Icariin

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Yijia Lou - One of the best experts on this subject based on the ideXlab platform.

  • involvement of p38mapk and reactive oxygen species in Icariin induced cardiomyocyte differentiation of murine embryonic stem cells in vitro
    Stem Cells and Development, 2008
    Co-Authors: Ling Ding, Danyan Zhu, Xingguang Liang, Yijia Lou
    Abstract:

    We previously reported that treatment of Icariin could significantly induce cardiomyocyte differentiation of murine embryonic stem (ES) cells in vitro. In the present study, the exact activity initiated by Icariin was further confirmed and the underlying molecular mechanism was investigated. We found that cardiomyocyte differentiation was efficiently stimulated only if Icariin was administrated between days 5 and 8 in differentiation course, which indicated with elevated percentage of embryoid bodies (EB) and with beating areas and up- regulated expression of alpha-actinin and troponin T. Exposure of Icariin triggered intracellular reactive oxygen species (ROS) generation of EBs in 3 h, which was abolished in the presence of either NADPH oxidase inhibitor DPI or antioxidant Trolox. Meanwhile, expression of NOX4, a membrane combined enzyme responsible for ROS generation, was promoted by Icariin in a dose-dependent manner. Although p38MAPK (mitogen-activated protein kinase), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal protein kinase (JNK) were spontaneously activated in early differentiation, only the phosphorylation of p38MAPK was enhanced and prolonged when Icariin was present, whereas both ERK and JNK showed no response to Icariin treatment. Moreover, the inducible effect of Icariin was blunted by SB203580, a specific inhibitor of p38MAPK. On the contrary, neither UO126 nor SP600125, the specific inhibitor of ERK and JNK, could abolish Icariin-stimulated differentiation. Nuclear location of MEF2C, which played a critical role in cardiomyocyte differentiation and could be activated by p38MAPK, was stimulated after Icariin exposure. Taken together, these results suggest that ROS generation and the subsequent activation of p38MAPK are essential for the inducible function of Icariin on cardiomyocyte differentiation of murine embryonic stem cells in vitro.

  • a novel anticancer agent icaritin induced cell growth inhibition g1 arrest and mitochondrial transmembrane potential drop in human prostate carcinoma pc 3 cells
    European Journal of Pharmacology, 2007
    Co-Authors: Xin Huang, Danyan Zhu, Yijia Lou
    Abstract:

    Abstract Icariin and icaritin with prenyl group have been demonstrated for their selective estrogen receptor modulating activities. We screened their effects on cell growth in human prostate carcinoma PC-3 cell line (estrogen receptor positive) in vitro . PC-3 cell line was used for the measurement of anti-carcinoma activities of 0–100 μmol/l icaritin and 30 μmol/l Icariin. 1 μmol/l 17-β estradiol (E 2 ) served as the estrogen positive control, and 1 μmol/l ICI 182,780 [7 α-[9 (4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl]-estra-1,3,5(10)-triene-3,17h-diol]] served as the specific estrogen receptor antagonist. Primary cultured rat prostate basal cells used as cell growth selective control. The growth-inhibitory effects were analyzed using MTT assay, and fluorochrome staining, flow cytometry, and immunoblotting were employed to illustrate the possible mechanisms. When treated with icaritin for 24 to 72 h, cell growth was strongly inhibited (at 48 h IC 50 was 10.74 ± 1.59 μmol/l, P Ψ m) drop. Meanwhile, few changes in IC 50 could be observed when co-incubated with ICI 182,780. Icaritin-induced growth inhibition was associated with G 1 arrest ( P 2 -M arrest depending upon doses. Consistently with G 1 arrest, icaritin increased protein expressions of pRb, p27 Kip1 and p16 Ink4a , while showed decrease in phosphorylated pRb, Cyclin D1 and CDK4. Comparatively, Icariin has much lower effects on PC-3 cells and showed only weak G 1 arrest, suggesting a possible structure–activity relationship. These findings suggested a novel anticancer efficacy of icaritin mediated selectively via induction of cell cycle arrest but not associated with estrogen receptors in PC-3 cells.

  • estrogenic effects of two derivatives of Icariin on human breast cancer mcf 7 cells
    Phytomedicine, 2005
    Co-Authors: Yijia Lou
    Abstract:

    The aims of the present study were to determine the estrogenic activities of Icariin (ICA) and its derivatives and their structure-estrogenic activity relationship. Therefore, icaritin (ICT) and desmethylicaritin (DICT) were derived from ICA. The estrogenic activities of ICA, ICT and DICT were examined by cell proliferation and progestogen receptor mRNA expression of estrogen-receptor-positive MCF-7 cells. Current studies exhibited that ICT and DICT both markedly enhanced the proliferation of MCF-7 cells; as compared to estradiol (100%), their relative proliferative effects (RPE) were 90% and 94%, respectively. Cell proliferation induced by ICT and DICT was completely antagonized by ICI182,780. ICT and DICT increased progestogen receptor (PR) at mRNA levels at 48 h after treatment, although the effects were not as prominent as 17beta-estradiol (E2). Those phenomena were not observed with ICA. Results demonstrate that ICT and DICT (nonconjugated forms) possess estrogen-like activity; however, ICA appears to have no estrogenicity in the MCF-7 cell line model in vitro.

  • determination of Icariin and metabolites in rat serum by capillary zone electrophoresis rat pharmacokinetic studies after administration of Icariin
    Journal of Pharmaceutical and Biomedical Analysis, 2004
    Co-Authors: Jian Liu, Yijia Lou
    Abstract:

    A simple and rapid method for determination of Icariin (ICA) and its two metabolites, icaritin (ICT) and desmethylicaritin (DICT), by capillary zone electrophoresis has been developed and validated. Optimum separation of ICA, ICT, and DICT was obtained on 43.6 cm x 50 microm capillary using sodium tetraborate (30 mmol/L), monobasic sodium phosphate (50 mmol/L)-acetonitrile (50:50, v/v) (pH 10.0) as running buffer. Carbamazepine (CMP) was used as internal standard (IS). The temperature and voltage were optimized at 25 degrees C and 12 kV, respectively. The limit of detection of ICA was 1.0 mg/L (S/N = 3) by UV detection at 270 nm. The elaborated method was tested in vivo after administration of a single dose of 120 mg ICA/kg to healthy rats. Calculated parameters confirmed usefulness of the method in rat pharmacokinetic studies on ICA.

Keming Chen - One of the best experts on this subject based on the ideXlab platform.

  • the flavonol glycoside Icariin promotes bone formation in growing rats by activating the camp signaling pathway in primary cilia of osteoblasts
    Journal of Biological Chemistry, 2017
    Co-Authors: Wengui Shi, Cory J Xian, Yuhai Gao, Yuanyuan Wang, Jian Zhou, Zhenlong Wei, Jufang Wang, Keming Chen
    Abstract:

    Icariin, a prenylated flavonol glycoside isolated from the herb Epimedium, has been considered as a potential alternative therapy for osteoporosis. Previous research has shown that, unlike other flavonoids, Icariin is unlikely to act via the estrogen receptor, but its exact mechanism of action is unknown. In this study, using rat calvarial osteoblast culture and rat bone growth models, we demonstrated that Icariin promotes bone formation by activating the cAMP/protein kinase A (PKA)/cAMP response element-binding protein (CREB) pathway requiring functional primary cilia of osteoblasts. We found that Icariin increases the peak bone mass attained by young rats and promotes the maturation and mineralization of rat calvarial osteoblasts. Icariin activated cAMP/PKA/CREB signaling of the osteoblasts by increasing intracellular cAMP levels and facilitating phosphorylation of both PKA and CREB. Blocking cAMP/PKA/CREB signaling with inhibitors of the cAMP-synthesizing adenylyl cyclase (AC) and PKA inhibitors significantly inhibited the osteogenic effect of Icariin in the osteoblasts. Icariin-activated cAMP/PKA/CREB signaling was localized to primary cilia, as indicated by localization of soluble AC and phosphorylated PKA. Furthermore, blocking ciliogenesis via siRNA knockdown of a cilium assembly protein, IFT88, inhibited Icariin-induced PKA and CREB phosphorylation and also abolished Icariin's osteogenic effect. Finally, several of these outcomes were validated in Icariin-treated rats. Together, these results provide new insights into Icariin function and its mechanisms of action and strengthen existing ties between cAMP-mediated signaling and osteogenesis.

  • Icariin stimulates the osteogenic differentiation of rat bone marrow stromal cells via activating the pi3k akt enos no cgmp pkg
    Bone, 2014
    Co-Authors: Yuankun Zhai, Cory J Xian, Jian Zhou, Xiaoyu Guo, Ping Zhen, Keming Chen
    Abstract:

    article Icariin, a prenylated flavonol glycoside isolated from Epimedii herba, has been found to be a potent stimulator of osteogenic differentiation and has potential application inpreventing bone loss. However, the signaling pathway underlying itsosteogeniceffect remainsunclear.Wehypothesizedthattheosteogenic activity of Icariin isrelated to the nitric oxide (NO) signal pathway and PI3K/AKT pathway in its upstream. Rat bone marrow stromal cells (rBMSCs) were cultured in osteogenic medium and treated with Icariin or together with L-NAME, ODQ, PDE5, and/or LY294002 (the inhibitor of NOS, sGC, cGMP, and PI3K respectively), and effects were examined on the ex- pressionofsignalmessengers(NOS,NO,sGC,cGMP,PKGandPI3K)andthe levelsofosteogenicmarkers(alkaline phosphatase or ALP, osteocalcin and calcified nodules). It was found that Icariin dose-dependently increased ALP activity,andtreatmentattheoptimal concentration(10 �5 M)increasedNOSactivity,iNOSandeNOSexpression, NO production, sGC and cGMP contents and PKG expression besides the phosphorylation of AKT. The addition of L-NAME, ODQ and PDE5 significantly inhibited the Icariin effects on above markers respectively. The addition of LY294002 decreased the p-AKT level, NOS activity, eNOS expression and NO production significantly, but had no significant effect on iNOS expression. The addition of any of the four inhibitors also abolished the osteogenic effect of Icariin on rBMSCs as indicatedby ALP activity, osteocalcin synthesis,calcium deposition and the number andareas of calcified nodules. These results suggest that the osteogenic effect of Icariin involves the PI3K-AKT-eNOS-NO- cGMP-PKG signal pathway. Furthermore, dosage response studies showed that Icariin at 10 �6 M (a physiologically achievable concentration in vivo) also activated this signal pathway.

  • functions and action mechanisms of flavonoids genistein and Icariin in regulating bone remodeling
    Journal of Cellular Physiology, 2013
    Co-Authors: Leiguo Ming, Keming Chen, Cory J Xian
    Abstract:

    Increasingly natural products particularly flavonoids are being explored for their therapeutic potentials in reducing bone loss and maintaining bone health. This study has reviewed previous studies on the two better known flavonoids, genistein and Icariin, their structures, functions, action mechanisms, relative potency, and potential application in regulating bone remodeling and preventing bone loss. Genistein, an isoflavone abundant in soy, has dual functions on bone cells, able to inhibit bone resorption activity of osteoclasts and stimulate osteogenic differentiation and maturation of bone marrow stromal progenitor cells (BMSCs) and osteoblasts. Genistein is an estrogen receptor (ER)-selective binding phytoestrogen, with a greater affinity to ERβ. Genistein inhibits tyrosine kinases and inhibits DNA topoisomerases I and II, and may act as an antioxidant. Genistein enhances osteoblastic differentiation and maturation by activation of ER, p38MAPK-Runx2, and NO/cGMP pathways, and it inhibits osteoclast formation and bone resorption through inducing osteoclastogenic inhibitor osteoprotegerin (OPG) and blocking NF-κB signaling. Icariin, a prenylated flavonol glycoside isolated from Epimedium herb, stimulates osteogenic differentiation of BMSCs and inhibits bone resorption activity of osteoclasts. Icariin, whose metabolites include icariside I, icariside II, icaritin, and desmethylicaritin, has no estrogenic activity. However, Icariin is more potent than genistein in promoting osteogenic differentiation and maturation of osteoblasts. The existence of a prenyl group on C-8 of Icariin molecular structure has been suggested to be the reason why Icariin is more potent than genistein in osteogenic activity. Thus, the prenylflavonoids may represent a class of flavonoids with a higher osteogenic activity.

  • Icariin is more potent than genistein in promoting osteoblast differentiation and mineralization in vitro
    Journal of Cellular Biochemistry, 2011
    Co-Authors: Leiguo Ming, Yuankun Zhai, Peng Song, Cory J Xian, Keming Chen
    Abstract:

    There has been a strong interest in searching for natural therapies for osteoporosis. Genistein, an isoflavone abundant in soy, and Icariin, a prenylated flavonol glycoside isolated from Epimedium Herb, have both been identified to exert beneficial effects in preventing postmenopausal bone loss. However, the relative potency in osteogenesis between the individual phytoestrogen flavonoids remains unknown. The present study compared ability of genistein and Icariin in enhancing differentiation and mineralization of cultured rat calvarial osteoblasts in vitro. Dose-dependent studies in osteoblast differentiation measuring alkaline phosphatase (ALP) activity revealed optimal concentrations of genistein and icarrin for stimulating osteogenesis to be both at 10(-5) M. Time course studies comparing the two compounds both at 10(-5) M demonstrated that Icariin treatment always produced higher ALP activity, more and larger areas of CFU-F(ALP) colonies and mineralized nodules, more osteocalcin secretion, and calcium deposition, and a higher level of mRNA expression of osteogenesis-related genes COL1α2, BMP-2, OSX, and RUNX-2. However, they inhibited the proliferation of osteoblasts to a similar degree. In conclusion, although future in vivo studies are required to investigate whether Icariin is more efficient in improving bone mass and/or preventing bone loss, our in vitro studies have demonstrated that Icariin has a stronger osteogenic activity than genistein. In addition, while the prenyl group on C-8 of Icariin could be the active group that takes part in osteoblastic differentiation and explains its greater potency in osteogenesis, mechanisms of action, and reasons for the relative potency of Icariin versus genistein need to be further studied.

Mei Hui Chen - One of the best experts on this subject based on the ideXlab platform.

  • Icariin promotes osteogenic differentiation of rat bone marrow stromal cells by activating the erα wnt β catenin signaling pathway
    Biomedicine & Pharmacotherapy, 2016
    Co-Authors: Qiushi Wei, Jin Zhang, Guoju Hong, Zhenqiu Chen, Weimin Deng, Mei Hui Chen
    Abstract:

    Icariin, the main effective component of Herba Epimedii, has been identified to regulate the osteogenic differentiation of rat bone marrow stromal cells (rBMSCs) and have potential application in preventing bone loss and promoting bone regeneration. However, the underlying signaling pathway of its osteogenic effect remains unclear. Here, we investigated whether Icariin could promote osteogenesis of rBMSCs through modulating the estrogen receptor alpha (ERα) and Wnt/β-catenin signaling pathways, which implicated in rBMSCs osteogenesis. rBMSCs were cultured in osteogenic induction medium and treated with Icariin or together with ICI 182780 or DKK1, the effects on the expression of osteogenic genes and Wnt/β-catenin signaling were detected. Results indicated that Icariin (0.1μM) markedly enhanced the proliferation of rBMSCs and alkaline phosphatase (ALP) activity. Additionally, Icariin (0.1μM) significantly up-regulated the expression of osteogenic genes (Runx2, osteopotin, DLX5, osteocalcin, collagen type I, and ERα) and Wnt signal members (β-catenin, Lef1, TCF7, c-jun, c-myc, and cyclin D). Furthermore, Icariin stimulated the activation of β-catenin as evidenced by increased total β-catenin protein and nuclear translocation. These osteogenesis-potentiating effects of Icariin were blocked by ICI 182780 or DKK1. Taken together, these results suggest that the osteogenic effects of Icariin on rBMSCs involves the ERα-Wnt/β-catenin signaling pathway.

Jingcheng Dong - One of the best experts on this subject based on the ideXlab platform.

  • Icariin inhibits tnf α ifn γ induced inflammatory response via inhibition of the substance p and p38 mapk signaling pathway in human keratinocytes
    International Immunopharmacology, 2015
    Co-Authors: Lingwen Kong, Baojun Liu, Qingli Luo, Jiaqi Liu, Jia Wang, Hongying Zhang, Qi Pang, Yingchao Liu, Jingcheng Dong
    Abstract:

    Pro-inflammatory cytokines play a crucial role in the etiology of atopic dermatitis. We demonstrated that Herba Epimedii has anti-inflammatory potential in an atopic dermatitis mouse model; however, limited research has been conducted on the anti-inflammatory effects and mechanism of Icariin, the major active ingredient in Herba Epimedii, in human keratinocytes. In this study, we evaluated the anti-inflammatory potential and mechanisms of Icariin in the tumor necrosis factor-α (TNF-α)/interferon-γ (IFN-γ)-induced inflammatory response in human keratinocytes (HaCaT cells) by observing these cells in the presence or absence of Icariin. We measured IL-6, IL-8, IL-1β, MCP-1 and GRO-α production by ELISA; IL-6, IL-8, IL-1β, intercellular adhesion molecule-1 (ICAM-1) and tachykinin receptor 1 (TACR1) mRNA expression by real-time PCR; and P38-MAPK, P-ERK and P-JNK signaling expression by western blot in TNF-α/IFN-γ-stimulated HaCaT cells before and after Icariin treatment. The expression of TNF-α-R1 and IFN-γ-R1 during the stimulation of the cell models was also evaluated before and after Icariin treatment. We investigated the effect of Icariin on these pro-inflammatory cytokines and detected whether this effect occurred via the mitogen-activated protein kinase (MAPK) signal transduction pathways. We further specifically inhibited the activity of two kinases with 20μM SB203580 (a p38 kinase inhibitor) and 50μM PD98059 (an ERK1/2 kinase inhibitor) to determine the roles of the two signal pathways involved in the inflammatory response. We found that Icariin inhibited TNF-α/IFN-γ-induced IL-6, IL-8, IL-1β, and MCP-1 production in a dose-dependent manner; meanwhile, the Icariin treatment inhibited the gene expression of IL-8, IL-1β, ICAM-1 and TACR1 in HaCaT cells in a time- and dose-dependent manner. Icariin treatment resulted in a reduced expression of p-P38 and p-ERK signal activation induced by TNF-α/IFN-γ; however, only SB203580, the p38 alpha/beta inhibitor, inhibited the secretion of inflammatory cytokines induced by TNF-α/IFN-γ in cultured HaCaT cells. The differential expression of TNF-α-R1 and IFN-γ-R1 was also observed after the stimulation of TNF-α/IFN-γ, which was significantly normalized after the Icariin treatment. Collectively, we illustrated the anti-inflammatory property of Icariin in human keratinocytes. These effects were mediated, at least partially, via the inhibition of substance P and the p38-MAPK signaling pathway, as well as by the regulation of the TNF-α-R1 and IFN-γ-R1 signals.

  • regulation of th17 treg function contributes to the attenuation of chronic airway inflammation by Icariin in ovalbumin induced murine asthma model
    Immunobiology, 2015
    Co-Authors: Ying Wei, Baojun Liu, Jing Sun, Qingli Luo, Feng Liu, Jingcheng Dong
    Abstract:

    Icariin which is a flavonoid glucoside isolated from Epimedium brevicornu Maxim, has been reported to have anti-osteoporotic, anti-inflammatory and anti-depressant-like activities. In this study, we observed the effect of Icariin on airway inflammation of ovalbumin (OVA)-induced murine asthma model and the associated regulatory mode on T-helper (Th)17 and regulatory T (Treg) cell function. Our data revealed that chronic OVA inhalation induced a dramatic increase in airway resistance (RL) and decrease in the lung dynamic compliance (Cdyn), and Icariin and DEX treatment caused significant attenuation of such airway hyperresponsiveness (AHR). BALF cell counts demonstrated that Icariin and DEX led to a prominent reduction in total leukocyte as well as lymphocyte, eosinophil, neutrophil, basophil and monocyte counts. Histological analysis results indicated that Icariin and DEX alleviated the inflammatory cells infiltrating into the peribronchial tissues and goblet cells hyperplasia and mucus hyper-production. Flow cytometry test demonstrated that Icariin or DEX administration resulted in a significant percentage reduction in CD4+RORγt+ T cells and elevation of CD4+Foxp3+ T cells in BALF. Furthermore, Icariin or DEX caused a significant reduction in IL-6, IL-17 and TGF-β level in BALF. Unfortunately, Icariin had no effect on IL-10 level in BALF. Western blot assay found that Icariin or DEX suppressed RORγt and promoted Foxp3 expression in the lung tissue. qPCR analysis revealed that Icariin and DEX resulted in a notable decrease in RORγt and increase in Foxp3 mRNA expression in isolated spleen CD4+ T cell. In conclusion, our results suggested that Icariin was effective in the attenuation of AHR and chronic airway inflammatory changes in OVA-induced murine asthma model, and this effect was associated with regulation of Th17/Treg responses, which indicated that Icariin may be used as a potential therapeutic method to treat asthma with Th17/Treg imbalance phenotype.

  • Icariin exerts an antidepressant effect in an unpredictable chronic mild stress model of depression in rats and is associated with the regulation of hippocampal neuroinflammation
    Neuroscience, 2015
    Co-Authors: Baohong Liu, Feng Liu, Jing Sun, J Tao, Jingcheng Dong
    Abstract:

    Icariin (ICA), a flavonoid extracted from the traditional Chinese herb Herba Epimedii that can freely cross the blood-brain barrier, inhibits neuroinflammation and attenuates oxidative stress damage. Our previous studies demonstrated that Icariin exerts an antidepressant-like activity in a social defeat mouse model. However, it is unknown whether Icariin is beneficial for the treatment of depression via its modulation of oxidative stress and neuroinflammation. The objective of this study was to investigate the effects of Icariin on the depression-like behaviors in an unpredictable chronic mild stress (CMS) model of depression in rats. Rats exposed to CMS showed behavioral deficits in physical state, the sucrose preference test (SPT) and the forced swimming test (FST) and exhibited a significant increase in oxidative-nitrosative stress markers, inflammatory mediators, including tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β), activation of the nuclear factor kappa B (NF-κB) signaling pathway and increased inducible nitric oxide synthase (iNOS) mRNA expression in the hippocampus, which was reversed by chronic treatment with Icariin (20 or 40 mg/kg). Interestingly, Icariin negatively regulated the activation of the nod-like receptor protein 3 (NLRP3) inflammasome/caspase-1/IL-1β axis in the hippocampus of CMS rats. These results confirm that Icariin exerts antidepressant-like effects, which may be mediated, at least in part, by enhanced antioxidant status and anti-inflammatory effects on the brain tissue via the inhibition of NF-κB signaling activation and the NLRP3-inflammasome/caspase-1/IL-1β axis. Our findings provide new information to understand the antidepressant action of Icariin, which is targeted to the NLRP3-inflammasom in brain.

  • neuroprotective effects of Icariin on corticosterone induced apoptosis in primary cultured rat hippocampal neurons
    Brain Research, 2011
    Co-Authors: Baojun Liu, Xiaohong Duan, Jianhua Huang, Hongying Zhang, Guang Yang, Jiang Tao, Yuxue Cao, Jingcheng Dong
    Abstract:

    Neurons are damaged following prolonged exposure to high concentrations of corticosterone, particularly during chronic inflammatory and immune diseases. One of the main mechanisms underlying neuronal injury is apoptosis. In the present study the neuroprotective effects of Icariin, an active natural ingredient from the Chinese plant Epimedium sagittatum maxim against corticosterone-induced apoptosis were examined in primary cultured rat hippocampal neuronal cells. Pre-treatment of neuronal cells with Icariin suppressed corticosterone-induced cytotoxicity in a dose-dependent manner. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick-end-labeling assay (TUNEL) labeling demonstrated that Icariin significantly reduced TUNEL-positive cell numbers induced by exposure of cultured neurons to corticosterone. Moreover, Icariin markedly inhibited corticosterone-induced mitochondrial dysfunction, including improved mitochondrial membrane potential and inhibition of caspase-3 activation. Using western blot analysis, corticosterone activated p38MAPK, extracellular regulated kinase 1/2(ERK1/2) ,and c-jun N-terminal protein kinase 1(JNK1) ,while Icariin blocked p38 MAPK, but not JNK1 or ERK1/2. Pharmacological approaches showed that the activation of p38MAPK plays a critical role in corticosterone-induced mitochondrial dysfunction and apoptosis. Taken together, the present results suggest that the protective effects of Icariin on apoptosis in hippocampal neuronal cells are potentially mediated through blockade of p38 MAPK phosphorylation.

  • Icariin attenuates lps induced acute inflammatory responses involvement of pi3k akt and nf κb signaling pathway
    European Journal of Pharmacology, 2010
    Co-Authors: Changqing Xu, Xiaohong Duan, Jinfeng Wu, Yanchun Xu, Jingcheng Dong
    Abstract:

    Abstract This study aimed to investigate the mechanism underlying the attenuation of LPS-induced lung inflammation by Icariin in vivo and in vitro. The anti-inflammatory effects of Icariin on LPS-induced acute inflammatory and the molecular mechanism were investigated. Pretreatment with icarrin (20 mg/kg) could attenuate acute lung inflammation by inhibiting mRNA expressions of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), metalloproteinase cycloxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the lung of LPS-treated mice. In addition, Icariin suppressed the secretion of TNF-α, prostaglandin E2 (PGE2) and nitric oxide (NO) as well as NF-κB p65 activation. Furthermore, decreased myeloperoxidase (MPO) activity was observed in the lung tissue and LPS-induced cytotoxicity in the RAW 264.7 macrophages cells was also markedly attenuated by Icariin. Western blotting analysis and confocal microscopy showed that Icariin pretreatment reduced the nucleus transportation and constant level of NF-κB p65 in the RAW 264.7 macrophage cells. However, the protective effects of Icariin were reversed by a PI3K/Akt inhibitor (wortmannin). Our in vitro and in vivo results suggested that activation of the PI3K/Akt pathway and the inhibition of NF-κB were involved in the protective effects of Icariin on LPS-induced acute inflammatory responses.

Teruyuki Nagamune - One of the best experts on this subject based on the ideXlab platform.

  • Icariin a potential osteoinductive compound for bone tissue engineering
    Tissue Engineering Part A, 2010
    Co-Authors: Jiyuan Zhao, Shinsuke Ohba, Yusuke Komiyama, Masashige Shinkai, Ungil Chung, Teruyuki Nagamune
    Abstract:

    To effectively treat bone diseases using bone regenerative medicine, there is an urgent need to develop safe and cheap drugs that can potently induce bone formation. Here, we demonstrate the osteogenic effects of Icariin, the main active compound of Epimedium pubescens. Icariin induced osteogenic differentiation of preosteoblastic cells. The combination of Icariin and a helioxanthin-derived small compound synergistically induced osteogenic differentiation of MC3T3-E1 cells to a similar extent to bone morphogenetic protein-2. Icariin enhanced the osteogenic induction activity of bone morphogenetic protein-2 in a fibroblastic cell line. Mineralization was enhanced by treatment with a combination of Icariin and calcium-enriched medium. The in vivo anabolic effect of Icariin was confirmed in a mouse calvarial defect model. Eight-week-old male C57BL/6N mice were transplanted with Icariin–calcium phosphate cement (CPC) tablets or CPC tablets only (n = 5 for each), and bone regeneration was evaluated after 4 and...

  • Icariin induces osteogenic differentiation in vitro in a bmp and runx2 dependent manner
    Biochemical and Biophysical Research Communications, 2008
    Co-Authors: Jiyuan Zhao, Shinsuke Ohba, Masashige Shinkai, Ungil Chung, Teruyuki Nagamune
    Abstract:

    To effectively treat bone diseases using bone regenerative medicine, there is an urgent need to develop safe cheap drugs that can potently induce bone formation. Here, we demonstrate the osteogenic effect of Icariin, the main active compound of Epimedium pubescens. Icariin induced osteogenic differentiation in pre-osteoblastic MC3T3-E1 cells and mouse primary osteoblasts. Icariin upregulated the mRNA expression levels of the osteoblast marker genes runt-related transcription factor 2 (Runx2) and inhibitor of DNA-binding 1 (Id-1). The osteogenic effect was inhibited by the introduction of Smad6 or dominant-negative Runx2, as well as Noggin treatment. Furthermore, Icariin induced the mRNA expression of bone morphogenetic protein (BMP)-4. These data suggest that Icariin exerts its potent osteogenic effect through induction of Runx2 expression, production of BMP-4 and activation of BMP signaling. The extremely low cost of Icariin and its high abundance make it appealing for bone regenerative medicine.