The Experts below are selected from a list of 2325 Experts worldwide ranked by ideXlab platform
Jing Gung Chung - One of the best experts on this subject based on the ideXlab platform.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Abstract Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 μM in human lung cancer A-549 cells. In contrast, treatment with 5–10 μM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca2+ levels and the mitochondrial membrane potential (ΔΨm), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
Song Shei Lin - One of the best experts on this subject based on the ideXlab platform.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Abstract Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 μM in human lung cancer A-549 cells. In contrast, treatment with 5–10 μM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca2+ levels and the mitochondrial membrane potential (ΔΨm), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
Helen F Galley - One of the best experts on this subject based on the ideXlab platform.
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the mitochondria targeted antioxidant mitoq protects against fluoroquinolone induced oxidative stress and mitochondrial membrane damage in human achilles tendon cells
Free Radical Research, 2009Co-Authors: Damon A Lowes, Carol Wallace, Nigel R. Webster, Michael P Murphy, Helen F GalleyAbstract:Tendinitis and tendon rupture during treatment with fluoroquinolone antibiotics is thought to be mediated via oxidative stress. This study investigated whether ciprofloxacin and moxifloxacin cause oxidative stress and mitochondrial damage in cultured normal human Achilles’ tendon cells and whether an antioxidant targeted to mitochondria (MitoQ) would protect against such damage better than a non-mitochondria targeted antioxidant. Human tendon cells from normal Achilles’ tendons were exposed to 0–0.3 mm antibiotic for 24 h and 7 days in the presence of 1 µm MitoQ or an untargeted form, idebenone. Both moxifloxacin and ciprofloxacin resulted in up to a 3-fold increase in the rate of oxidation of Dichlorodihydrofluorescein, a marker of general oxidative stress in tenocytes (p<0.0001) and loss of mitochondrial membrane permeability (p<0.001). In cells treated with MitoQ the oxidative stress was less and mitochondrial membrane potential was maintained. Mitochondrial damage to tenocytes during fluoroquinolone t...
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the mitochondria targeted antioxidant mitoq protects against fluoroquinolone induced oxidative stress and mitochondrial membrane damage in human achilles tendon cells
Free Radical Research, 2009Co-Authors: Damon A Lowes, Carol Wallace, Nigel R. Webster, Michael P Murphy, Helen F GalleyAbstract:Tendinitis and tendon rupture during treatment with fluoroquinolone antibiotics is thought to be mediated via oxidative stress. This study investigated whether ciprofloxacin and moxifloxacin cause oxidative stress and mitochondrial damage in cultured normal human Achilles' tendon cells and whether an antioxidant targeted to mitochondria (MitoQ) would protect against such damage better than a non-mitochondria targeted antioxidant. Human tendon cells from normal Achilles' tendons were exposed to 0-0.3 mM antibiotic for 24 h and 7 days in the presence of 1 microM MitoQ or an untargeted form, idebenone. Both moxifloxacin and ciprofloxacin resulted in up to a 3-fold increase in the rate of oxidation of Dichlorodihydrofluorescein, a marker of general oxidative stress in tenocytes (p<0.0001) and loss of mitochondrial membrane permeability (p<0.001). In cells treated with MitoQ the oxidative stress was less and mitochondrial membrane potential was maintained. Mitochondrial damage to tenocytes during fluoroquinolone treatment may be involved in tendinitis and tendon rupture.
Hsuan Pang Huang - One of the best experts on this subject based on the ideXlab platform.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Abstract Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 μM in human lung cancer A-549 cells. In contrast, treatment with 5–10 μM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca2+ levels and the mitochondrial membrane potential (ΔΨm), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
Jai Sing Yang - One of the best experts on this subject based on the ideXlab platform.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
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dna damage and endoplasmic reticulum stress mediated curcumin induced cell cycle arrest and apoptosis in human lung carcinoma a 549 cells through the activation caspases cascade and mitochondrial dependent pathway
Cancer Letters, 2008Co-Authors: Song Shei Lin, Hsuan Pang Huang, Jai Sing Yang, Te Chun Hsai, Chin Chung Lin, Cheng Wen Lin, Chao Lin Kuo, Gibson W Wood, Jing Gung ChungAbstract:Abstract Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 μM in human lung cancer A-549 cells. In contrast, treatment with 5–10 μM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca2+ levels and the mitochondrial membrane potential (ΔΨm), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.