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Jin Won Hyun - One of the best experts on this subject based on the ideXlab platform.
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articles hyperoside protects cells against gamma ray radiation induced apoptosis in hamster Lung Fibroblast
Natural product sciences, 2013Co-Authors: Mei Jing Piao, Sungwook Chae, Sam Sik Kang, Ki Cheon Kim, Suk Ju Cho, Jin Won HyunAbstract:Ionizing radiation, including that evoked by gamma (γ)-rays, induces oxidative stress through the generation of reactive oxygen species, resulting in apoptosis, or programmed cell death. This study aimed to elucidate the radioprotective effects of hyperoside (quercetin-3-O-galactoside) against γ-ray radiation-induced apoptosis in Chinese hamster Lung Fibroblasts, V79-4 and demonstrated that the compound reduced levels of intracellular reactive oxygen species in γ-ray-irradiated cells. Hyperoside also protected irradiated cells against DNA damage (evidenced by pronounced DNA tails and elevated phospho-histone H2AX and 8-oxoguanine content) and membrane lipid peroxidation. Furthermore, hyperoside prevented the γ-ray-provoked reduction in cell viability via the inhibition of apoptosis through the increased levels of Bcl-2, the decreased levels of Bax and cytosolic cytochrome c, and the decrease of the active caspase 9 and caspase 3 expression. Taken together, these results suggest that hyperoside defend cells against γ-ray radiation-induced apoptosis by inhibiting oxidative stress.
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butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Kyoung Ah Kang, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster Lung Fibroblast (V79-4) cells, butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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hyperoside prevents oxidative damage induced by hydrogen peroxide in Lung Fibroblast cells via an antioxidant effect
Biochimica et Biophysica Acta, 2008Co-Authors: Mei Jing Piao, Rui Zhang, Hee-sun Kim, Kyoung Ah Kang, Zhi Hong Wang, Ho Jin You, Ju Sun Kim, Sam Sik Kang, Jin Won HyunAbstract:Abstract We elucidated the cytoprotective effects of hyperoside (quercetin-3- O -galactoside) against hydrogen peroxide (H 2 O 2 )-induced cell damage. We found that hyperoside scavenged the intracellular reactive oxygen species (ROS) detected by fluorescence spectrometry, flow cytometry, and confocal microscopy. In addition, we found that hyperoside scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO 4 + H 2 O 2 ) in a cell-free system, which was detected by electron spin resonance (ESR) spectrometry. Hyperoside was found to inhibit H 2 O 2 -induced apoptosis in Chinese hamster Lung Fibroblast (V79-4) cells, as shown by decreased apoptotic nuclear fragmentation, decreased sub-G 1 cell population, and decreased DNA fragmentation. In addition, hyperoside pretreatment inhibited the H 2 O 2 -induced activation of caspase-3 measured in terms of levels of cleaved caspase-3. Hyperoside prevented H 2 O 2 -induced lipid peroxidation as well as protein carbonyl. In addition, hyperoside prevented the H 2 O 2 -induced cellular DNA damage, which was established by comet tail, and phospho histone H2A.X expression. Furthermore, hyperoside increased the catalase and glutathione peroxidase activities. Conversely, the catalase inhibitor abolished the cytoprotective effect of hyperoside from H 2 O 2 -induced cell damage. In conclusion, hyperoside was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing antioxidant enzyme activity.
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cytoprotective activity of carpinus tschonoskii against h o induced oxidative stress
Natural product sciences, 2007Co-Authors: Rui Zhang, Jae Woo Park, Byoungsam Yoo, Mei Jing Piao, Kyoung Ah Kang, Taekyun Shin, Young-taek Yang, Jin Won HyunAbstract:We have studied the cytoprotective effect on HO induced oxidative stress from leaves of Carpinus tschonoskii. The methanol extract of Carpinus tschonoskii was found to scavenge intracellular reactive oxygen species (ROS) using flow cytometry and confocal microscope. This extract prevented lipid peroxidation and thus reduced cell death of Chinese hamster Lung Fibroblast (V79-4) induced by HO treatment. The extract increased catalase activity and phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that Carpinus tschonoskii protects V79-4 cells against oxidative damage by HO through scavenging ROS.
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induction of antioxidant enzymes in phloroglucinol treated cells
한국환경성돌연변이·발암원학회지, 2005Co-Authors: Kyoung Ah Kang, Nam Ho Lee, Kyoung Hwa Lee, Sungwook Chae, Young Min Ham, Jong Seok Baik, Rui Zhang, Myung Sun Jung, Jin Won HyunAbstract:We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster Lung Fibroblast (V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by γ-ray radiation. In addition, phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity. Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.
Rui Zhang - One of the best experts on this subject based on the ideXlab platform.
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butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Kyoung Ah Kang, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster Lung Fibroblast (V79-4) cells, butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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hyperoside prevents oxidative damage induced by hydrogen peroxide in Lung Fibroblast cells via an antioxidant effect
Biochimica et Biophysica Acta, 2008Co-Authors: Mei Jing Piao, Rui Zhang, Hee-sun Kim, Kyoung Ah Kang, Zhi Hong Wang, Ho Jin You, Ju Sun Kim, Sam Sik Kang, Jin Won HyunAbstract:Abstract We elucidated the cytoprotective effects of hyperoside (quercetin-3- O -galactoside) against hydrogen peroxide (H 2 O 2 )-induced cell damage. We found that hyperoside scavenged the intracellular reactive oxygen species (ROS) detected by fluorescence spectrometry, flow cytometry, and confocal microscopy. In addition, we found that hyperoside scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO 4 + H 2 O 2 ) in a cell-free system, which was detected by electron spin resonance (ESR) spectrometry. Hyperoside was found to inhibit H 2 O 2 -induced apoptosis in Chinese hamster Lung Fibroblast (V79-4) cells, as shown by decreased apoptotic nuclear fragmentation, decreased sub-G 1 cell population, and decreased DNA fragmentation. In addition, hyperoside pretreatment inhibited the H 2 O 2 -induced activation of caspase-3 measured in terms of levels of cleaved caspase-3. Hyperoside prevented H 2 O 2 -induced lipid peroxidation as well as protein carbonyl. In addition, hyperoside prevented the H 2 O 2 -induced cellular DNA damage, which was established by comet tail, and phospho histone H2A.X expression. Furthermore, hyperoside increased the catalase and glutathione peroxidase activities. Conversely, the catalase inhibitor abolished the cytoprotective effect of hyperoside from H 2 O 2 -induced cell damage. In conclusion, hyperoside was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing antioxidant enzyme activity.
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cytoprotective activity of carpinus tschonoskii against h o induced oxidative stress
Natural product sciences, 2007Co-Authors: Rui Zhang, Jae Woo Park, Byoungsam Yoo, Mei Jing Piao, Kyoung Ah Kang, Taekyun Shin, Young-taek Yang, Jin Won HyunAbstract:We have studied the cytoprotective effect on HO induced oxidative stress from leaves of Carpinus tschonoskii. The methanol extract of Carpinus tschonoskii was found to scavenge intracellular reactive oxygen species (ROS) using flow cytometry and confocal microscope. This extract prevented lipid peroxidation and thus reduced cell death of Chinese hamster Lung Fibroblast (V79-4) induced by HO treatment. The extract increased catalase activity and phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that Carpinus tschonoskii protects V79-4 cells against oxidative damage by HO through scavenging ROS.
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induction of antioxidant enzymes in phloroglucinol treated cells
한국환경성돌연변이·발암원학회지, 2005Co-Authors: Kyoung Ah Kang, Nam Ho Lee, Kyoung Hwa Lee, Sungwook Chae, Young Min Ham, Jong Seok Baik, Rui Zhang, Myung Sun Jung, Jin Won HyunAbstract:We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster Lung Fibroblast (V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by γ-ray radiation. In addition, phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity. Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.
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Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in Lung Fibroblast cells.
FEBS Letters, 2005Co-Authors: Kyoung Hwa Lee, Hong-gu Joo, Sungwook Chae, Rui Zhang, Myung Sun Jung, Young-ki Lee, So Young Kim, Hee-sun Kim, Jae Woo ParkAbstract:We have investigated the cytoprotective effect of eckol, which was isolated from Ecklonia cava, against oxidative stress induced cell damage in Chinese hamster Lung Fibroblast (V79-4) cells. Eckol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl radical, hydrogen peroxide (H2O2), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, eckol reduced H2O2 induced cell death in V79-4 cells. In addition, eckol inhibited cell damage induced by serum starvation and radiation by scavenging ROS. Eckol was found to increase the activity of catalase and its protein expression. Further, molecular mechanistic study revealed that eckol increased phosphorylation of extracellular signal-regulated kinase and activity of nuclear factor κ B. Taken together, the results suggest that eckol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathway.
Robin J Mcanulty - One of the best experts on this subject based on the ideXlab platform.
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stat3 mediated signaling dysregulates Lung Fibroblast myoFibroblast activation and differentiation in uip ipf
American Journal of Pathology, 2012Co-Authors: Geoffrey J Laurent, Robin J Mcanulty, Dmitri V Pechkovsky, Cecilia M Prele, John B Wong, Cory M Hogaboam, Samuel Shaomin Zhang, Moises Selman, Steven E MutsaersAbstract:STAT3 is a latent transcription factor that plays a role in regulating Fibroblast function in fibrotic Lung diseases. To further understand the role of STAT3 in the phenotypic divergence and function of human Lung Fibroblasts (LFs), we investigated the effect of basal and cytokine-induced STAT3 activity on indices of LF differentiation and activation, including expression of α-smooth muscle actin (α-SMA), collagen, and adhesion molecules Thy-1/CD90 and α v β 3 and β 5 integrins. We identified a population of Fibroblasts from usual interstitial pneumonia (UIP)/idiopathic pulmonary fibrosis (IPF) Lungs characterized by constitutively phosphorylated STAT3, lower proliferation rates, and diminished expression of α-SMA, Thy-1/CD90, and β 3 integrins compared with control LFs. Staining of UIP Lung biopsy specimens demonstrated that phosphorylated STAT3 was not present in α-SMA–positive Fibroblastic foci but was observed in the nuclei of cells located in the areas of dense fibrosis. STAT3 activation in LFs did not significantly influence basal or transforming growth factor β 1 –induced collagen I expression but inhibited expression of α-SMA, Thy-1/CD90, and αv β 3 integrins. Suppression of STAT3 signaling diminished resistance of IPF LFs to staurosporine-induced apoptosis and responsiveness to transforming growth factor β 1 but increased basal α-SMA and restored β 3 integrin expression in LFs via an ALK-5–dependent, SMAD3/7-independent mechanism. These data suggest that STAT3 activation regulates several pathways in human LFs associated with normal wound healing, whereas aberrant STAT3 signaling plays a critical role in UIP/IPF pathogenesis.
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mast cell tryptase stimulates human Lung Fibroblast proliferation via protease activated receptor 2
American Journal of Physiology-lung Cellular and Molecular Physiology, 2000Co-Authors: Ian A Akers, Morley D. Hollenberg, Maddy Parsons, Michael Hill, Shahin Sanjar, Geoffrey J Laurent, Robin J McanultyAbstract:Mast cells play a potentially important role in fibroproliferative diseases, releasing mediators including tryptase that are capable of stimulating Fibroblast proliferation and procollagen synthesi...
Shihchieh Hung - One of the best experts on this subject based on the ideXlab platform.
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involvement of er stress pi3k akt activation and Lung Fibroblast proliferation in bleomycin induced pulmonary fibrosis
Scientific Reports, 2017Co-Authors: Han Shui Hsu, Chen Chi Liu, Jiun Han Lin, Tien Wei Hsu, Jyuan Wei Hsu, Shihchieh HungAbstract:Pulmonary fibrosis is characterized by Fibroblast proliferation and extracellular matrix remodelling, leading to respiratory insufficiency. The mechanisms underlying this progressive and devastating disease remain unclear. Conditions that can impair the function of the endoplasmic reticulum (ER) cause accumulation of unfolded or misfolded proteins, resulting in ER stress and activation of the unfolded protein response (UPR). ER stress has been implicated in many conditions including cancer, diabetes, obesity, and inflammation. It is also involved in Lung fibrosis, through myoFibroblastic differentiation of Fibroblasts; however, the precise role of ER stress in Lung fibrosis is unknown. The current study aimed to investigate the underlying mechanisms of ER stress inhibitors in the treatment of bleomycin-induced Lung fibrosis. We demonstrated that bleomycin can activate ER stress associated proteins, including GRP78, CHOP, and ATF-4, both in vitro and in vivo. PI3K/AKT acts upstream of ER stress to affect Lung Fibroblast proliferation, resulting in bleomycin-induced pulmonary fibrosis. Treatment with ER stress inhibitors or a PI3K inhibitor caused a reduction in Fibroblast proliferation and improved pulmonary function. The relationship between PI3K/AKT/mTOR and ER stress in pulmonary fibrosis, and the application of PI3K inhibitors and ER stress inhibitors in the treatment of pulmonary fibrosis require further investigation.
Sungwook Chae - One of the best experts on this subject based on the ideXlab platform.
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articles hyperoside protects cells against gamma ray radiation induced apoptosis in hamster Lung Fibroblast
Natural product sciences, 2013Co-Authors: Mei Jing Piao, Sungwook Chae, Sam Sik Kang, Ki Cheon Kim, Suk Ju Cho, Jin Won HyunAbstract:Ionizing radiation, including that evoked by gamma (γ)-rays, induces oxidative stress through the generation of reactive oxygen species, resulting in apoptosis, or programmed cell death. This study aimed to elucidate the radioprotective effects of hyperoside (quercetin-3-O-galactoside) against γ-ray radiation-induced apoptosis in Chinese hamster Lung Fibroblasts, V79-4 and demonstrated that the compound reduced levels of intracellular reactive oxygen species in γ-ray-irradiated cells. Hyperoside also protected irradiated cells against DNA damage (evidenced by pronounced DNA tails and elevated phospho-histone H2AX and 8-oxoguanine content) and membrane lipid peroxidation. Furthermore, hyperoside prevented the γ-ray-provoked reduction in cell viability via the inhibition of apoptosis through the increased levels of Bcl-2, the decreased levels of Bax and cytosolic cytochrome c, and the decrease of the active caspase 9 and caspase 3 expression. Taken together, these results suggest that hyperoside defend cells against γ-ray radiation-induced apoptosis by inhibiting oxidative stress.
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butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Kyoung Ah Kang, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster Lung Fibroblast (V79-4) cells, butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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induction of antioxidant enzymes in phloroglucinol treated cells
한국환경성돌연변이·발암원학회지, 2005Co-Authors: Kyoung Ah Kang, Nam Ho Lee, Kyoung Hwa Lee, Sungwook Chae, Young Min Ham, Jong Seok Baik, Rui Zhang, Myung Sun Jung, Jin Won HyunAbstract:We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster Lung Fibroblast (V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by γ-ray radiation. In addition, phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity. Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.
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Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in Lung Fibroblast cells.
FEBS Letters, 2005Co-Authors: Kyoung Hwa Lee, Hong-gu Joo, Sungwook Chae, Rui Zhang, Myung Sun Jung, Young-ki Lee, So Young Kim, Hee-sun Kim, Jae Woo ParkAbstract:We have investigated the cytoprotective effect of eckol, which was isolated from Ecklonia cava, against oxidative stress induced cell damage in Chinese hamster Lung Fibroblast (V79-4) cells. Eckol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl radical, hydrogen peroxide (H2O2), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, eckol reduced H2O2 induced cell death in V79-4 cells. In addition, eckol inhibited cell damage induced by serum starvation and radiation by scavenging ROS. Eckol was found to increase the activity of catalase and its protein expression. Further, molecular mechanistic study revealed that eckol increased phosphorylation of extracellular signal-regulated kinase and activity of nuclear factor κ B. Taken together, the results suggest that eckol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathway.
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triphlorethol a from ecklonia cava protects v79 4 Lung Fibroblast against hydrogen peroxide induced cell damage
Free Radical Research, 2005Co-Authors: Kyoung Hwa Lee, Nam Ho Lee, Sungwook Chae, Youngsang Koh, Byoungsam Yoo, Ju Ho Kim, Young Min Ham, Jong Seok Baik, Jin Won HyunAbstract:In the present study, triphlorethol-A, a phlorotannin, was isolated from Ecklonia cava and its antioxidant properties were investigated. Triphlorethol-A was found to scavenge intracellular reactive oxygen species (ROS) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thus prevented lipid peroxidation. The radical scavenging activity of triphlorethol-A protected the Chinese hamster Lung Fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) against cell death, via the activation of ERK protein. Furthermore, triphlorethol-A reduced the apoptotic cells formation induced by H2O2. Triphlorethol-A increased the activities of cellular antioxidant enzymes like, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Hence, from the present study, it is suggestive that triphlorethol-A protects V79-4 cells against H2O2 damage by enhancing the cellular antioxidative activity.
