200 ㎍/㎖using Raw 264.7 cells. CHT showed dose-dependent DPPH scavenging activity, with more than 90% scavenging activities at 800 ㎍/㎖concentrations. CHT showed dose-dependent suppression activity of ROS production, especially at 200 ㎍/㎖of 37.5%. CHT decreased NO production activity, with significant decrease of 33.2% at 200 ㎍/㎖. IL-6, MCP-1, TNF-α production rate were decreased by approximately 25% when Raw 264.7 cells were treated with LPS and with CHT of 200 ㎍/㎖. Also, IL-1β production rate was decreased by 25% at 100 ㎍/㎖. The results above indicate that CHT significantly reduces the effect of oxidative and inflammatory cytokines. The use of CHT in dermatitis can be widely suggested.