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Pengjun Zhao - One of the best experts on this subject based on the ideXlab platform.
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Hyperoside exhibits anticancer activity in non‑small cell lung cancer cells with T790M mutations by upregulating FoxO1 via CCAT1.
Oncology reports, 2019Co-Authors: Pengjun ZhaoAbstract:Acquired epidermal growth factor receptor (EGFR) T790M mutation is the most common mechanism that accounts for EGFR‑TKI (tyrosine kinase inhibitor) resistance of non‑small cell lung cancer (NSCLC). High expense and acquired resistance weaken support for the use of osimertinib for T790M‑positive NSCLC treatment, and limit the efficacy and application of this drug. Hyperoside, a flavonol glycoside compound, extracted from Hypericum perforatum, has been reported to inhibit the growth of a variety of tumors. The present study aimed to investigate the role of Hyperoside in treating NSCLC with T790M mutations, and to elucidate the underlying molecular mechanisms. Cell viability assays, apoptosis analysis, reverse transcription‑quantitative PCR, western blot analysis, animal experiments and immunohistochemistry were performed to examine the anticancer activity of Hyperoside. Hyperoside inhibited the proliferation and induced the apoptosis of T790M‑positive NSCLC cells. Hyperoside upregulated forkhead box protein O1 (FoxO1) expression and downregulated the level of long non‑coding RNA (lncRNA) colon cancer associated transcript 1 (CCAT1) in T790M‑positive NSCLC cells. In the in vivo study, Hyperoside inhibited the growth of T790M‑positive NSCLC xenografts. In conclusion, Hyperoside inhibited proliferation and induced apoptosis by upregulating FoxO1 via CCAT1 in T790M‑positive NSCLC both in vitro and in vivo, suggesting that Hyperoside is a novel candidate for T790M‑positive NSCLC treatment.
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Hyperoside exhibits anticancer activity in non small cell lung cancer cells with t790m mutations by upregulating foxo1 via ccat1
Oncology Reports, 2019Co-Authors: Pengjun ZhaoAbstract:Acquired epidermal growth factor receptor (EGFR) T790M mutation is the most common mechanism that accounts for EGFR‑TKI (tyrosine kinase inhibitor) resistance of non‑small cell lung cancer (NSCLC). High expense and acquired resistance weaken support for the use of osimertinib for T790M‑positive NSCLC treatment, and limit the efficacy and application of this drug. Hyperoside, a flavonol glycoside compound, extracted from Hypericum perforatum, has been reported to inhibit the growth of a variety of tumors. The present study aimed to investigate the role of Hyperoside in treating NSCLC with T790M mutations, and to elucidate the underlying molecular mechanisms. Cell viability assays, apoptosis analysis, reverse transcription‑quantitative PCR, western blot analysis, animal experiments and immunohistochemistry were performed to examine the anticancer activity of Hyperoside. Hyperoside inhibited the proliferation and induced the apoptosis of T790M‑positive NSCLC cells. Hyperoside upregulated forkhead box protein O1 (FoxO1) expression and downregulated the level of long non‑coding RNA (lncRNA) colon cancer associated transcript 1 (CCAT1) in T790M‑positive NSCLC cells. In the in vivo study, Hyperoside inhibited the growth of T790M‑positive NSCLC xenografts. In conclusion, Hyperoside inhibited proliferation and induced apoptosis by upregulating FoxO1 via CCAT1 in T790M‑positive NSCLC both in vitro and in vivo, suggesting that Hyperoside is a novel candidate for T790M‑positive NSCLC treatment.
Ying Jin - One of the best experts on this subject based on the ideXlab platform.
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Hyperoside exerts anti inflammatory and anti arthritic effects in lps stimulated human fibroblast like synoviocytes in vitro and in mice with collagen induced arthritis
Acta Pharmacologica Sinica, 2016Co-Authors: Xiang-nan Jin, Hai-juan Sui, Zhou Liu, Enzhi Yan, Hanming Wang, Wei Gao, Ying JinAbstract:Hyperoside is a flavonol glycoside mainly found in plants of the genera Hypericum and Crataegus, which has shown anti-oxidant, anti-cancer and anti-inflammatory activities. In this study, we investigated the effects of Hyperoside on human rheumatoid fibroblast-like synoviocytes (FLSs) in vitro and on mouse collagen-induced arthritis (CIA) in vivo. FLSs were isolated from primary synovial tissues obtained from rheumatoid arthritis (RA) patients and exposed to LPS (1 μg/mL). Cell viability and proliferation were measured with MTT and BrdU assay. Cell migration was assessed using wound-healing assay and Transwell assay. DNA binding of NF-κB was measured using a TransAM-NFkappaB kit. The localization of p65 subunit was detected with immunocytochemistry. CIA was induced in mice by primary immunization with Bovine Type II collagen (CII) emulsified in CFA, followed by a booster injection 3 weeks later. The arthritic mice were treated with Hyperoside (25, 50 mg·kg−1·d−1, ip) for 3 weeks, and the joint tissues were harvested for histological analysis. Hyperoside (10, 50, 100 μmol/L) dose-dependently inhibited LPS-induced proliferation and migration of human RA FLSs in vitro. Furthermore, Hyperoside decreased LPS-stimulated production of TNF-α, IL-6, IL-1 and MMP-9 in the cells. Moreover, Hyperoside inhibited LPS-induced phosphorylation of p65 and IκBα, and suppressed LPS-induced nuclear translocation of p65 and DNA biding of NF-κB in the cells. Three-week administration of Hyperoside significantly decreased the clinical scores, and alleviated synovial hyperplasia, inflammatory cell infiltration and cartilage damage in mice with CIA. Hyperoside inhibits LPS-induced proliferation, migration and inflammatory responses in human RA FLSs in vitro by suppressing activation of the NF-κB signaling pathway, which contributes to the therapeutic effects observed in mice with CIA.
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Hyperoside induces both autophagy and apoptosis in non-small cell lung cancer cells in vitro.
Acta pharmacologica Sinica, 2016Co-Authors: Ling Wang, Xiang-nan Jin, Hai-juan Sui, Zhou Liu, Ying JinAbstract:Hyperoside (quercetin-3-O-β-D-galactopyranoside) is a flavonol glycoside found in plants of the genera Hypericum and Crataegus, which exhibits anticancer, anti-oxidant, and anti-inflammatory activities. In this study we investigated whether autophagy was involved in the anticancer mechanisms of Hyperoside in human non-small cell lung cancer cells in vitro. Human non-small cell lung cancer cell line A549 was tested, and human bronchial epithelial cell line BEAS-2B was used for comparison. The expression of LC3-II, apoptotic and signaling proteins was measured using Western blotting. Autophagosomes were observed with MDC staining, LC3 immunocytochemistry, and GFP-LC3 fusion protein techniques. Cell viability was assessed using MTT assay. Hyperoside (0.5, 1, 2 mmol/L) dose-dependently increased the expression of LC3-II and autophagosome numbers in A549 cells, but had no such effects in BEAS-2B cells. Moreover, Hyperoside dose-dependently inhibited the phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, but increased the phosphorylation of ERK1/2 in A549 cells. Insulin (200 nmol/L) markedly enhanced the phosphorylation of Akt and decreased LC3-II expression in A549 cells, which were reversed by pretreatment with Hyperoside, whereas the MEK1/2 inhibitor U0126 (20 μmol/L) did not blocked Hyperoside-induced LC3-II expression. Finally, Hyperoside dose-dependently suppressed the cell viability and induced apoptosis in A549 cells, which were significantly attenuated by pretreatment with the autophagy inhibitor 3-methyladenine (2.5 mmol/L). Hyperoside induces both autophagy and apoptosis in human non-small cell lung cancer cells in vitro. The autophagy is induced through inhibiting the Akt/mTOR/p70S6K signal pathways, which contributes to anticancer actions of Hyperoside.
Yanli Song - One of the best experts on this subject based on the ideXlab platform.
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Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy.
Frontiers in pharmacology, 2020Co-Authors: Aiwu Wei, Huidongzi Xiao, Jingjing Guo, Zhuqing Jing, Shaoqi Shi, Yanli SongAbstract:Anticardiolipin antibody (aCL), an important characterization of antiphospholipid syndrome, shows an intense association with vascular endothelial injury. Hyperoside is a flavonoid extracted from medicinal plants traditionally used in Chinese medicines, displaying anti-inflammatory, anti-cancer, and anti-oxidative properties in various diseases. Recent studies have shifted the focus on the protective effects of Hyperoside on vascular endothelial injury. However, little is known about the mechanisms involved. In the present study, we investigated the effect of Hyperoside on aCL-induced injury of human umbilical vein endothelial cells (HUVECs) in vitro. Our data illustrated that aCL induced HUVEC injury via inhibiting autophagy. Hyperoside reduced aCL-induced secretion of proinflammatory cytokines IL-1β and IL-8 and endothelial adhesion cytokines TF, ICAM1, and VCAM1 in HUVECs. Additionally, Hyperoside activated autophagy and suppressed the mTOR/S6K and TLR4/Myd88/NF-κB signaling transduction pathways in aCL-induced HUVECs. To the best of our knowledge, this is the first study to investigate the effect of Hyperoside on aCL-induced injury, as well as offer insights into the involved mechanisms, which is of great significance for the treatment of antiphospholipid syndrome.
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Hyperoside attenuates pregnancy loss through activating autophagy and suppressing inflammation in a rat model.
Life sciences, 2020Co-Authors: Aiwu Wei, Huidongzi Xiao, Yanli Song, Yanrong Wan, Xingxing RenAbstract:Abstract Aims Recurrent pregnancy loss (RPL) is one of the most common obstetrical diseases, which is a manifestation of antiphospholipid syndrome (APS) with no effective therapy methods. Autophagy and inflammatory responses both play an important role in the pathogenesis of RPL and Hyperoside has been demonstrated to have multifarious bioactivities including enhancing autophagy and anti-inflammation. This study aims to investigate the effect of Hyperoside on anticardiolipin (aCL)-IgG fractions-induced pregnancy loss. Main methods In the present study, the effect of Hyperoside was evaluated in a rat model of pregnancy loss induced by aCL-IgG fractions isolated from serum of APS patients. The fetuses were counted and the placentas were weighted and the protein expressions of inflammation and autophagy were measured by western blot analysis. Key findings Treatment with Hyperoside (40 mg/kg) improved pregnancy outcome manifest as increasing the weight of fetuses and decreasing the fetal resorption rate. In addition, Hyperoside treatment downregulated the expressions of phosphorylated mammalian target of rapamycin (mTOR), phosphorylated p70S6 Kinase (S6K) and inhibited the expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and NF-kB p-p65 in pregnancy loss animal models. Significance Hyperoside attenuated pregnancy loss through regulating mTOR/S6K and TLR4/MyD88/NF-kB signaling pathways, which may provide a potential drug candidate for recurrent pregnancy loss therapy.
Aiwu Wei - One of the best experts on this subject based on the ideXlab platform.
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Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy.
Frontiers in pharmacology, 2020Co-Authors: Aiwu Wei, Huidongzi Xiao, Jingjing Guo, Zhuqing Jing, Shaoqi Shi, Yanli SongAbstract:Anticardiolipin antibody (aCL), an important characterization of antiphospholipid syndrome, shows an intense association with vascular endothelial injury. Hyperoside is a flavonoid extracted from medicinal plants traditionally used in Chinese medicines, displaying anti-inflammatory, anti-cancer, and anti-oxidative properties in various diseases. Recent studies have shifted the focus on the protective effects of Hyperoside on vascular endothelial injury. However, little is known about the mechanisms involved. In the present study, we investigated the effect of Hyperoside on aCL-induced injury of human umbilical vein endothelial cells (HUVECs) in vitro. Our data illustrated that aCL induced HUVEC injury via inhibiting autophagy. Hyperoside reduced aCL-induced secretion of proinflammatory cytokines IL-1β and IL-8 and endothelial adhesion cytokines TF, ICAM1, and VCAM1 in HUVECs. Additionally, Hyperoside activated autophagy and suppressed the mTOR/S6K and TLR4/Myd88/NF-κB signaling transduction pathways in aCL-induced HUVECs. To the best of our knowledge, this is the first study to investigate the effect of Hyperoside on aCL-induced injury, as well as offer insights into the involved mechanisms, which is of great significance for the treatment of antiphospholipid syndrome.
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Hyperoside attenuates pregnancy loss through activating autophagy and suppressing inflammation in a rat model.
Life sciences, 2020Co-Authors: Aiwu Wei, Huidongzi Xiao, Yanli Song, Yanrong Wan, Xingxing RenAbstract:Abstract Aims Recurrent pregnancy loss (RPL) is one of the most common obstetrical diseases, which is a manifestation of antiphospholipid syndrome (APS) with no effective therapy methods. Autophagy and inflammatory responses both play an important role in the pathogenesis of RPL and Hyperoside has been demonstrated to have multifarious bioactivities including enhancing autophagy and anti-inflammation. This study aims to investigate the effect of Hyperoside on anticardiolipin (aCL)-IgG fractions-induced pregnancy loss. Main methods In the present study, the effect of Hyperoside was evaluated in a rat model of pregnancy loss induced by aCL-IgG fractions isolated from serum of APS patients. The fetuses were counted and the placentas were weighted and the protein expressions of inflammation and autophagy were measured by western blot analysis. Key findings Treatment with Hyperoside (40 mg/kg) improved pregnancy outcome manifest as increasing the weight of fetuses and decreasing the fetal resorption rate. In addition, Hyperoside treatment downregulated the expressions of phosphorylated mammalian target of rapamycin (mTOR), phosphorylated p70S6 Kinase (S6K) and inhibited the expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and NF-kB p-p65 in pregnancy loss animal models. Significance Hyperoside attenuated pregnancy loss through regulating mTOR/S6K and TLR4/MyD88/NF-kB signaling pathways, which may provide a potential drug candidate for recurrent pregnancy loss therapy.
Jianxin Sun - One of the best experts on this subject based on the ideXlab platform.
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Induction of Nur77 by Hyperoside inhibits vascular smooth muscle cell proliferation and neointimal formation.
Biochemical pharmacology, 2014Co-Authors: Yan Huo, Ming Chen, Nadan Wang, Pengguo Chen, Cheng Guo, Jianxin SunAbstract:Abstract Nur77 is an orphan nuclear receptor that belongs to the nuclear receptor 4A (NR4A) subfamily, which has been implicated in a variety of biological events, such as cell apoptosis, proliferation, inflammation, and metabolism. Activation of Nur77 has recently been shown to be beneficial for the treatment of cardiovascular and metabolic diseases. The purpose of this study is to identify novel natural Nur77 activators and investigate their roles in preventing vascular diseases. By measuring Nur77 expression using quantitative RT-PCR, we screened active ingredients extracted from Chinese herb medicines with beneficial cardiovascular effects. Hyperoside (quercetin 3- D -galactoside) was identified as one of the potent activators for inducing Nur77 expression and activating its transcriptional activity in vascular smooth muscle cells (VSMCs). We demonstrated that Hyperoside, in a time and dose dependent manner, markedly increased the expression of Nur77 in rat VSMCs, with an EC 50 of ∼0.83 μM. Mechanistically, we found that Hyperoside significantly increased the phosphorylation of ERK 1/2 MAP kinase and its downstream target cAMP response element-binding protein (CREB), both of which contributed to the Hyperoside-induced Nur77 expression in rat VSMCs. Moreover, through activation of Nur77 receptor, Hyperoside markedly inhibited both vascular smooth muscle cell proliferation in vitro and the carotid artery ligation–induced neointimal formation in vivo. These findings demonstrate that Hyperoside is a potent natural activator of Nur77 receptor, which can be potentially used for prevention and treatment of occlusive vascular diseases.