The Experts below are selected from a list of 135 Experts worldwide ranked by ideXlab platform
In Sang Song - One of the best experts on this subject based on the ideXlab platform.
-
Chrysophanic Acid blocks proliferation of colon cancer cells by inhibiting egfr mtor pathway
Phytotherapy Research, 2011Co-Authors: In Sang SongAbstract:Inactivation of epidermal growth factor receptor (EGFR) is a prime method used in colon cancer therapy. Here it is shown that Chrysophanic Acid, a natural anthraquinone, has anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanic Acid preferentially blocked proliferation in SNU-C5 cells but not in other cell lines (HT7, HT29, KM12C, SW480, HCT116 and SNU-C4) with low levels of EGFR expression. Chrysophanic Acid treatment in SNU-C5 cells inhibited EGF-induced phosphorylation of EGFR and suppressed activation of downstream signaling molecules, such as AKT, extracellular signal-regulated kinase (ERK) and the mammalian target of rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanic Acid (80 and 120 µm) significantly blocked cell proliferation when combined with the mTOR inhibitor, rapamycin. These findings offer the first evidence of anticancer activity for Chrysophanic Acid via EGFR/mTOR mediated signaling transduction pathway. Copyright © 2010 John Wiley & Sons, Ltd.
-
Chrysophanic Acid blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway.
Phytotherapy Research, 2010Co-Authors: In Sang SongAbstract:Inactivation of epidermal growth factor receptor (EGFR) is a prime method used in colon cancer therapy. Here it is shown that Chrysophanic Acid, a natural anthraquinone, has anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanic Acid preferentially blocked proliferation in SNU-C5 cells but not in other cell lines (HT7, HT29, KM12C, SW480, HCT116 and SNU-C4) with low levels of EGFR expression. Chrysophanic Acid treatment in SNU-C5 cells inhibited EGF-induced phosphorylation of EGFR and suppressed activation of downstream signaling molecules, such as AKT, extracellular signal-regulated kinase (ERK) and the mammalian target of rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanic Acid (80 and 120 µm) significantly blocked cell proliferation when combined with the mTOR inhibitor, rapamycin. These findings offer the first evidence of anticancer activity for Chrysophanic Acid via EGFR/mTOR mediated signaling transduction pathway. Copyright © 2010 John Wiley & Sons, Ltd.
Jaeyoung Um - One of the best experts on this subject based on the ideXlab platform.
-
Chrysophanic Acid reduces testosterone induced benign prostatic hyperplasia in rats by suppressing 5α reductase and extracellular signal regulated kinase
Oncotarget, 2017Co-Authors: Donghyun Youn, Jinbong Park, Yunu Jung, Jongwook Kang, Miyoung Jeong, Gautam Sethi, Jaeyoung UmAbstract:// Dong-Hyun Youn 1, * , Jinbong Park 1, * , Hye-Lin Kim 2 , Yunu Jung 1 , JongWook Kang 1 , Mi-Young Jeong 2 , Gautam Sethi 3 , Kwang Seok Ahn 2 , Jae-Young Um 1, 2 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea 2 College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea 3 Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore * These authors have contributed equally to this work Correspondence to: Jae-Young Um, email: jyum@khu.ac.kr Keywords: benign prostatic hyperplasia-BPH, Chrysophanic Acid, prostate specific antigen, 5α-reductase, extracellular signal-regulated kinase Received: April 28, 2016 Accepted: October 31, 2016 Published: November 17, 2016 ABSTRACT Benign prostatic hyperplasia (BPH) is one of the most common chronic diseases in male population, of which incidence increases gradually with age. In this study, we investigated the effect of Chrysophanic Acid (CA) on BPH. BPH was induced by a 4-week injection of testosterone propionate (TP). Four weeks of further injection with vehicle, TP, TP + CA, TP + finasteride was carried on. In the CA treatment group, the prostate weight was reduced and the TP-induced histological changes were restored as the normal control group. CA treatment suppressed the TP-elevated prostate specific antigen (PSA) expression. In addition, 5α-reductase, a crucial factor in BPH development, was suppressed to the normal level close to the control group by CA treatment. The elevated expressions of androgen receptor (AR), estrogen receptor α and steroid receptor coactivator 1 by TP administration were also inhibited in the CA group when compared to the TP-induced BPH group. Then we evaluated the changes in three major factors of the mitogen-activated protein kinase chain during prostatic hyperplasia; extracellular signal-regulated kinase (ERK), c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38). While ERK was elevated in the process of BPH, JNK and p38 was not changed. This up-regulated ERK was also reduced as normal by CA treatment. Further in vitro studies with RWPE-1 cells confirmed TP-induced proliferation and elevated AR, PSA and p-ERK were all reduced by CA treatment. Overall, these results suggest a potential pharmaceutical feature of CA in the treatment of BPH.
-
Chrysophanic Acid suppresses adipogenesis and induces thermogenesis by activating amp activated protein kinase alpha in vivo and in vitro
Frontiers in Pharmacology, 2016Co-Authors: Jinbong Park, Donghyun Youn, Yunu Jung, Jongwook Kang, Miyoung Jeong, Seongkyu Choe, Seungheon Hong, Jaeyoung UmAbstract:Chrysophanic Acid (CA) is a member of the anthraquinone family abundant in rhubarb, a widely used herb for obesity treatment in Traditional Korean Medicine. Though several studies have indicated numerous features of CA, no study has yet reported the effect of CA on obesity. In this study, we tried to identify the anti-obesity effects of CA. By using 3T3-L1 adipocytes and primary cultured brown adipocytes as in vitro models, high-fat diet (HFD)-induced obese mice, and zebrafish as in vivo models, we determined the anti-obesity effects of CA. CA reduced weight gain in HFD-induced obese mice. They also decreased lipid accumulation and the expressions of adipogenesis factors including peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) in 3T3-L1 adipocytes. In addition, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), the brown fat specific thermogenic genes, were up-regulated in brown adipocytes by CA treatment. Furthermore, when co-treated with Compound C, the AMP-activated protein kinase (AMPK) inhibitor, CA was able to restore the activation of AMPKα in both types of adipocytes, indicating the multi-controlling effect of CA was partially via the AMPKα pathway. Given all together, these results indicate that CA can ameliorate obesity by controlling the adipogenic and thermogenic pathway at the same time. On these bases we suggest the new potential of CA as an anti-obese pharmacotherapy.
Karl Ludwig Platt - One of the best experts on this subject based on the ideXlab platform.
-
The inhibition by naphthoquinones and anthraquinones of 2-amino-3-methylimidazo[4,5-f ]quinoline metabolic activation to a mutagen: a structure-activity relationship study
Zeitschrift f�r Lebensmitteluntersuchung und -Forschung A, 1998Co-Authors: R. Edenharder, Claudia Speth, Michaela Decker, Karl Ludwig PlattAbstract:Nine naphthoquinones, 19 anthraquinones, and nine structurally related monoketonic compounds such as anthrone, xanthone, etc., inhibited mutagenicity induced by 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) in Salmonella typhimurium TA 98 in the presence of rat liver S9 with distinct structure-activity relationships. A carbonyl function was a prerequisite for antimutagenicity while, in general, anthraquinones (IC50 values: 2.3–>213 nmol/ml top agar) were more potent antimutagens than structurally related monoketonic compounds (IC50 values: 25.3–94.9 nmol/ml top agar) and naphthoquinones (IC50 values: 3.7–90.7 nmol/ml top agar). The parent compounds and methyl substituted derivatives were already the most potent while introduction of polar substituents such as COOH and SO3H considerably reduced antimutagenicity. Introduction of OH functions had equivocal effects: with increasing numbers, antimutagenic potencies were concomitantly reduced; however, anthraflavic Acid, chrysazin, quinizarin, and especially 5,8-dihydroxy-1,4-naphthoquinone were more potent than the parent compounds. The patterns of inhibition by quinones of 7-ethoxyresorufin-O-dealkylase activities in rat liver microsomes, linked to cytochrome P-450-dependent oxidation of IQ to N-hydroxy-IQ (N-OH-IQ), were in general identical with those obtained in the Salmonella/reversion assay except for Chrysophanic Acid, emodin, and some naphthoquinones which were very potent in this assay (IC50: 0.20–45.0 μM). On the other hand, mutagenicity of N-OH-IQ in S. typhimurium TA 98NR was not inhibited by nonpolar quinones (except 1,4-naphthoquinone) but rather by polar compounds and especially by hydroxyquinones (IC50 values: 5.3–106.7 nmol/ml top agar or not reached). Inhibition of mutagenic activities of IQ, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline, 2-amino-6-methyldipyrido[1,2-a:3′,2′-d]imidazole, and 3-amino-1-methyl-5H-pyrido[4,3-b]indole by chrysazin, Chrysophanic Acid, physicon, and purpurin varied, but no clearcut structure-activity relationships of the mutagens were observed.
-
The inhibition by naphthoquinones and anthraquinones of 2-amino-3-methylimidazo[4,5-f ]quinoline metabolic activation to a mutagen: a structure-activity relationship study
Zeitschrift für Lebensmitteluntersuchung und -Forschung A, 1998Co-Authors: R. Edenharder, Claudia Speth, Michaela Decker, Karl Ludwig PlattAbstract:Nine naphthoquinones, 19 anthraquinones, and nine structurally related monoketonic compounds such as anthrone, xanthone, etc., inhibited mutagenicity induced by 2-amino-3-methylimidazo[4,5- f ]quinoline (IQ) in Salmonella typhimurium TA 98 in the presence of rat liver S9 with distinct structure-activity relationships. A carbonyl function was a prerequisite for antimutagenicity while, in general, anthraquinones (IC_50 values: 2.3–>213 nmol/ml top agar) were more potent antimutagens than structurally related monoketonic compounds (IC_50 values: 25.3–94.9 nmol/ml top agar) and naphthoquinones (IC_50 values: 3.7–90.7 nmol/ml top agar). The parent compounds and methyl substituted derivatives were already the most potent while introduction of polar substituents such as COOH and SO_3H considerably reduced antimutagenicity. Introduction of OH functions had equivocal effects: with increasing numbers, antimutagenic potencies were concomitantly reduced; however, anthraflavic Acid, chrysazin, quinizarin, and especially 5,8-dihydroxy-1,4-naphthoquinone were more potent than the parent compounds. The patterns of inhibition by quinones of 7-ethoxyresorufin- O -dealkylase activities in rat liver microsomes, linked to cytochrome P-450-dependent oxidation of IQ to N -hydroxy-IQ (N-OH-IQ), were in general identical with those obtained in the Salmonella /reversion assay except for Chrysophanic Acid, emodin, and some naphthoquinones which were very potent in this assay (IC_50: 0.20–45.0 μM). On the other hand, mutagenicity of N-OH-IQ in S. typhimurium TA 98NR was not inhibited by nonpolar quinones (except 1,4-naphthoquinone) but rather by polar compounds and especially by hydroxyquinones (IC_50 values: 5.3–106.7 nmol/ml top agar or not reached). Inhibition of mutagenic activities of IQ, 2-amino-3,8-dimethylimidazo[4,5- f ]quinoxaline, 2-amino-6-methyldipyrido[1,2- a :3′,2′- d ]imidazole, and 3-amino-1-methyl-5 H -pyrido[4,3- b ]indole by chrysazin, Chrysophanic Acid, physicon, and purpurin varied, but no clearcut structure-activity relationships of the mutagens were observed.
Jinbong Park - One of the best experts on this subject based on the ideXlab platform.
-
Chrysophanic Acid reduces testosterone induced benign prostatic hyperplasia in rats by suppressing 5α reductase and extracellular signal regulated kinase
Oncotarget, 2017Co-Authors: Donghyun Youn, Jinbong Park, Yunu Jung, Jongwook Kang, Miyoung Jeong, Gautam Sethi, Jaeyoung UmAbstract:// Dong-Hyun Youn 1, * , Jinbong Park 1, * , Hye-Lin Kim 2 , Yunu Jung 1 , JongWook Kang 1 , Mi-Young Jeong 2 , Gautam Sethi 3 , Kwang Seok Ahn 2 , Jae-Young Um 1, 2 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea 2 College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea 3 Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore * These authors have contributed equally to this work Correspondence to: Jae-Young Um, email: jyum@khu.ac.kr Keywords: benign prostatic hyperplasia-BPH, Chrysophanic Acid, prostate specific antigen, 5α-reductase, extracellular signal-regulated kinase Received: April 28, 2016 Accepted: October 31, 2016 Published: November 17, 2016 ABSTRACT Benign prostatic hyperplasia (BPH) is one of the most common chronic diseases in male population, of which incidence increases gradually with age. In this study, we investigated the effect of Chrysophanic Acid (CA) on BPH. BPH was induced by a 4-week injection of testosterone propionate (TP). Four weeks of further injection with vehicle, TP, TP + CA, TP + finasteride was carried on. In the CA treatment group, the prostate weight was reduced and the TP-induced histological changes were restored as the normal control group. CA treatment suppressed the TP-elevated prostate specific antigen (PSA) expression. In addition, 5α-reductase, a crucial factor in BPH development, was suppressed to the normal level close to the control group by CA treatment. The elevated expressions of androgen receptor (AR), estrogen receptor α and steroid receptor coactivator 1 by TP administration were also inhibited in the CA group when compared to the TP-induced BPH group. Then we evaluated the changes in three major factors of the mitogen-activated protein kinase chain during prostatic hyperplasia; extracellular signal-regulated kinase (ERK), c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38). While ERK was elevated in the process of BPH, JNK and p38 was not changed. This up-regulated ERK was also reduced as normal by CA treatment. Further in vitro studies with RWPE-1 cells confirmed TP-induced proliferation and elevated AR, PSA and p-ERK were all reduced by CA treatment. Overall, these results suggest a potential pharmaceutical feature of CA in the treatment of BPH.
-
Chrysophanic Acid suppresses adipogenesis and induces thermogenesis by activating amp activated protein kinase alpha in vivo and in vitro
Frontiers in Pharmacology, 2016Co-Authors: Jinbong Park, Donghyun Youn, Yunu Jung, Jongwook Kang, Miyoung Jeong, Seongkyu Choe, Seungheon Hong, Jaeyoung UmAbstract:Chrysophanic Acid (CA) is a member of the anthraquinone family abundant in rhubarb, a widely used herb for obesity treatment in Traditional Korean Medicine. Though several studies have indicated numerous features of CA, no study has yet reported the effect of CA on obesity. In this study, we tried to identify the anti-obesity effects of CA. By using 3T3-L1 adipocytes and primary cultured brown adipocytes as in vitro models, high-fat diet (HFD)-induced obese mice, and zebrafish as in vivo models, we determined the anti-obesity effects of CA. CA reduced weight gain in HFD-induced obese mice. They also decreased lipid accumulation and the expressions of adipogenesis factors including peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) in 3T3-L1 adipocytes. In addition, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), the brown fat specific thermogenic genes, were up-regulated in brown adipocytes by CA treatment. Furthermore, when co-treated with Compound C, the AMP-activated protein kinase (AMPK) inhibitor, CA was able to restore the activation of AMPKα in both types of adipocytes, indicating the multi-controlling effect of CA was partially via the AMPKα pathway. Given all together, these results indicate that CA can ameliorate obesity by controlling the adipogenic and thermogenic pathway at the same time. On these bases we suggest the new potential of CA as an anti-obese pharmacotherapy.
Jungsup Choi - One of the best experts on this subject based on the ideXlab platform.
-
herbicidal activity of natural compound Chrysophanic Acid under the greenhouse condition
Korean Journal of Weed Science, 2011Co-Authors: Chungkil Kang, Mooki Hong, Jungsup ChoiAbstract:A series of experiments was conducted to investigate the herbicidal activity of natural compound Chrysophanic Acid under the greenhouse condition in 16 weed species. Chrysophanic Acid showed non-selective herbicidal activity. While Chrysophanic Acid exhibited severe injury by foliar treatment, little or no injury was found by the soil treatment. Among the tested weeds, the most effective activity was found in grass and broad leaf weeds, a lower significant difference in herbicidal activity was found in sedge. At early post-emergence, weeds appeared to be very susceptible to Chrysophanic Acid with . The higher the natural compound concentrations, the lower weed growth. At middle post-emergence, weeds appeared to be very effective to Chrysophanic Acid with .
-
herbicidal activity of Chrysophanic Acid in semi field condition
Korean Journal of Weed Science, 2010Co-Authors: Jungsup Choi, Hyunwoo Jang, Hyunjin Hwang, Jaechul ChunAbstract:ABSTRACT Herbicidal activity and characteristics of Chrysophanic Acid were investigated in semi-field condition. At early and middle post-emergence, Trifolium repens appeared to be very susceptible to Chrysophanic Acid of 2,000 μg mL -1 . However, herbicidal activity of Chrysophanic Acid of 2,000 μg mL -1 estimated by visual injury to Artemisia princeps was not caused considerable phytotoxicity. Also by foliar application, the concentration of crysophanic Acid for effectively control to Polygonum aviculare was much higher than 2,000 μg mL -1 . Herbicidal activity of Chrysophanic Acid to Echinochloa crus-galli, Cypres difformis, Setaria viridis, Digitaria sangguinalis, Bidens tripartita by foliar application was more effective at concentration ranges from 4,000 to 6,000 μg mL -1 . These results suggest that Chrysophanic Acid demanded for higher than 2,000 μg mL -1 to successful weed control in the field condition.Key words: Chrysophanic Acid; impermeability; natural herbicide; semi-field condition; treatment dosage.
-
herbicidal activity of natural product Chrysophanic Acid
Korean Journal of Weed Science, 2010Co-Authors: Hyunwoo Jang, Hyunjin Hwang, Jaechul Chun, Jungsup ChoiAbstract:Herbicidal characterisitcs of natural product Chrysophanic Acid were investigated in a greenhouse condition. At early- and middle-stage post-emergence treatments, several grasses and broadleaf weeds appeared to be very susceptible to Chrysophanic Acid. However, any significant herbicidal activity treated by pre-emergence did not occur at concentration ranges from 31.3 to 1,000 ug . Herbicidal activity of Chrysophanic Acid estimated by visual injury for large crabgrass was much higher when applied at 7 to 14 days after seeding than at 21 and 28 days after seeding. By post-emergence treatment, Chrysophanic Acid caused very considerable phytotoxicity on several grasses and broadleaf crops. In herbicidal interaction experiments determined by Colby`s method, the effect of Chrysophanic Acid and caryophyllene oxide tank-mixture showed very high synergistic activity. Although Chrysophanic Acid did not give any pre-emergence effect, herbicidal spectrum tended to be very wide and strong when treated by post-emergence. These results suggest that Chrysophanic Acid possesses a possible potential to develop as a natural herbicide.