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논문분류 춘계학술대회 초록집
제목 Nicotine Induces Apoptosis in Human Proximal Tubular Cells
저자 Joon Seok Choi1, Soo Yeon Joo2, Hoon In Choi2, Chang Seong Kim1, Eun Hui Bae1, Seong Kwon Ma1, Jong Un Lee2, Soo Wan Kim1
출판정보 2013; 2013(1):
키워드 Nicotine, Apoptosis, Reactive oxygen species
초록 Background: Cigarette smoking is considered as independent risk factor for progression of chronic kidney disease and nicotine is the major compound of cigarette. The present study was aimed to investigate the effect of nicotine on renal tubular epithelial cell apoptosis in vitro and explore the potential mechanisms involved. Methods: Human proximal tubular epithelial (HK-2) cells were treated with 200 μM of nicotine. Cell viability was examined using MTT assay. The DCF-DA staining was used to measure intracellular levels of reactive oxygen species (ROS). The protein expression of extracellular signal-regulated kinase (ERK), P38 and c-Jun N-terminal kinase (JNK), NF-κB, Bax and Bcl-2 was determined by semiquantitative immunoblotting. Results: Nicotine treatment resulted in dose-dependent decreases of cell viability and increases of ROS. Nicotine increased the expression of p-ERK, p-JNK and p-P38. Nicotine induced expression of p-ERK and p-JNK in HK-2 cells, which was attenuated by pretreatement of N-acetyl-cysteine. The expression of NF-κB started to increase 1 hour after nicotine exposure. Increased nuclear NF-κB activation was counteracted by inhibitors of ERK (PD98059) or JNK (SP6 00125), but not affected by p38 MAPK inhibitor (SB203580). Nicotine decreased the expression of Bcl-2, while increased that of Bax, which was attenuated by the treatment of NF-κB inhibitor (Bay 11-7082) or N-acetyl-L-cysteine (NAC). Flow cytometry analysis revealed nicotine-induced apoptosis. Conclusion: These results suggest that nicotine induce apoptosis by increased ROS generation through activation of NF-κB and mitogen-activated protein kinase signaling pathways in HK-2 cells.
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