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Yung-Chieh Tsai,Yen-Mei Lee,Sy-Ying Leu,Hsiao-Yen Chiang,Mao-Hsiung Yen,Pao-Yun Cheng,Chih-Hsiung Hsu 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
Leptin is a peptide hormone, which has a central role in the regulation of body weight; it also exerts many potentially atherogenic effects. Ferulic acid ethyl ester (FAEE) has been approved for antioxidant properties. The aim of this study was to investigate whether FAEE can inhibit the atherogenic effects of leptin and the possible molecular mechanism of its action. Both of cell proliferation and migration were measured when the aortic smooth muscle cell (A10 cell) treated with leptin and/or FAEE. Phosphorylated p44/42MAPK, cell cycle-regulatory protein (for example, cyclin D1, p21, p27), β-catenin and matrix metalloproteinase-9 (MMP-9) proteins levels were also measured. Results demonstrated that leptin (10, 100 ng ml−1) significantly increased the proliferation of cells and the phosphorylation of p44/42MAPK in A10 cells. The proliferative effect of leptin was significantly reduced by the pretreatment of U0126 (0.5 μM), a MEK inhibitor, in A10 cells. Meanwhile, leptin significantly increased the protein expression of cyclin D1, p21, β-catenin and decreased the expression of p27 in A10 cells. In addition, leptin (10 ng ml−1) significantly increased the migration of A10 cells and the expression of MMP-9 protein. Above effects of leptin were significantly reduced by the pretreatment of FAEE (1 and 10 μM) in A10 cells. In conclusion, FAEE exerts multiple effects on leptin-induced cell proliferation and migration, including the inhibition of p44/42MAPK phosphorylation, cell cycle-regulatory proteins and MMP-9, thereby suggesting that FAEE may be a possible therapeutic approach to the inhibition of obese vascular disease.
Hui-Ling Tung,Hsu-Mei Lee,Munkhzaya Narantsetseg 한국데이터전략학회 2024 Journal of information technology applications & m Vol.31 No.1
How to create high levels of employee engagement and how to avoid burnout in the workplace is main issue in human resource management. According to Job Demands-Resources (JD-R) model, this study aims to investigate when self-efficacy plays as a mitigator on the impact of job demand on burnout, and explains why job resources are translated into work engagement. A sample of 237 Mongolian employees is used to test hypotheses. Results show that self-efficacy does offset the relationship between job demands and burnout. Meanwhile, self-efficacy plays as a mediator on the impact of job resources on work engagement. The implications of these findings for the context of JD-R model are discussed.