Hyeon-Gyun Jo1,2, Cheol Park3, Hyesook Lee2,4, Gi-Young Kim5, Young-Sam Keum6, Jin Won Hyun7, Taeg Kyu Kwon8, Yung Hyun Choi9,10, Su Hyun Hong11,12. 1. Cheong-Choon Korean Medical Clinic, 47388, Busan, Republic of Korea. 2. Department of Biochemistry, Dong-eui University College of Korean Medicine, 47227, Busan, Republic of Korea. 3. Division of Basic Sciences, College of Liberal Studies, Dong-eui University, 47340, Busan, Republic of Korea. 4. Anti-Aging Research Center, Dong-eui University, 47340, Busan, Republic of Korea. 5. Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, 63243, Jeju, Republic of Korea. 6. College of Pharmacy and Integrated Research Institute for Drug Development, Dongguk University, 10326, Goyang, Republic of Korea. 7. Department of Biochemistry, College of Medicine, Jeju National University, 63243, Jeju, Republic of Korea. 8. Department of Immunology, School of Medicine, Keimyung University, 42601, Daegu, Republic of Korea. 9. Department of Biochemistry, Dong-eui University College of Korean Medicine, 47227, Busan, Republic of Korea. choiyh@deu.ac.kr. 10. Anti-Aging Research Center, Dong-eui University, 47340, Busan, Republic of Korea. choiyh@deu.ac.kr. 11. Department of Biochemistry, Dong-eui University College of Korean Medicine, 47227, Busan, Republic of Korea. hongsh@deu.ac.kr. 12. Anti-Aging Research Center, Dong-eui University, 47340, Busan, Republic of Korea. hongsh@deu.ac.kr.
Abstract
BACKGROUND: Coptisine is a natural alkaloid compound and is known to have multiple beneficial effects including antioxidant activity. However, whether it can protect lung fibroblasts from oxidative damage has not been studied yet. OBJECTIVES: To investigate the potential inhibitory effect of coptisine against oxidative stress in V79-4 lung fibroblast cells. METHODS: V79-4 cells were treated with H2O2 (1 mM) in the presence or absence of coptisine (50 µg/ml), N-acetyl cysteine (NAC, 10 mM) or zinc protoporphyrin IX (ZnPP, 10 µM) for the indicated times. The alleviating effects of coptisine on cytotoxicity, cell cycle arrest, apoptosis, reactive oxygen species (ROS) production, DNA damage, mitochondrial dynamics, and inhibition of ATP production against H2O2 were investigated. Western blot analysis was used to analyze the expression levels of specific proteins. RESULTS: Coptisine inhibited H2O2-induced cytotoxicity and DNA damage by blocking abnormal ROS generation. H2O2 treatment caused cell cycle arrest at the G2/M phase accompanied by increased expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1 and decreased expression of cyclin B1 and cyclin A. However, these effects were attenuated in the presence of coptisine or NAC. Coptisine also prevented apoptosis by decreasing the rate of Bax/Bcl-2 expression in H2O2-stimulated cells and suppressing the loss of mitochondrial membrane potential and the cytosolic release of cytochrome c. In addition, the activation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was markedly promoted by coptisine in the presence of H2O2. However, zinc protoporphyrin IX, a potent inhibitor of HO-1, attenuated the ROS scavenging and anti-apoptotic effects of coptisine. CONCLUSIONS: Based on current data, we suggest that coptisine can be used as a potential treatment for oxidative stress-related lung disease.
BACKGROUND:Coptisine is a natural alkaloid compound and is known to have multiple beneficial effects including antioxidant activity. However, whether it can protect lung fibroblasts from oxidative damage has not been studied yet. OBJECTIVES: To investigate the potential inhibitory effect of coptisine against oxidative stress in V79-4 lung fibroblast cells. METHODS: V79-4 cells were treated with H2O2 (1 mM) in the presence or absence of coptisine (50 µg/ml), N-acetyl cysteine (NAC, 10 mM) or zinc protoporphyrin IX (ZnPP, 10 µM) for the indicated times. The alleviating effects of coptisine on cytotoxicity, cell cycle arrest, apoptosis, reactive oxygen species (ROS) production, DNA damage, mitochondrial dynamics, and inhibition of ATP production against H2O2 were investigated. Western blot analysis was used to analyze the expression levels of specific proteins. RESULTS:Coptisine inhibited H2O2-induced cytotoxicity and DNA damage by blocking abnormal ROS generation. H2O2 treatment caused cell cycle arrest at the G2/M phase accompanied by increased expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1 and decreased expression of cyclin B1 and cyclin A. However, these effects were attenuated in the presence of coptisine or NAC. Coptisine also prevented apoptosis by decreasing the rate of Bax/Bcl-2 expression in H2O2-stimulated cells and suppressing the loss of mitochondrial membrane potential and the cytosolic release of cytochrome c. In addition, the activation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was markedly promoted by coptisine in the presence of H2O2. However, zinc protoporphyrin IX, a potent inhibitor of HO-1, attenuated the ROS scavenging and anti-apoptotic effects of coptisine. CONCLUSIONS: Based on current data, we suggest that coptisine can be used as a potential treatment for oxidative stress-related lung disease.
Entities:
Keywords:
Apoptosis; Coptisine; DNA damage; Nrf2/HO-1; ROS
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