Product Name Naringin
CAS No.: 10236-47-2
Catalog No.: CFN99555
Molecular Formula: C27H32O14
Molecular Weight: 580.53 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: p21 | Wnt/β-catenin | p38MAPK | JNK | NF-kB | p65 | AP-1 | IkB | EGFR | IKK
Source: The peels of Citrus maxima.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $30/20mg
Naringin exhibits antioxidant, anti-atherogenic, antiulcer, anti-hypocholesterolemic, anti-lipoperoxidative, and anti-hyperglycemia effects. Naringin reduces Ara-C-induced oxidative stress through both an inhibition of the generation of ROS production and an increase in antioxidant enzyme activities, it blocks apoptosis caused by Ara-C-induced oxidative stress, resulting in the inhibition of the cytotoxicity of Ara-C. Naringin attenuates epidermal growth factor (EGF)-induced MUC5AC secretion in A549 cells by suppressing the cooperative activities of MAPKs-AP-1 and IKKs-IκB-NF-κB signaling pathways.
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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.

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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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    J Pharmacol Sci. 2003 Jun;92(2):166-70.
    Effects of naringin on hydrogen peroxide-induced cytotoxicity and apoptosis in P388 cells.[Pubmed: 12832847]
    Flavonoids are widely recognized as naturally occurring antioxidants. Naringin (NG) is one of the flavonoid components in citrus fruits such as grapefruit. Hydrogen peroxide (H2O2) causes cytotoxicity through oxidative stress and apoptosis.
    In this paper, we examined the effects of NG on H2O2-induced cytotoxicity and apoptosis in mouse leukemia P388 cells. Cytotoxicity was determined by mitochondrial activity (MTT assay). Apoptosis and DNA damage were analyzed by measuring chromatin condensation and Comet assay (alkaline single cell gel electrophoresis), respectively. H2O2-induced cytotoxicity was significantly attenuated by NG or the reduced form of glutathione (GSH), a typical intracellular antioxidant. NG suppressed chromatin condensation and DNA damage induced by H2O2.
    These results indicate that NG from natural products is a useful drug having antioxidant and anti-apoptopic properties.
    2015 Nov 30;10(11):e0143868.
    Naringin Alleviates Diabetic Kidney Disease through Inhibiting Oxidative Stress and Inflammatory Reaction[Pubmed: 26619044]
    Naringin, a flavanone glycoside extracted from Citrus grandis Osbeck, has a wide range of pharmacological effects. In the present study we aimed at demonstrating the protective effect of Naringin against diabetic kidney disease (DKD) and elucidating its possible molecular mechanism underlying. The beneficial effect of Naringin was assessed in rats with streptozotocin (STZ)-induced diabetes and high glucose-induced HBZY-1 cells. According to our results, first we found that Naringin relieved kidney injury, improved renal function and inhibited collagen formation and renal interstitial fibrosis. Second, we confirmed that Naringin restrained oxidative stress by activating Nrf2 antioxidant pathway. Moreover, the results suggested that Naringin significantly resisted inflammatory reaction by inhibiting NF- κ B signaling pathway. Taken together, our results demonstrate that Naringin effectively alleviates DKD, which provide theoretical basis for Naringin clinically used to treatment of DKD.
    2015 Sep;47(3):1061-9.
    Naringin induces autophagy-mediated growth inhibition by downregulating the PI3K/Akt/mTOR cascade via activation of MAPK pathways in AGS cancer cells[Pubmed: 26201693]
    Naringin, one of the major bioflavonoid of Citrus, has been demonstrated as potential anticancer agent. However, the underlying anticancer mechanism still needs to be explored further. This study investigated the inhibitory effect of Naringin on human AGS cancer cells. AGS cell proliferation was inhibited by Naringin in a dose- and time-dependent manner. Naringin did not induce apoptotic cell death, determined by no DNA fragmentation and the reduced Bax/Bcl-xL ratio. Growth inhibitory role of Naringin was observed by western blot analysis demonstrating downregulation of PI3K/Akt/mTOR cascade with an upregulated p21CIPI/WAFI. Formation of cytoplasmic vacuoles and autophagosomes were observed in Naringin-treated AGS cells, further confirmed by the activation of autophagic proteins Beclin 1 and LC3B with a significant phosphorylation of mitogen activated protein kinases (MAPKs). Collectively, our observed results determined that anti-proliferative activity of Naringin in AGS cancer cells is due to suppression of PI3K/Akt/mTOR cascade via induction of autophagy with activated MAPKs. Thus, the present finding suggests that Naringin induced autophagy- mediated growth inhibition shows potential as an alternative therapeutic agent for human gastric carcinoma.
    J Pharm Bioallied Sci. 2015 Apr-Jun;7(2):121-7.
    Effect of naringin on hemodynamic changes and left ventricular function in renal artery occluded renovascular hypertension in rats.[Pubmed: 25883516]
    Renal artery occlusion (RAO) induced hypertension is a major health problem associated with structural and functional variations of the renal and cardiac vasculature. Naringin a flavanone glycoside derived possesses metal-chelating, antioxidant and free radical scavenging properties. The objective of this study was to investigate the antihypertensive activity of Naringin in RAO induced hypertension in rats.
    Male Wistar rats (180-200 g) were divided into five groups Sham, RAO, Naringin (20, 40 and 80 mg/kg). Animals were pretreated with Naringin (20, 40 and 80 mg/kg p.o) for 4 weeks. On the last day of the experiment, left renal artery was occluded with renal bulldog clamp for 4 h. After assessment of hemodynamic and left ventricular function various biochemical (superoxide dismutase [SOD], glutathione [GSH] and malondialdehyde [MDA]) and histological parameters were determined in the kidney. RESULTS: RAO group significantly (P < 0.001) increased hemodynamic parameters at 15, 30 and 45 min of clamp removal. Naringin (40 and 80 mg/kg) treated groups showed a significant decrease in hemodynamic parameters at 15 min. after clamp removal that remained sustained for 60 min. Naringin (40 and 80 mg/kg) treated groups showed significant improvement in left ventricular function at 15, 30 and 45 min after clamp removal. Alteration in level of SOD, GSH and MDA was significantly restored by Naringin (40 and 80 mg/kg) treatment. It also reduced histological aberration induced in kidney by RAO.
    It is concluded that the antihypertensive activity of Naringin may result through inhibition of oxidative stress.
    Life Sci. 2010 Jun 19;86(25-26):928-35.
    Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice.[Pubmed: 20433854 ]
    The present study has been designed to explore the nitric oxide mechanism in the protective effect of Naringin against I/R induced neurobehavioral alterations, oxidative damage and mitochondrial dysfunction in mice.
    Laca mice (25-30 g) were subjected twice to BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. Naringin (50 and 100 mg/kg) was administered for 10 days, starting 7 days before the animals were subjected to I/R injury. On day 10, various neurobehavioral parameters followed by biochemical parameters and mitochondrial enzyme complex activities were assessed. Ischemia reperfusion injury caused significant (increased immobility period, neurological score and decreased locomotor activity) oxidative damage (increased lipid peroxidation and nitrite concentration and depleted reduced glutathione, glutathione-S-transferase, superoxide dismutase and catalase) and altered mitochondrial enzyme complex activities (complex I to IV) as compared to sham treatment. Naringin (50 and 100 mg/kg) treatment significantly attenuated neurobehavioral alterations, oxidative damage and restored mitochondrial enzyme complex activities as compared to control (ischemia reperfusion) group. Further, protective effect of Naringin (50 mg/kg) was attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with Naringin (50 mg/kg) significantly potentiated their protective effect as compared to their treatment alone.
    The present study suggests the involvement of nitric oxide mechanism in the protective effect of Naringin against post-stroke depression induced neurobehavioral, biochemical and cellular alterations in mice.
    Toxicology. 2007 Feb 12;230(2-3):178-88.
    Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats.[Pubmed: 17188415 ]
    Diets rich in natural antioxidants are associated with reduced risk of heart diseases.
    This study was aimed to evaluate the preventive role of Naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85mg/kg) at an interval of 24h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of beta-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with Naringin (10, 20 or 40mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats.
    Thus, Naringin possess cardioprotective effect in ISO-induced MI in rats.
    Pharmacology. 1994 Sep;49(3):144-50.
    Antiulcer effect of naringin on gastric lesions induced by ethanol in rats.[Pubmed: 7972328]
    This study was designed to determine the gastroprotective properties of Naringin on and the involvement of endogenous prostaglandins in mucosal injury produced by absolute ethanol.
    Oral pretreatment with the highest dose of Naringin (400 mg/kg), 60 min before absolute ethanol was the most effective antiulcer treatment. Subcutaneous administration of indomethacin (10 mg/kg) to the animals treated with Naringin (400 mg/kg) partially inhibited gastric protection, but the prostaglandin E2 determination did not show any increase in prostanoid levels. The contents of gastric mucus and total proteins were not significantly modified. Naringin-treated rats showed a marked increase in hexosamine levels, but this increase was less in animals pretreated with indomethacin.
    These results show that Naringin has a 'cytoprotective' effect against ethanol injury in the rat, but this property appears to be mediated by non-prostaglandin-dependent mechanisms.
    2015 Nov;409(1-2):199-211.
    Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells[Pubmed: 26280522]
    Oxidative stress and mitochondrial dysfunction are implicated in neuronal apoptosis associated with Huntington's disease. Naringin is the flavanone present in grapefruit and related citrus species possess diverse pharmacological and therapeutic properties including antioxidant, anti-apoptotic, and neuroprotective properties. The aim of this study was to investigate the protective effect of Naringin on 3-nitropropionic acid (3-NP)-induced neurotoxicity in pheochromocytoma cells (PC12) cells and to explore its mechanism of action. Naringin protects PC12 cells from 3-NP neurotoxicity, as evaluated the by cell viability assays. The lactate dehydrogenase release was decreased upon Naringin treatment in 3-NP-induced PC12 cells. Naringin treatment enhances the antioxidant defense by increasing the activities of enzymatic antioxidants and the level of reduced glutathione. The increase in levels of reactive oxygen species and lipid peroxidation induced by 3-NP were significantly decreased by Naringin. PC12 cells induced with 3-NP showed decrease in the mitochondrial membrane potential and mitochondrial respiratory complex enzymes, succinate dehydrogenase and cytochrome c oxidase activities, and it was significantly altered to near normal upon Naringin treatment. Naringin reduced the 3-NP-induced apoptosis through the modulation in expressions of B-cell lymphoma 2 and Bcl-2-associated X protein. Further, Naringin enhances the nuclear translocation of Nrf2 and induces the Nad(p)h: quinone oxidoreductase-1 and Heme oxygenase-1 expressions through the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway. Taken together, the above findings suggest that Naringin augments cellular antioxidant defense capacity and reduces the 3-NP-induced neurotoxicity in PC12 cells through the PI-3K/Akt-dependent Nrf2 activation in PC12 cells. Keywords: 3-Nitropropionic acid; Apoptosis; Mitochondrial dysfunction; Naringin; Nrf2; Oxidative stress; PI-3K/Akt.
    Toxicol Lett. 2013 Jul 18;220(3):219-28.
    Naringin inhibits growth potential of human triple-negative breast cancer cells by targeting β-catenin signaling pathway.[Pubmed: 23694763 ]
    Triple-negative (ER-/PR-/HER2-) breast cancer (TNBC) is a severe clinical problem because of its relatively poorer prognosis, aggressive behavior and lack of targeted therapies. Naringin, a major flavonoid extracted from citrus fruits, has been reported to exert promising anticancer activities. However, the detailed antitumor mechanism of Naringin still remains enigmatic.
    In this study, TNBC cell lines-based in vitro and in vivo models were used to explore the anticancer effect and mechanism of Naringin. Our data demonstrated that Naringin inhibited cell proliferation, and promoted cell apoptosis and G1 cycle arrest, accompanied by increased p21 and decreased survivin. Meanwhile, β-catenin signaling pathway was found to be suppressed by Naringin. In contrast, over-expressing β-catenin by adenoviral vector system in TNBC cells reversed the antitumor activity of Naringin, and regulated p21 and survivin. Correspondingly, the antitumor potential of Naringin was also observed in Naringin-treated MDA-MB-231 xenograft mice, while immunohistochemical analysis of tumors from Naringin-treated mice showed higher expression of p21 and lower expression of survivin and active β-catenin.
    Taken together, these results indicate that Naringin could inhibit growth potential of TNBC cells by modulating β-catenin pathway, which suggests Naringin might be used as a potential supplement for the prevention and treatment of breast cancer.
    Eur J Pharmacol. 2012 Sep 5;690(1-3):207-13.
    Naringin attenuates EGF-induced MUC5AC secretion in A549 cells by suppressing the cooperative activities of MAPKs-AP-1 and IKKs-IκB-NF-κB signaling pathways.[Pubmed: 22766066 ]
    Naringenin, the aglycone of Naringin, has been reported to attenuate MUC5AC secretion by inhibiting activity of nuclear factor kappa B (NF-κB) via EGFR-PI3K-Akt/ERK MAPKinase signaling pathways. However, previous studies demonstrated that the MUC5AC promoter was located in two different regions: an activator protein-1 (AP-1) binding site and a NF-κB binding site.
    The current study comprehensively determined the involvement of MAPKs/AP-1 and IKKs/IκB/NF-κB in epidermal growth factor (EGF)-induced A549 cells, and sought to ascertain the signaling pathways of Naringin imparted in suppression of EGF-induced MUC5AC secretion. The results showed that Naringin of 100 μM not only significantly decreased EGF-induced overexpressions of both MUC5AC mucin and mRNA in A549 cells, but also suppressed the phosphorylation of EGF receptor, p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK1/2), and c-Jun N-terminal kinase (JNK), as well as nucleus NF-κB p65 and AP-1. Moreover, any of three MAPKs inhibitors (PD98059, SB203580, and SP600125) significantly inhibited EGF-induced MUC5AC secretion. And as compared to MG132, the inhibitor κB (IκB) phosphorylation inhibitor of SN50 was more effective in reducing EGF-induced MUC5AC secretion because of suppression of nucleus AP-1. Meanwhile, as compared to Naringin, both SP600125 and azithromycin were less effective in suppressing EGF-induced secretion of MUC5AC because of the unchanged nucleus NF-κB p65.
    These results indicated that Naringin attenuates EGF-induced MUC5AC secretion in A549 cells by suppressing the cooperative activities of MAPKs/AP-1 and IKKs/IκB/NF-κB signaling pathways.
    J. Nutr., 2004, 134(10):2499-503.
    The hypoglycemic effects of hesperidin and naringin are partly mediated by hepatic glucose-regulating enzymes in C57BL/KsJ-db/db mice.[Pubmed: 15465737]
    Dietary antioxidant compounds such as bioflavonoids may offer some protection against the early stage of diabetes mellitus and the development of complications.
    We investigated the effect of citrus bioflavonoids on blood glucose level, hepatic glucose-regulating enzymes activities, hepatic glycogen concentration, and plasma insulin levels, and assessed the relations between plasma leptin and body weight, blood glucose, and plasma insulin. Male C57BL/KsJ-db/db mice (db/db mice, 5 wk old), an animal model for type 2 diabetes, were fed a nonpurified diet for 2 wk and then were fed an AIN-76 control diet or the control diet supplemented with hesperidin (0.2 g/kg diet) or Naringin (0.2 g/kg diet). Hesperidin and Naringin supplementation significantly reduced blood glucose compared with the control group. Hepatic glucokinase activity and glycogen concentration were both significantly elevated in the hesperidin- and the Naringin-supplemented groups compared with the control group. Naringin also markedly lowered the activity of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxykinase compared with the control group. Plasma insulin, C-peptide, and leptin levels in the db/db mice from the 2 bioflavonoid-supplemented groups were significantly higher than those of the control group. Furthermore, plasma leptin was positively correlated with plasma insulin level (r = 0.578, P < 0.01) and body weight (r = 0.541, P < 0.05), and was inversely correlated with the blood glucose level (r = -0.46, P < 0.05).
    The current results suggest that hesperidin and Naringin both play important roles in preventing the progression of hyperglycemia, partly by increasing hepatic glycolysis and glycogen concentration and/or by lowering hepatic gluconeogenesis.
    Clin Nutr. 2004 Oct;23(5):1025-34.
    Antihypercholesterolemic property of naringin alters plasma and tissue lipids, cholesterol-regulating enzymes, fecal sterol and tissue morphology in rabbits.[Pubmed: 15380892 ]
    Hyperlipidemia is a major risk factor for cardiovascular diseases. This study was designed to confirm the hypocholesterolemic role of Naringin.
    Male rabbits were fed 0.5% high-cholesterol diet or high-cholesterol diet supplemented with either 0.05% Naringin or 0.03% lovastatin for 8 weeks. The Naringin and lovastatin supplements significantly lowered plasma total- and LDL-cholesterol and hepatic lipids levels, while significantly increasing HDL-C/total-C ratio compared to the control group. Hepatic 3-hydroxy-3-methylglutaryl CoA reductase and acyl-CoA: cholesterol acyltransferase activities were significantly higher and lower, respectively, in both supplemented groups than the control group. Total fecal sterol content was significantly increased in lovastatin and especially Naringin group. In histopathological analyses, only control group exhibited hepatic lipid droplets, cardiac adipocyte infiltration and slight damage of endothelial lining in aortic wall, but two supplements retarded these atherogenic signs.
    It would appear that both Naringin and lovastatin contributed to hypocholesterolemic action via down-regulated ACAT activity and higher excretion of fecal sterols in response to high-cholesterol feeding. Also, Naringin supplement seemed to preserve tissue morphology from damages induced by high cholesterol diet.
    J Med Food. 2010 Aug;13(4):976-84.
    Protective effect of naringin, a citrus flavonoid, against colchicine-induced cognitive dysfunction and oxidative damage in rats.[Pubmed: 20673063 ]
    Alzheimer's disease is a neurodegenerative disorder. Central administration of colchicine is well known to cause cognitive impairment and oxidative damage, which simulates sporadic dementia of the Alzheimer type in humans.
    The present study has been designed to investigate the protective effects of Naringin against the colchicine-induced cognitive impairment and oxidative damage in rats. Colchicine (15 microg/5 microL), administered intracerebroventricularly, resulted in poor memory retention in both the Morris water maze and elevated plus maze task paradigms and caused marked oxidative damage. It also caused a significant decrease in acetylcholinesterase activity. Naringin (40 and 80 mg/kg, p.o.) treatment was given daily for a period of 25 days beginning 4 days prior to colchicine administration. Chronic treatment with Naringin caused significant improvement in the cognitive performance and attenuated oxidative damage, as evidenced by lowering of malondialdehyde level and nitrite concentration and restoration of superoxide dismutase, catalase, glutathione S-transferase, and reduced glutathione levels, and acetylcholinesterase activity compared to control.
    The present study highlights the therapeutic potential of Naringin against colchicine-induced cognitive impairment and associated oxidative damage.

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