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    Natural Products
    Hesperidin
    Information
    CAS No. 520-26-3 Price $30 / 20mg
    Catalog No.CFN98839Purity>=98%
    Molecular Weight610.6 Type of CompoundFlavonoids
    FormulaC28H34O15Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)  (SDF)
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    Size /Price /Stock 10 mM * 1 mL in DMSO / $15.4 / In-stock
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  • Biological Activity
    Description: Hesperidin has antioxidative, anti-inflammatory, vasoprotective,and anticarcinogenic effects, it induces apoptosis and triggers autophagic markers through inhibition of Aurora-A mediated phosphoinositide-3-kinase/Akt/mammalian target of rapamycin and glycogen synthase kinase-3 beta signalling cascades in experimental colon carcinogenesis. Hesperidin also exerts its protective effect against CYP-induced hepatotoxicity through upregulation of hepatic PPARγ expression and abrogation of inflammation and oxidative stress.
    Targets: P450 (e.g. CYP17) | PPAR | NF-kB | NOS | Bcl-2/Bax | Caspase | PI3K | mTOR | Akt | Wnt/β-catenin | GSK-3 | c-Myc | COX | TNF-α
    In vitro:
    Oncol Lett . 2018 Nov;16(5):6299-6306.
    Hesperidin exhibits in vitro and in vivo antitumor effects in human osteosarcoma MG-63 cells and xenograft mice models via inhibition of cell migration and invasion, cell cycle arrest and induction of mitochondrial-mediated apoptosis[Pubmed: 30405765]
    The objective of the present study was to investigate the anticancer properties of Hesperidin against human osteosarcoma MG-63 cells. Its effects on apoptosis, cell migration, cell invasion and cell cycle arrest, and its effects on tumor volume and weight were also evaluated in the present study. MTS assay was used to study the cytotoxic effects of the compound on cell viability. Effects on apoptosis and cell cycle arrest were evaluated by flow cytometry. In vitro wound healing assay and Matrigel assay were performed to study the effects of Hesperidin on cell migration and cell invasion, respectively. Hesperidin exerted dose-dependent and time-dependent growth inhibitory effects on cervical cancer cells with IC50 values of 33.5, 23.8 and 17.6 μM, respectively, at 24, 48 and 72 h time intervals. Hesperidin led to early and late apoptosis induction in these cells. Hesperidin-treated cells also led to G2/M phase cell cycle arrest, which exhibited strong dose-dependence. Hesperidin treatment also led to inhibition of cell migration and invasion.
    In vivo:
    Nutrition. 2014 Nov-Dec;30(11-12):1415-22.
    Protective effect of hesperidin in a model of Parkinson's disease induced by 6-hydroxydopamine in aged mice.[Pubmed: 25280422]
    The aim of this study was to evaluate the role of the flavonoid Hesperidin in an animal model of PD induced by 6-hidroxidopamine (6-OHDA).
    METHODS AND RESULTS:
    Aged mice were treated with Hesperidin (50 mg/kg) during 28 d after an intracerebroventricular injection of 6-OHDA. The enzymatic activities of superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and glutathione S-transferase, the levels of glutathione, reactive oxygen species, total reactive antioxidant potential, dopamine and its levels of metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid, was analyzed in the striatum. The behavioral parameters (depressive-like, memory, and locomotor) were measured. This study demonstrated that Hesperidin (50 mg/kg) treatment was effective in preventing memory impairment in the Morris water maze test, as well as, depressive-like behavior in the tail suspension test. Hesperidin attenuated the 6-OHDA-induced reduction in glutathione peroxidase and catalase activity, total reactive antioxidant potential and the dopamine and its metabolite levels in the striatum of aged mice. 6-OHDA increased reactive oxygen species levels and glutathione reductase activity in the striatum, and these alterations were mitigated by chronic administration of Hesperidin.
    CONCLUSIONS:
    This study demonstrated a protective effect of Hesperidin on the neurotoxicity induced by 6-OHDA in aged mice, indicating that it could be useful as a therapy for the treatment of PD.
    Can J Physiol Pharmacol. 2014 Sep;92(9):717-24.
    Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARγ and abrogation of oxidative stress and inflammation.[Pubmed: 25079140]
    This study was undertaken to evaluate the protective effects of Hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats.
    METHODS AND RESULTS:
    The rats received a single intraperitoneal dose of CYP of 200 mg/kg body mass, followed by treatment with Hesperidin, orally, at doses of 25 and 50 mg/kg for 11 consecutive days. CYP induced hepatic damage, as evidenced by the significantly elevated levels of serum pro-inflammatory cytokines, serum transaminases, liver lipid peroxidation, and nitric oxide. As a consequence, there was reduced glutathione content, and the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were markedly reduced. In addition, CYP administration induced a considerable downregulation of peroxisome proliferator activated receptor gamma (PPARγ) and upregulation of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) mRNA expression. Hesperidin, in a dose-dependent manner, rejuvenated the altered markers to an almost normal state.
    CONCLUSIONS:
    In conclusion, Hesperidin showed a potent protective effect against CYP-induced oxidative stress and inflammation leading to hepatotoxicity. The study suggests that Hesperidin exerts its protective effect against CYP-induced hepatotoxicity through upregulation of hepatic PPARγ expression and abrogation of inflammation and oxidative stress.
    Environ Toxicol Pharmacol. 2014 May;37(3):907-15.
    Effect of hesperidin and neohesperidin from bittersweet orange (Citrus aurantium var. bigaradia) peel on indomethacin-induced peptic ulcers in rats.[Pubmed: 24691249]
    Hesperidin and neoHesperidin are the major flavanones isolated from bittersweet orange. It was recently reported that they have potent anti-inflammatory effects in various inflammatory models.
    METHODS AND RESULTS:
    In the present study, the effects of Hesperidin and neoHesperidin on indomethacin-induced ulcers in rats and the underlying mechanisms were investigated. Gastric ulcers were induced in rats with a single dose of indomethacin. The effects of pretreatment with Hesperidin and neoHesperidin were assessed in comparison with omeprazole as reference standard. Ulcer index, gene expression of gastric cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), lipid peroxidation product, malondialdhyde (MDA), and reduced glutathione (GSH) content in stomach were measured. Furthermore, gross and histopathological examination was performed.
    CONCLUSIONS:
    Our results indicated that both Hesperidin and neoHesperidin significantly aggravated gastric damage caused by indomethacin administration as evidenced by increased ulcer index and histopathological changes of stomach.
    Med Sci Monit . 2018 Dec 17;24:9177-9186.
    Effects of Hesperidin on H₂O₂-Treated Chondrocytes and Cartilage in a Rat Osteoarthritis Model[Pubmed: 30557884]
    BACKGROUND The purpose of this research was to investigate the effects of Hesperidin on hydrogen peroxide (H₂O₂)-induced chondrocytes injury and cartilage degeneration in a rat model of osteoarthritis (OA). MATERIAL AND METHODS Chondrocytes were isolated from rat knee joints and treated with Hesperidin alone or combined with H₂O₂. Then, Cell Counting Kit-8 (CCK-8) assay was used to assess cell viability. Activity of reactive oxygen species (ROS) and levels of malondialdehyde (MDA) were estimated. Cell apoptosis was assessed by flow cytometry assay. In addition, gene expression levels were measured for caspase 3, tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), collagen type II (Col2a1), aggrecan, (sex-determining region Y)-box 9 (SOX9), matrix metalloproteinase (MMP)-13, and inducible nitric oxide synthase (iNOS) through quantitative real-time polymerase chain reaction (qPCR). To examine the effects on cartilage destruction in vivo, Hesperidin or vehicle control were orally administrated in a surgically-induced osteoarthritis (OA) model. RESULTS The results indicated that Hesperidin pretreatment of chondrocytes reduce H₂O₂-induced cytotoxicity and apoptosis. Hesperidin pretreatment decreased the formation of MDA and intracellular ROS, including chondrocyte apoptosis. Hesperidin also reversed the activity of H₂O₂ on inhibiting the Col2a1, aggrecan, and SOX9 gene expression and increasing the gene expression of caspase 3, IL-1β, TNFα, iNOS, and MMP13. In addition, Hesperidin administration markedly attenuated cartilage destruction and reduced IL-1β and TNF-α levels in a surgically-induced OA model. CONCLUSIONS Our study suggests that Hesperidin can prevent H₂O₂-induced chondrocytes injury through its antioxidant effects in vitro and reduce cartilage damage in a rat model of OA.
    Hesperidin Description
    Source: The peels of Citrus sinensis.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.6377 mL 8.1887 mL 16.3773 mL 32.7547 mL 40.9433 mL
    5 mM 0.3275 mL 1.6377 mL 3.2755 mL 6.5509 mL 8.1887 mL
    10 mM 0.1638 mL 0.8189 mL 1.6377 mL 3.2755 mL 4.0943 mL
    50 mM 0.0328 mL 0.1638 mL 0.3275 mL 0.6551 mL 0.8189 mL
    100 mM 0.0164 mL 0.0819 mL 0.1638 mL 0.3275 mL 0.4094 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Eur J Cancer. 2014 Sep;50(14):2489-507.
    Hesperidin induces apoptosis and triggers autophagic markers through inhibition of Aurora-A mediated phosphoinositide-3-kinase/Akt/mammalian target of rapamycin and glycogen synthase kinase-3 beta signalling cascades in experimental colon carcinogenesis.[Pubmed: 25047426]
    Abnormalities in the homeostasis mechanisms involved in cell survival and apoptosis are contributing factors for colon carcinogenesis. Interventions of these mechanisms by pharmacologically safer agents gain predominance in colon cancer prevention. We previously reported the chemopreventive efficacy of Hesperidin against colon carcinogenesis.
    METHODS AND RESULTS:
    In the present study, we aimed at investigating the potential of Hesperidin over the abrogated Aurora-A coupled pro-survival phosphoinositide-3-kinase (PI3K)/Akt signalling cascades. Further, the role of Hesperidin over apoptosis and mammalian target of rapamycin (mTOR) mediated autophagic responses were studied. Azoxymethane (AOM) induced mouse model of colon carcinogenesis was involved in this study. Hesperidin treatment was provided either in initiation/post-initiation mode respectively. Hesperidin significantly altered AOM mediated anti-apoptotic scenario by modulating Bax/Bcl-2 ratio together with enhanced cytochrome-c release and caspase-3, 9 activations. In addition, Hesperidin enhanced p53-p21 axis with concomitant decrease in cell cycle regulator. Hesperidin treatment caused significant up-regulation of tumour suppressor phosphatase and tensin homologue (PTEN) with a reduction in the expression of AOM mediated p-PI3K and p-Akt. Additionally, Hesperidin administration exhibited inhibition against p-mTOR expression which in turn led to stimulation of autophagic markers Beclin-1 and LC3-II. Aurora-A an upstream regulator of PI3K/Akt pathway was significantly inhibited by Hesperidin. Furthermore, Hesperidin administration restored glycogen synthase kinase-3 beta (GSK-3β) activity which in turn prevented the accumulation of oncoproteins β-catenin, c-jun and c-myc.
    CONCLUSIONS:
    Taken together, Hesperidin supplementation initiated apoptosis via targeted inhibition of constitutively activated Aurora-A mediated PI3K/Akt/GSK-3β and mTOR pathways coupled with autophagic stimulation against AOM induced colon carcinogenesis.
    Animal Research:
    Tissue Cell. 2014 Oct;46(5):304-10.
    Protective effect of hesperidin against lung injury induced by intestinal ischemia/reperfusion in adult albino rats: histological, immunohistochemical and biochemical study.[Pubmed: 25063207 ]
    Hesperidin is a naturally common flavonoid. It is an abundant and cheap by-product of citrus cultivation. It is reported to have antioxidative, anti-inflammatory and anticarcinogenic effects. This work was performed to investigate the possible protective role of Hesperidin in ameliorating the effect of experimentally induced intestinal ischemia/reperfusion injury (I/R) on lung tissue, histologically, immunohistochemically and biochemically.
    METHODS AND RESULTS:
    Thirty male Wistar adult albino rats were randomized into three groups named: group I (control group); group II (I/R); and group III (I/R with Hesperidin). Intestinal I/R was induced by occluding the superior mesenteric artery for 60 min, followed by 120 min of reperfusion period. Animals were given Hesperidin orally 1h before the onset of ischemia. At the end of the reperfusion period the lung tissues were extracted for histopathological examination and immunohistochemical detection of the distribution of inducible nitric oxide synthase (iNOS). Pulmonary edema was evaluated by lung tissue wet/dry weight ratios. The levels of malondialdehyde (MDA, a biomarker of oxidative damage), myeloperoxidase (MPO, an index of the degree of neutrophil accumulation) and glutathione (GSH, a biomarker of protective oxidative injury) were also determined in all dissected tissues. Pretreatment with Hesperidin (in group III) alleviated lung morphological changes noticed in I/R group and the levels of MDA and MPO were significantly decreased whereas those of GSH were significantly increased. Immunohistochemical study revealed a significant decrease in the iNOS. Hesperidin also significantly alleviated the formation of pulmonary edema as evidenced by the decreased organ wet/dry weight ratios.
    CONCLUSIONS:
    Hesperidin exerts a protective effect against lung damage induced by intestinal I/R injury in rats by reducing oxidative stress.
    J Nutr. 2003 Jun;133(6):1892-7.
    Hesperidin, a citrus flavonoid, inhibits bone loss and decreases serum and hepatic lipids in ovariectomized mice.[Pubmed: 12771335]
    The purpose of this study was to examine whether Hesperidin inhibits bone loss in ovariectomized mice (OVX), an animal model of postmenopausal osteoporosis.
    METHODS AND RESULTS:
    Forty 8-wk-old female ddY mice were assigned to five groups: a sham-operated group fed the control diet (AIN-93G), an OVX group fed the control diet, an OVX+HesA group fed the control diet containing 0.5 g/100 g Hesperidin, and an OVX+HesB group fed the control diet containing 0.7 g/100 g alpha-glucosylHesperidin and an OVX+17beta-estradiol (E(2)) group fed the control diet and administered 0.03 micro g E(2)/d with a mini-osmotic pump. After 4 wk, the mice were killed and blood, femoral, uterine and liver were sampled immediately. Hesperidin administration did not affect the uterine weight. In OVX mice, the bone mineral density of the femur was lower than in the sham group (P < 0.05) and this bone loss was significantly prevented by dietary Hesperidin or alpha-glucosylHesperidin. The Ca, P and Zn concentrations in the femur were significantly higher in the Hesperidin-fed and E(2) groups than in the OVX group. Histomorphometric analyses showed that the trabecular bone volume and trabecular thickness in the femoral distal metaphysis were markedly decreased (P < 0.05) by OVX, and alpha-glucosylHesperidin significantly prevented this bone loss. Furthermore, Hesperidin decreased the osteoclast number of the femoral metaphysis in OVX mice, as did E(2). Serum and hepatic lipids were lower in mice that consumed the Hesperidin-containing diets (P < 0.05) than in the OVX group fed the control diet.
    CONCLUSIONS:
    These results suggest a possible role for citrus flavonoids in the prevention of lifestyle-related diseases because of their beneficial effects on bone and lipids.