The Experts below are selected from a list of 1815 Experts worldwide ranked by ideXlab platform
Jae Myung Cha - One of the best experts on this subject based on the ideXlab platform.
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amelioration of trinitrobenzene sulfonic acid induced colitis in mice by Liquiritigenin
Journal of Gastroenterology and Hepatology, 2015Co-Authors: Joon Ki Min, Chi Hoon Lee, Seeun Jang, Jaewoo Park, Sungjig Lim, Donghyun Kim, Hyunsu Bae, Hyojong Kim, Jae Myung ChaAbstract:Background and Aim The anti-inflammatory effects of Liquiritigenin, a major flavonoid isolated from Glycyrrhizae uralensis, have been reported in many inflammation models. However, its protective effects have not been reported in a colitis model. This study investigated the anti-inflammatory effect and mechanism of Liquiritigenin for trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods Male mice imprinting control regions (ICR) were randomly divided into five groups: normal, TNBS-induced colitis, colitis treated with Liquiritigenin at low dose (10 mg/kg) and high dose (20 mg/kg), or mesalazine (10 mg/kg). TNBS colitis induction was performed except for in the normal group, and they were treated with Liquiritigenin or mesalazine except control group. The treatment effect was measured after three days treatment, by body weight, colon length, macroscopic score, histological score, levels of cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10) in colon tissue as well as the nuclear factor kappa-light-chain-enhancer pathway of activated B cells (NF-κB) activation. Results Mice treated with high-dose Liquiritigenin showed significant body weight gain, inhibition of colon shortening, protective effect on histological damages, and myeloperoxidase activity of colon tissue compared with the control group. Furthermore, mice treated with high-dose Liquiritigenin experienced significantly suppressed tumor necrosis factor-α, IL-1β, and IL-6 as well as enhanced IL-10 expression (all P < 0.05). High-dose Liquiritigenin treatment group showed significant decreases in TNBS-induced phosphorylation of IKKβ, p65, and IκB-α. Conclusion Liquiritigenin may ameliorate TNBS-induced colitis in mice by suppressing expression of pro-inflammatory cytokines through NF-κB pathway.
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Amelioration of trinitrobenzene sulfonic acid-induced colitis in mice by Liquiritigenin.
Journal of gastroenterology and hepatology, 2015Co-Authors: Joon Ki Min, Chi Hoon Lee, Seeun Jang, Jaewoo Park, Sungjig Lim, Donghyun Kim, Hyunsu Bae, Hyojong Kim, Jae Myung ChaAbstract:Background and Aim The anti-inflammatory effects of Liquiritigenin, a major flavonoid isolated from Glycyrrhizae uralensis, have been reported in many inflammation models. However, its protective effects have not been reported in a colitis model. This study investigated the anti-inflammatory effect and mechanism of Liquiritigenin for trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods Male mice imprinting control regions (ICR) were randomly divided into five groups: normal, TNBS-induced colitis, colitis treated with Liquiritigenin at low dose (10 mg/kg) and high dose (20 mg/kg), or mesalazine (10 mg/kg). TNBS colitis induction was performed except for in the normal group, and they were treated with Liquiritigenin or mesalazine except control group. The treatment effect was measured after three days treatment, by body weight, colon length, macroscopic score, histological score, levels of cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10) in colon tissue as well as the nuclear factor kappa-light-chain-enhancer pathway of activated B cells (NF-κB) activation. Results Mice treated with high-dose Liquiritigenin showed significant body weight gain, inhibition of colon shortening, protective effect on histological damages, and myeloperoxidase activity of colon tissue compared with the control group. Furthermore, mice treated with high-dose Liquiritigenin experienced significantly suppressed tumor necrosis factor-α, IL-1β, and IL-6 as well as enhanced IL-10 expression (all P
Gang Chen - One of the best experts on this subject based on the ideXlab platform.
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Liquiritigenin reverses depression like behavior in unpredictable chronic mild stress induced mice by regulating pi3k akt mtor mediated bdnf trkb pathway
Behavioural Brain Research, 2016Co-Authors: Weiwei Tao, Jinao Duan, Yu Dong, Hanqing Wang, Yanyan Chen, Wenda Xue, Chang Chen, Baomei Xia, Gang ChenAbstract:Major depression is a common long-lasting or recurrent psychiatric disease with high lifetime prevalence and high incidence of suicide. The main purpose of the current study was to verify whether Liquiritigenin conferred an antidepressant-like effect on the depressive mouse model established by unpredictable chronic mild stress (UCMS) and explore its possible mechanism. The results of depression-related behaviors including sucrose preference test (SPT), open field test (OFT), forced swimming test (FST) and tail suspension test (TST) indicated that both Liquiritigenin (7.5mg/kg, 15mg/kg) and fluoxetine (20mg/kg) dramatically improved the depression symptoms. Enzyme-linked immunosorbent assay (ELISA) revealed that treatment with Liquiritigenin significantly reduced the concentrations of pro-inflammatory cytokines including interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α in serum and hippocampus. Compared with the UCMS group, the administrations of Liquiritigenin, increased levels of superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and decreased Malondialdehyde (MDA) content. Meanwhile, glucocorticoids (GC) content was reduced in the Liquiritigenin group, which suggested that Liquiritigenin exhibiting the ameliorative effect on activated hypothalamic-pituitary-adrenal (HPA) axis stimulated with UCMS. Mice treated with Liquiritigenin showed restored levels of neurotransmitter norepinephrine (NE) and serotonin (5-HT). Western blot analysis displayed up-regulated expressions of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, p- mammalian target of rapamycin (mTOR), p-tropomyosin-related kinase B (TrkB), brain-derived neurotrophic factor (BDNF). Thus, it was supposed that Liquiritigenin might be useful for the treatment of chronic depression possibly through PI3K/Akt/mTOR mediated BDNF/TrkB pathway.
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Liquiritigenin reverses depression-like behavior in unpredictable chronic mild stress-induced mice by regulating PI3K/Akt/mTOR mediated BDNF/TrkB pathway.
Behavioural brain research, 2016Co-Authors: Weiwei Tao, Jinao Duan, Yu Dong, Hanqing Wang, Yanyan Chen, Wenda Xue, Chang Chen, Baomei Xia, Gang ChenAbstract:Major depression is a common long-lasting or recurrent psychiatric disease with high lifetime prevalence and high incidence of suicide. The main purpose of the current study was to verify whether Liquiritigenin conferred an antidepressant-like effect on the depressive mouse model established by unpredictable chronic mild stress (UCMS) and explore its possible mechanism. The results of depression-related behaviors including sucrose preference test (SPT), open field test (OFT), forced swimming test (FST) and tail suspension test (TST) indicated that both Liquiritigenin (7.5mg/kg, 15mg/kg) and fluoxetine (20mg/kg) dramatically improved the depression symptoms. Enzyme-linked immunosorbent assay (ELISA) revealed that treatment with Liquiritigenin significantly reduced the concentrations of pro-inflammatory cytokines including interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α in serum and hippocampus. Compared with the UCMS group, the administrations of Liquiritigenin, increased levels of superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and decreased Malondialdehyde (MDA) content. Meanwhile, glucocorticoids (GC) content was reduced in the Liquiritigenin group, which suggested that Liquiritigenin exhibiting the ameliorative effect on activated hypothalamic-pituitary-adrenal (HPA) axis stimulated with UCMS. Mice treated with Liquiritigenin showed restored levels of neurotransmitter norepinephrine (NE) and serotonin (5-HT). Western blot analysis displayed up-regulated expressions of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, p- mammalian target of rapamycin (mTOR), p-tropomyosin-related kinase B (TrkB), brain-derived neurotrophic factor (BDNF). Thus, it was supposed that Liquiritigenin might be useful for the treatment of chronic depression possibly through PI3K/Akt/mTOR mediated BDNF/TrkB pathway.
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Protective effect of Liquiritigenin on depressive-like behavior in mice after lipopolysaccharide administration
Psychiatry research, 2016Co-Authors: Weiwei Tao, Huang Huang, Xing Chu, Gang ChenAbstract:Liquiritigenin (Liq), the main active ingredient of traditional Chinese medicine licorice, possesses anti-inflammatory and neuroprotective properties. The current investigation was designed to explore whether Liquiritigenin could relieve lipopolysaccharide (LPS)-induced depression-like behavior in mice and the underlying mechanism. Liquiritigenin (7.5mg/kg, 15mg/kg) and fluoxetine (20mg/kg) were pretreated intragastrically once daily for 7 consecutive days. LPS (0.5mg/kg) was injected subcutaneously to establish the depression model 30min after pretreatment on day 7. Interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels in serum and hippocampus were detected by enzyme-linked immunosorbent assay (ELISA). Behavioral assessment was conduct 24h post LPS injection. The expressions of p65NF-κB, IκBα, brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase B (TrkB) in hippocampus were determined by western blot. The obtained results showed that Liquiritigenin effectively reduced the levels of pro-inflammatory cytokines and the expressions of p-p65NF-κB and p-IκBα. Furthermore, Liquiritigenin preconditioning could down-regulate the immobility time in tail suspension test (TST), forced swimming test (FST) and up-regulate BDNF and TrkB contents in hippocampus. Thus, it is assumed that the antidepressant activity of Liquiritigenin might be attributed to its anti-inflammatory property and BDNF/TrkB signaling pathway.
Li Bo Zou - One of the best experts on this subject based on the ideXlab platform.
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Liquiritigenin Attenuates Alzheimer’s-Like Neuropathology in an Amyloid Protein Precursor Transgenic Mouse Model and the Underlying Mechanisms
Drug Development - A Case Study Based Insight into Modern Strategies, 2011Co-Authors: Rui Ting Liu, Jin Tian Tang, Li Bo ZouAbstract:Estrogen plays a key regulatory role in a number of biological processes and, in addition to its classic function as a sex hormone, it has been linked to neurodegenerative diseases, including Alzheimer's disease (AD) (Wickelgren, 1997; Brann et al., 2007; Zhang et al., 2007). However, long-term compliance with estrogen therapy is often estimated to be no more than 15%–40%, due to its undesirable side-effects, such as an increased risk of developing breast and uterine cancer (Warren, 2004). Therefore, the body of recent research has focused on finding neuro-selective estrogen receptor agonists (Zhao et al., 2005) that mimic the beneficial effects of estrogen in the brain but which also exert negligible adverse effects on non-neural estrogen-responsive tissues. For instance, propylpyrazole triol and diarylpropionitrile – each of which exhibits relative specificity for the estrogen receptors ER┙ and ER┚ respectively – have been proven to differentially regulate AD-like changes in female AD model mice (Carroll and Pike, 2008). Additionally, some phytoestrogens with fewer side-effects and potential neuroprotective effects have been developed for use in alternative treatment strategies (Zhao et al., 2002; Bang et al., 2004). Liquiritigenin (7, 4’-dihydroxyflavanone) is a flavonoid extracted from the radix of Glycyrrhiza, an herbal that is frequently used to treat injury or swelling, or for detoxification in traditional Oriental medicine. Liquiritigenin is also one of the major active compounds of MF101 (Kupfer et al., 2008), an herbal extract currently used in clinical trials for the treatment of hot flushes and night-sweats in post-menopausal women. Our interest in Liquiritigenin is based upon the following observations. First, Liquiritigenin is shown to be a selective agonist of estrogen receptor-┚ (ER┚) (Mersereau et al., 2008). ER┚ is expressed in the brain centre related to learning and memory, but it is unlikely to be related to sex (Shughrue et al., 1997; Gustafsson et al., 2003). Second, studies have already proven that Liquiritigenin exerts cytoprotective effects in vitro and in vivo (Kim et al., 2004; Kim et al.,
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Liquiritigenin attenuates the learning and memory deficits in an amyloid protein precursor transgenic mouse model and the underlying mechanisms
European Journal of Pharmacology, 2011Co-Authors: Rui Ting Liu, Jin Tian Tang, Li Bo ZouAbstract:The present paper is to examine whether Liquiritigenin is able to attenuate the Alzheimer's-like learning and memory deficits in a transgenic (Tg) mouse model that over-expresses amyloid protein precursor (APP), and explores the underlying mechanisms. Consistent with our previous observations, we found that treatment with Liquiritigenin improved the behavioral performance of Tg mice and it attenuated the protein expression of oligomeric form of amyloid β-peptide (Aβ). Furthermore, treatment with Liquiritigenin inhibited astrocytosis in the hippocampus, and it may through its inhibitory activities on Notch-2, an important molecular regulating neural proliferation and differentiation. These findings provide evidence for beneficial activity of Liquiritigenin in a mouse model of Alzheimer's disease and support the continued investigation of Notch signaling pathway as a target for treatment of Alzheimer's disease.
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Promotion of rat brain-derived progenitor cell neurogenesis by Liquiritigenin treatment: underlying mechanisms.
Neuroscience letters, 2010Co-Authors: Rui Ting Liu, Li Bo ZouAbstract:The purpose of the present study was to determine if Liquiritigenin, which is a newly discovered estrogen receptor β (ERβ) agonist, can induce differentiation of brain-derived progenitor cells from rats and to investigate the mechanisms involved. Treatment of brain-derived progenitor cell cultures with Liquiritigenin increased the number of cells that differentiated into neurons; but the treatment did not alter the growth of astrocytes. Furthermore, treatment with Liquiritigenin decreased Notch-2 mRNA and protein expression, which could promote the growth of new neurons. Using RNA interference (RNAi), we determined that inhibition of Notch-2 by Liquiritigenin was probably ERβ-dependent. These findings highlight the possible role of Liquiritigenin in the repair and regeneration of injured brain tissue of patients with neurodegenerative diseases and support further investigation of the Notch-2 signaling pathway using ERβ agonists.
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effects of Liquiritigenin treatment on the learning and memory deficits induced by amyloid β peptide 25 35 in rats
Behavioural Brain Research, 2010Co-Authors: Rui Ting Liu, Li Bo ZouAbstract:Considerable evidence has emerged supporting the neuroprotective and cognition-preserving effects of estrogen, but these benefits are complicated by the evidence that estrogen increases the risk of certain cancers. Selective estrogen receptor modulators (SERMs) that specifically target the brain while avoiding peripheral organs offer a way to allow the application of estrogen treatment to neurodegenerative diseases with fewer undesirable effects. In an attempt to find such estrogen substitutes, Liquiritigenin was discovered as a relatively selective estrogen receptor beta (ERbeta) agonist. In the present study, we extend our previous findings to investigate the effects of Liquiritigenin on the learning and memory deficits and related neuropathology in Abeta(25-35) hippocampal-injected rats. Our results show that Liquiritigenin treatment improves the behavioral performance of the model rats and attenuates neuronal loss in the brain. More importantly, Liquiritigenin treatment decreases mRNA levels and protein expression of Notch-2, an effect that could promote the generation of new neurons. These findings provide evidence for the beneficial activity of Liquiritigenin in a brain-injured rat model and support the continued investigation of SERMs such as Liquiritigenin as an alternative to estrogen-based hormone therapy in reducing the risk of neurodegenerative diseases such as Alzheimer's disease.
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Effects of Liquiritigenin treatment on the learning and memory deficits induced by amyloid β-peptide (25–35) in rats
Behavioural brain research, 2010Co-Authors: Rui Ting Liu, Li Bo ZouAbstract:Considerable evidence has emerged supporting the neuroprotective and cognition-preserving effects of estrogen, but these benefits are complicated by the evidence that estrogen increases the risk of certain cancers. Selective estrogen receptor modulators (SERMs) that specifically target the brain while avoiding peripheral organs offer a way to allow the application of estrogen treatment to neurodegenerative diseases with fewer undesirable effects. In an attempt to find such estrogen substitutes, Liquiritigenin was discovered as a relatively selective estrogen receptor beta (ERbeta) agonist. In the present study, we extend our previous findings to investigate the effects of Liquiritigenin on the learning and memory deficits and related neuropathology in Abeta(25-35) hippocampal-injected rats. Our results show that Liquiritigenin treatment improves the behavioral performance of the model rats and attenuates neuronal loss in the brain. More importantly, Liquiritigenin treatment decreases mRNA levels and protein expression of Notch-2, an effect that could promote the generation of new neurons. These findings provide evidence for the beneficial activity of Liquiritigenin in a brain-injured rat model and support the continued investigation of SERMs such as Liquiritigenin as an alternative to estrogen-based hormone therapy in reducing the risk of neurodegenerative diseases such as Alzheimer's disease.
Joon Ki Min - One of the best experts on this subject based on the ideXlab platform.
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amelioration of trinitrobenzene sulfonic acid induced colitis in mice by Liquiritigenin
Journal of Gastroenterology and Hepatology, 2015Co-Authors: Joon Ki Min, Chi Hoon Lee, Seeun Jang, Jaewoo Park, Sungjig Lim, Donghyun Kim, Hyunsu Bae, Hyojong Kim, Jae Myung ChaAbstract:Background and Aim The anti-inflammatory effects of Liquiritigenin, a major flavonoid isolated from Glycyrrhizae uralensis, have been reported in many inflammation models. However, its protective effects have not been reported in a colitis model. This study investigated the anti-inflammatory effect and mechanism of Liquiritigenin for trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods Male mice imprinting control regions (ICR) were randomly divided into five groups: normal, TNBS-induced colitis, colitis treated with Liquiritigenin at low dose (10 mg/kg) and high dose (20 mg/kg), or mesalazine (10 mg/kg). TNBS colitis induction was performed except for in the normal group, and they were treated with Liquiritigenin or mesalazine except control group. The treatment effect was measured after three days treatment, by body weight, colon length, macroscopic score, histological score, levels of cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10) in colon tissue as well as the nuclear factor kappa-light-chain-enhancer pathway of activated B cells (NF-κB) activation. Results Mice treated with high-dose Liquiritigenin showed significant body weight gain, inhibition of colon shortening, protective effect on histological damages, and myeloperoxidase activity of colon tissue compared with the control group. Furthermore, mice treated with high-dose Liquiritigenin experienced significantly suppressed tumor necrosis factor-α, IL-1β, and IL-6 as well as enhanced IL-10 expression (all P < 0.05). High-dose Liquiritigenin treatment group showed significant decreases in TNBS-induced phosphorylation of IKKβ, p65, and IκB-α. Conclusion Liquiritigenin may ameliorate TNBS-induced colitis in mice by suppressing expression of pro-inflammatory cytokines through NF-κB pathway.
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Amelioration of trinitrobenzene sulfonic acid-induced colitis in mice by Liquiritigenin.
Journal of gastroenterology and hepatology, 2015Co-Authors: Joon Ki Min, Chi Hoon Lee, Seeun Jang, Jaewoo Park, Sungjig Lim, Donghyun Kim, Hyunsu Bae, Hyojong Kim, Jae Myung ChaAbstract:Background and Aim The anti-inflammatory effects of Liquiritigenin, a major flavonoid isolated from Glycyrrhizae uralensis, have been reported in many inflammation models. However, its protective effects have not been reported in a colitis model. This study investigated the anti-inflammatory effect and mechanism of Liquiritigenin for trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods Male mice imprinting control regions (ICR) were randomly divided into five groups: normal, TNBS-induced colitis, colitis treated with Liquiritigenin at low dose (10 mg/kg) and high dose (20 mg/kg), or mesalazine (10 mg/kg). TNBS colitis induction was performed except for in the normal group, and they were treated with Liquiritigenin or mesalazine except control group. The treatment effect was measured after three days treatment, by body weight, colon length, macroscopic score, histological score, levels of cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10) in colon tissue as well as the nuclear factor kappa-light-chain-enhancer pathway of activated B cells (NF-κB) activation. Results Mice treated with high-dose Liquiritigenin showed significant body weight gain, inhibition of colon shortening, protective effect on histological damages, and myeloperoxidase activity of colon tissue compared with the control group. Furthermore, mice treated with high-dose Liquiritigenin experienced significantly suppressed tumor necrosis factor-α, IL-1β, and IL-6 as well as enhanced IL-10 expression (all P
Yun-qing Cai - One of the best experts on this subject based on the ideXlab platform.
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Liquiritigenin inhibits serum induced hif 1α and vegf expression via the akt mtor p70s6k signalling pathway in hela cells
Phytotherapy Research, 2012Co-Authors: Sirou Xie, Yu Wang, Changwei Liu, Kang Luo, Yun-qing CaiAbstract:Liquiritigenin (LQ) is a non-toxic dietary flavonoid with chemopreventive and anticancer properties. However, the mechanism of its antiangiogenesis remains unclear. Hypoxia-inducible factor-1α (HIF-1α) and its downstream target, vascular endothelial growth factor (VEGF), play a critical role in tumour angiogenesis and represent an attractive chemotherapeutic target. In this study, we investigated the effect of LQ on the molecular mechanism of angiogenesis. We found that LQ inhibited VEGF expression at both mRNA and protein levels. Liquiritigenin did not affect HIF-1α expression at the mRNA level, but it dramatically inhibited both serum- and mimicked hypoxic-induced HIF-1α protein accumulation in HeLa cells. Furthermore, we showed that LQ inhibited serum-induced expression of HIF-1α by reducing its stability and decreased the synthesis in a dose-dependent manner. Mechanistically, we demonstrated that LQ inhibited HIF-1α and VEGF expression involved in blocking the protein kinase B (PKB/Akt) signalling pathway, and the mechanisms correlated with dephosphorylation of the mammalian target of rapamycin (mTOR) and its effector ribosomal protein S6 kinase (p70S6K). In addition, LQ inhibited VEGF-induced formation of capillary-like structures in human umbilical vein endothelial cells (HUVEC). Taken together, our study provided valuable insights into the mechanism of antiangiogenic effect of LQ.
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Liquiritigenin inhibits tumor growth and vascularization in a mouse model of HeLa cells.
Molecules (Basel Switzerland), 2012Co-Authors: Yuxin Liu, Yu Wang, Sirou Xie, Kang Luo, Yang Wang, Yun-qing CaiAbstract:Angiogenesis is one of the crucial steps in the transition of a tumor from a small, harmless cluster of mutated cells to a large, malignant growth, capable of spreading to other organs throughout the body. Vascular endothelial growth factor (VEGF) that stimulates vasculogenesis and angiogenesis is thought to be as an anti-angiogenic target for cancer therapy. Liquiritigenin (LQ), a flavanone existing in Radix glycyrrhiza, shows extensive biological activities, such as anti-inflammatory and anti-cancer properties. In our studies, Liquiritigenin effectively inhibited the growth of tumors xenografted in nude mice from human cervical cancer cell line HeLa cells, and microvascular density (MVD) of the tumor exposed to Liquiritigenin was reduced in a dose dependent manner, especially in the high dose group. Moreover, the expression and secretion of VEGF were down-regulated by the drug in vivo and in vitro. Therefore, Liquiritigenin can be further studied on cancer and other diseases associated with VEGF up-regulation.
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Liquiritigenin inhibits serum-induced HIF-1α and VEGF expression via the AKT/mTOR-p70S6K signalling pathway in HeLa cells
Phytotherapy research : PTR, 2011Co-Authors: Sirou Xie, Yu Wang, Changwei Liu, Kang Luo, Yun-qing CaiAbstract:Liquiritigenin (LQ) is a non-toxic dietary flavonoid with chemopreventive and anticancer properties. However, the mechanism of its antiangiogenesis remains unclear. Hypoxia-inducible factor-1α (HIF-1α) and its downstream target, vascular endothelial growth factor (VEGF), play a critical role in tumour angiogenesis and represent an attractive chemotherapeutic target. In this study, we investigated the effect of LQ on the molecular mechanism of angiogenesis. We found that LQ inhibited VEGF expression at both mRNA and protein levels. Liquiritigenin did not affect HIF-1α expression at the mRNA level, but it dramatically inhibited both serum- and mimicked hypoxic-induced HIF-1α protein accumulation in HeLa cells. Furthermore, we showed that LQ inhibited serum-induced expression of HIF-1α by reducing its stability and decreased the synthesis in a dose-dependent manner. Mechanistically, we demonstrated that LQ inhibited HIF-1α and VEGF expression involved in blocking the protein kinase B (PKB/Akt) signalling pathway, and the mechanisms correlated with dephosphorylation of the mammalian target of rapamycin (mTOR) and its effector ribosomal protein S6 kinase (p70S6K). In addition, LQ inhibited VEGF-induced formation of capillary-like structures in human umbilical vein endothelial cells (HUVEC). Taken together, our study provided valuable insights into the mechanism of antiangiogenic effect of LQ.
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Liquiritigenin induces mitochondria-mediated apoptosis via cytochrome c release and caspases activation in HeLa Cells.
Phytotherapy research : PTR, 2011Co-Authors: Changwei Liu, Yi-jing Zhou, Yu Wang, Sirou Xie, Xiangmei Ren, Yun-qing CaiAbstract:It has been demonstrated that many flavonoids possess a potent and broad spectrum of antitumor activity. Liquiritigenin is a flavanone extracted from Glycyrrhizae. This study investigated the effects of Liquiritigenin on cell viability and apoptosis induction in human cervical carcinoma (HeLa) cells. The results show that Liquiritigenin significantly suppressed cell proliferation in a dose- and time-dependent manner in HeLa cells. In addition, Liquiritigenin promoted apoptosis in HeLa cells, evidenced by apoptotic morphological changes and Annexin-V binding. The apoptosis induction with Liquiritigenin is associated with the up-regulation of p53 and Bax, along with down-regulation of Bcl-2 and survivin. Finally, examination of the mitochondrial pathway of apoptosis revealed that cytochrome c is released from mitochondria to cytosol, associated with the activation of caspase-9 and -3, and the cleavage of poly (ADP-ribose) polymerase (PARP). Overall, the results indicate that Liquiritigenin induces apoptosis in part via the mitochondrial pathway, which is associated with p53 up-regulation, release of cytochrome c and elevated activity of caspase-9 and -3 in HeLa cells.
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Inhibition of hepatoma 22 tumor by Liquiritigenin.
Phytotherapy research : PTR, 2009Co-Authors: Ming Zhou, Haruo Higo, Yun-qing CaiAbstract:The purpose of this study was to evaluate the in vivo antitumor effects of Liquiritigenin (LQ) on H(22) Hepatocarcinoma. After mice were administrated Liquiritigenin (10, 20 and 40 mg/kg) intragastrically for 15 days, tumor volume, indices of thymus and spleen, MDA level in serum, optical microscopy, electron microscopy were determined. We have found that LQ had inhibitory effects on transplanted tumors and that the middle dose of LQ was more effective than the others. All LQ groups could increase thymus weight but it had no obvious effect on the spleen. MDA content decreased with LQ treatment but there wasn't a significant difference. In the group treated with LQ, we observed that the nuclei changed markedly and had ultrastructural morphological changes to apoptosis. The study supports that LQ significantly inhibits the growth of H(22) in vivo, and might be a promising antihepatoma agent.
