NaringeninCAS# 480-41-1 |
2D Structure
- (±)-Naringenin
Catalog No.:BCN9061
CAS No.:67604-48-2
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 480-41-1 | SDF | Download SDF |
PubChem ID | 932 | Appearance | Powder |
Formula | C15H12O5 | M.Wt | 272.3 |
Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
Synonyms | 67604-48-2;4',5,7-Trihydroxyflavanone; Naringenine; (+/-)-Naringenin; Naringetol | ||
Solubility | DMSO : ≥ 50 mg/mL (183.65 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 5,7-dihydroxy-2-(4-hydroxyphenyl)-2,3-dihydrochromen-4-one | ||
SMILES | C1C(OC2=CC(=CC(=C2C1=O)O)O)C3=CC=C(C=C3)O | ||
Standard InChIKey | FTVWIRXFELQLPI-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C15H12O5/c16-9-3-1-8(2-4-9)13-7-12(19)15-11(18)5-10(17)6-14(15)20-13/h1-6,13,16-18H,7H2 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Naringenin is a weak estrogen that also exhibits partial antiestrogenic activity in the female rat uterus and MCF-7 human breast cancer cells. Naringenin is also a agent for the treatment of hepatitis C virus (HCV) infection. Naringenin has hypocholesterolemic, antioxidant, free radical scavenger, anti-cancer, anti-inflammatory, neuroprotective, carbohydrate metabolism promoter, and immune system modulator properties. Naringenin possesses potent antidepressant-like property via the central serotonergic and noradrenergic systems. |
Targets | NOS | COX | TNF-α | PGE | IL Receptor | PI3K | Akt | Caspase | NF-kB | NO | p65 | LDL |
In vitro | Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases.[Pubmed: 22552813 ]Int J Mol Med. 2012 Jul;30(1):204-10.Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, has been reported to exhibit anti-inflammatory and antitumor activities. However, the cellular and molecular mechanisms underlying the Naringenin anti-inflammatory activity are poorly understood.
Secretion of hepatocyte apoB is inhibited by the flavonoids, naringenin and hesperetin, via reduced activity and expression of ACAT2 and MTP.[Pubmed: 11352979]J Lipid Res. 2001 May;42(5):725-34.The citrus flavonoids, Naringenin and hesperetin, lower plasma cholesterol in vivo. However, the underlying mechanisms are not fully understood.
|
In vivo | Naringenin attenuates cisplatin nephrotoxicity in rats.[Pubmed: 15826879 ]Life Sci. 2005 Mar 18;76(18):2125-35.
Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin.[Pubmed: 19409769]Exp Toxicol Pathol. 2010 Mar;62(2):171-81.This experiment pertains to the protective role of Naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties.
Neuroprotective properties of the natural phenolic antioxidants curcumin and naringenin but not quercetin and fisetin in a 6-OHDA model of Parkinson's disease.[Pubmed: 16298737 ]Free Radic Res. 2005 Oct;39(10):1119-25.
Although the cause of dopaminergic cell death in Parkinson's disease (PD) remains unknown, oxidative stress has been strongly implicated. Because of their ability to combat oxidative stress, diet derived phenolic compounds continue to be considered as potential agents for long-term use in PD.
This study was aimed at investigating whether the natural phenolic compounds curcumin, Naringenin, quercetin, fisetin can be neuroprotective in the 6-OHDA model of PD.
|
Animal Research | Anti-atherogenic effect of citrus flavonoids, naringin and naringenin, associated with hepatic ACAT and aortic VCAM-1 and MCP-1 in high cholesterol-fed rabbits.[Pubmed: 11396955]Naringenin: a weakly estrogenic bioflavonoid that exhibits antiestrogenic activity.[Pubmed: 7503800]Involvement of monoaminergic system in the antidepressant-like effect of the flavonoid naringenin in mice.[Pubmed: 20603175 ]Prog Neuropsychopharmacol Biol Psychiatry. 2010 Oct 1;34(7):1223-8.Dietary flavonoids possess a multiplicity of neuroprotective actions in various central nervous pathophysiological conditions including depression.
Biochem Pharmacol. 1995 Oct 26;50(9):1485-93.
Biochem Biophys Res Commun. 2001 Jun 15;284(3):681-8.The anti-atherogenic effects of the citrus flavonoids, naringin and Naringenin, were evaluated in high cholesterol-fed rabbits.
|
Naringenin Dilution Calculator
Naringenin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.6724 mL | 18.3621 mL | 36.7242 mL | 73.4484 mL | 91.8105 mL |
5 mM | 0.7345 mL | 3.6724 mL | 7.3448 mL | 14.6897 mL | 18.3621 mL |
10 mM | 0.3672 mL | 1.8362 mL | 3.6724 mL | 7.3448 mL | 9.1811 mL |
50 mM | 0.0734 mL | 0.3672 mL | 0.7345 mL | 1.469 mL | 1.8362 mL |
100 mM | 0.0367 mL | 0.1836 mL | 0.3672 mL | 0.7345 mL | 0.9181 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
Naringenin is the predominant flavanone in grapefruit; displays strong anti-inflammatory and antioxidant activities.
In Vitro:Naringenin is shown to inhibit the proliferation of HepG2 cells resulted partly from an accumulation of cells in the G0/G1 and G2/M phase of the cell cycle. Naringenin has been shown to induce apoptosis as evidenced by nuclei damage and increased proportion of apoptotic cells. Naringenin triggers the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, subsequent release of cytochrome C, and sequential activation of caspase-3[1]. Naringenin exposure significantly reduces the cell viability of A431 cells with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. Cell cycle study shows that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis reveal a dose dependent increment in caspase-3 activity which leads to cell apoptosis[2].
In Vivo:Naringenin supplementation causes a significant reduction in the amount of total triglyceride and cholesterol in plasma and liver. In addition, naringenin supplementation lowers adiposity and triglyceride contents in parametrial adipose tissue. Naringenin-fed animals show a significant increase in PPARα protein expression in the liver. The expression of CPT-1 and UCP2, known to be regulated by PPARα, is markedly enhanced by naringenin treatment[3]. Naringenin increases hepatic fatty acid oxidation through a PPARγ coactivator 1α/PPARα-mediated transcription program. It prevents sterol regulatory element-binding protein 1c–mediated lipogenesis in both liver and muscle by reducing fasting hyperinsulinemia. Naringenin decreases hepatic cholesterol and cholesterol ester synthesis[4]. Naringenin inhibits TNF-α-induced VSMC proliferation and migration in a dose-dependent manner. Mechanistic study demonstrates that naringenin prevents ERK/MAPK and Akt phosphorylation while left p38 MAPK and JNK unchanged. Naringenin also blocks the increase of ROS generation induced by TNF-α[5].
References:
[1]. Arul D, et al. Naringenin (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. Pathol Oncol Res. 2013 Oct;19(4):763-70.
[2]. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS generation and cell cycle arrest. PLoS One. 2014 Oct 16;9(10):e110003.
[3]. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α proteinexpression and decreases plasma triglyceride and adiposity in rats. Eur J Nutr. 2011 Mar;50(2):81-8.
[4]. Mulvihill EE, et al. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDLreceptor-null mice with diet-induced insulin resistance. Diabetes. 2009 Oct;58(10):2198-210.
[5]. Chen S, et al. Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1. Food Chem Toxicol. 2012 Sep;50(9):3025-31.
- Chrysin
Catalog No.:BCN5557
CAS No.:480-40-0
- Pinocembrin
Catalog No.:BCN5556
CAS No.:480-39-7
- Pinostrobin
Catalog No.:BCN5555
CAS No.:480-37-5
- Linarin
Catalog No.:BCN5554
CAS No.:480-36-4
- Eugenin
Catalog No.:BCN2921
CAS No.:480-34-2
- Mellein
Catalog No.:BCN4785
CAS No.:480-33-1
- Orobol
Catalog No.:BCN5553
CAS No.:480-23-9
- Aromadendrin
Catalog No.:BCN5552
CAS No.:480-20-6
- Isorhamnetin
Catalog No.:BCN5551
CAS No.:480-19-3
- Taxifolin
Catalog No.:BCN5550
CAS No.:480-18-2
- Morin
Catalog No.:BCN1028
CAS No.:480-16-0
- Izalpinine
Catalog No.:BCN3682
CAS No.:480-14-8
- Isosakuranetin
Catalog No.:BCN5559
CAS No.:480-43-3
- Acacetin
Catalog No.:BCN5560
CAS No.:480-44-4
- Hydrangenol
Catalog No.:BCN5561
CAS No.:480-47-7
- Retrorsine
Catalog No.:BCN2119
CAS No.:480-54-6
- Lecanoric acid
Catalog No.:BCN5562
CAS No.:480-56-8
- Orsellinic acid
Catalog No.:BCN6574
CAS No.:480-64-8
- 2',4',6'-Trihydroxyacetophenone
Catalog No.:BCN3996
CAS No.:480-66-0
- Jaconine
Catalog No.:BCN2089
CAS No.:480-75-1
- Jacoline
Catalog No.:BCN2088
CAS No.:480-76-2
- Platyphylline
Catalog No.:BCN2115
CAS No.:480-78-4
- Integerrimine
Catalog No.:BCN2131
CAS No.:480-79-5
- Seneciphylline
Catalog No.:BCN5563
CAS No.:480-81-9
Secretion of hepatocyte apoB is inhibited by the flavonoids, naringenin and hesperetin, via reduced activity and expression of ACAT2 and MTP.[Pubmed:11352979]
J Lipid Res. 2001 May;42(5):725-34.
The citrus flavonoids, Naringenin and hesperetin, lower plasma cholesterol in vivo. However, the underlying mechanisms are not fully understood. The ability of these flavonoids to modulate apolipoprotein B (apoB) secretion and cellular cholesterol homeostasis was determined in the human hepatoma cell line, HepG2. apoB accumulation in the media decreased in a dose-dependent manner following 24-h incubations with Naringenin (up to 82%, P < 0.00001) or hesperetin (up to 74%, P < 0.002). Decreased apoB secretion was associated with reduced cellular cholesteryl ester mass. Cholesterol esterification was decreased, dose-dependently, up to 84% (P < 0.0001) at flavonoid concentrations of 200 microM. Neither flavonoid demonstrated selective inhibition of either form of acyl CoA:cholesterol acyltransferase (ACAT) as determined using CHO cells stably transfected with either ACAT1 or ACAT2. However, in HepG2 cells, ACAT2 mRNA was selectively decreased (- 50%, P < 0.001) by both flavonoids, whereas ACAT1 mRNA was unaffected. In addition, Naringenin and hesperetin decreased both the activity (- 20% to - 40%, P < 0.00004) and expression (- 30% to - 40%, P < 0.02) of microsomal triglyceride transfer protein (MTP). Both flavonoids caused a 5- to 7-fold increase (P < 0.02) in low density lipoprotein (LDL) receptor mRNA, which resulted in a 1.5- to 2-fold increase in uptake and degradation of (125)I-LDL. We conclude that both Naringenin and hesperetin decrease the availability of lipids for assembly of apoB-containing lipoproteins, an effect mediated by 1) reduced activities of ACAT1 and ACAT2, 2) a selective decrease in ACAT2 expression, and 3) reduced MTP activity. Together with an enhanced expression of the LDL receptor, these mechanisms may explain the hypocholesterolemic properties of the citrus flavonoids.
Naringenin: a weakly estrogenic bioflavonoid that exhibits antiestrogenic activity.[Pubmed:7503800]
Biochem Pharmacol. 1995 Oct 26;50(9):1485-93.
Treatment of immature 21-day-old female Sprague-Dawley rats with 17 beta-estradiol (E2) (0.5 microgram/rat) caused a significant increase in uterine wet weight, DNA synthesis, progesterone receptor (PR) binding, and peroxidase activity. At doses as high as 40 mg/rat, the bioflavonoid Naringenin did not cause a significant increase in any of these E2-induced responses. However, in rats cotreated with E2 (0.5 microgram/rat) plus Naringenin (30 mg/rat); there was a significant decrease in E2-induced uterine wet weight, DNA synthesis, PR binding, and peroxidase activity, indicating that Naringenin exhibits antiestrogenic activity in the immature rodent uterus. The binding of uterine nuclear extracts to a 32P-labeled estrogen responsive element (ERE) or progesterone responsive element (PRE) was determined using gel electrophoretic band shift assays. Incubation of [32P]ERE with uterine nuclear extracts from rats treated with Naringenin or E2 resulted in the formation of estrogen receptor (ER):ERE complexes; a higher mobility complex was prominent in the extracts from E2-treated rats, whereas a lower mobility complex was observed using nuclear extracts from Naringenin-treated animals. There was a significant decrease in the intensity of the E2-induced complex using nuclear extracts from rats treated with E2 plus Naringenin. In contrast, transformed cytosol from control rats gave an intense ER:ERE complex, whereas the intensity of the band was decreased markedly using transformed uterine cytosol from treated rats. Formation of a PR:PRE complex was also determined using transformed uterine cytosol. Cytosol from E2-treated rats gave an intense retarded band, whereas only weak bands were observed using cytosols from DMSO- (solvent), Naringenin-, or Naringenin plus E2-treated cells. The results of in vitro studies showed that 1 nM E2 increased (3- to 4-fold) the growth of MCF-7 human breast cancer cells, whereas 1-1000 nM Naringenin had no effect on cell proliferation. In cells cotreated with 1 nM E2 plus 1000 nM Naringenin, there was a significant decrease in E2-induced cell growth. In MCF-7 cells transiently transfected with a pS2 promoter-regulated luciferase reporter gene, Naringenin exhibited weak estrogenic activity. In cells cotreated with 0.1 or 1.0 microM Naringenin plus 1 nM E2, Naringenin inhibited E2-induced luciferase activity. The results of these studies confirmed that Naringenin is a weak estrogen that also exhibits partial antiestrogenic activity in the female rat uterus and MCF-7 human breast cancer cells.
Anti-atherogenic effect of citrus flavonoids, naringin and naringenin, associated with hepatic ACAT and aortic VCAM-1 and MCP-1 in high cholesterol-fed rabbits.[Pubmed:11396955]
Biochem Biophys Res Commun. 2001 Jun 15;284(3):681-8.
The anti-atherogenic effects of the citrus flavonoids, naringin and Naringenin, were evaluated in high cholesterol-fed rabbits. At 3 months of age, 30 male New Zealand White (NZW) rabbits were divided into three groups (n = 10 per group). The rabbits were fed a 1% cholesterol diet alone (control group) or a diet supplemented with either 0.1% naringin or 0.05% Naringenin for 8 weeks. The plasma lipoprotein levels, total cholesterol, triglyceride, and high-density lipoprotein showed no significant differences in the control and experimental groups. Hepatic acyl-CoA:cholesterol acyltransferase (ACAT) activity was slightly low in naringin (5.0%)- and Naringenin (15.0%)-fed rabbits, compared to control group. The aortic fatty streak areas were significantly lower in both the naringin (19.2 +/- 5.6%)- and Naringenin (18.1 +/- 6.5%)-supplemented groups than in the control group (60.4 +/- 14.0%). The expression levels of vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1), by semiquantitative RT-PCR analysis of the thoracic aorta, were significantly lower in the flavonoids supplemented groups than in the control group. These results suggest that the anti-atherogenic effect of the citrus flavonoids, naringin and Naringenin, is involved with a decreased hepatic ACAT activity and with the downregulation of VCAM-1 and MCP-1 gene expression.
Neuroprotective properties of the natural phenolic antioxidants curcumin and naringenin but not quercetin and fisetin in a 6-OHDA model of Parkinson's disease.[Pubmed:16298737]
Free Radic Res. 2005 Oct;39(10):1119-25.
Although the cause of dopaminergic cell death in Parkinson's disease (PD) remains unknown, oxidative stress has been strongly implicated. Because of their ability to combat oxidative stress, diet derived phenolic compounds continue to be considered as potential agents for long-term use in PD. This study was aimed at investigating whether the natural phenolic compounds curcumin, Naringenin, quercetin, fisetin can be neuroprotective in the 6-OHDA model of PD. Unilateral infusion of 6-OHDA into the medial forebrain bundle produced a significant loss of tyrosine hydroxylase (TH)-positive cells in the substantia nigra (SN) as well as a decreased of dopamine (DA) content in the striata in the vehicle-treated animals. Rats pretreated with curcumin or Naringenin showed a clear protection of the number of TH-positive cells in the SN and DA levels in the striata. However, neither pretreatment with quercetin nor fisetin had any effects on TH-positive cells or DA levels. The ability of curcumin and Naringenin to exhibit neuroprotection in the 6-OHDA model of PD may be related to their antioxidant capabilities and their capability to penetrate into the brain.
Involvement of monoaminergic system in the antidepressant-like effect of the flavonoid naringenin in mice.[Pubmed:20603175]
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Oct 1;34(7):1223-8.
Dietary flavonoids possess a multiplicity of neuroprotective actions in various central nervous pathophysiological conditions including depression. In this study, the neuropharmacological mechanism of the dietary flavonoid Naringenin was investigated in the mouse behavioral models of depression. For this purpose, we investigated the influence of pretreatment with the inhibitors of serotonin or noradrenaline synthesis, p-chlorophenylalanine methyl ester or alpha-methyl-p-tyrosine, respectively in the anti-immobility effect of Naringenin. Compared to the control group, Naringenin significantly decreased the immobility time after acute treatment in the mouse tail suspension test (10, 20 and 50 mg/kg), but not in the forced swimming test, without producing locomotor alteration in the open-field test. In addition, pretreatment of mice with p-chlorophenylalanine methyl ester (100 mg/kg) or alpha-methyl-p-tyrosine (100 mg/kg) prevented the anti-immobility effect of Naringenin (20 mg/kg) in the tail suspension test. Taken together, this data demonstrated that Naringenin possessed potent antidepressant-like property via the central serotonergic and noradrenergic systems. Thus, our findings suggest the therapeutic potential of this dietary flavonoid in central nervous system disorders especially depression where monoaminergic systems are involved.
Inhibitory effects of naringenin on tumor growth in human cancer cell lines and sarcoma S-180-implanted mice.[Pubmed:15744083]
Biol Pharm Bull. 2005 Mar;28(3):527-30.
We have investigated the effect of Naringenin (NGEN) on tumor growth in various human cancer cell lines and sarcoma S-180-implanted mice. NGEN showed cytotoxicity in cell lines derived from cancer of the breast (MCF-7, MDA-MB-231), stomach (KATOIII, MKN-7), liver (HepG2, Hep3B, Huh7), cervix (Hela, Hela-TG), pancreas (PK-1), and colon (Caco-2) as well as leukemia (HL-60, NALM-6, Jurkat, U937). NGEN-induced cytotoxicity was low in Caco-2 and high in leukemia cells compared to other cell lines. NGEN dose-dependently induced apoptosis, with hypodiploid cells detected in both Caco-2 and HL-60 by flow cytometric analysis. In vivo, NGEN inhibited tumor growth in sarcoma S-180-implanted mice, following intraperitoneal or peroral injection once a day for 5 d. Naringin (NG) also inhibited tumor growth by peroral injection but not intraperitoneal injection. NGEN, one of the most abundant flavonoids in citrus fruits, may have a potentially useful inhibitory effect on tumor growth.
Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin.[Pubmed:19409769]
Exp Toxicol Pathol. 2010 Mar;62(2):171-81.
This experiment pertains to the protective role of Naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5mg/kg) was administered orally for 4 weeks to induce hepatotoxicity. Liver damage induced by cadmium was clearly shown by the increased activities of serum hepatic marker enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and serum total bilirubin (TB) along with the increased level of lipid peroxidation indices (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) and protein carbonyl contents in liver. The toxic effect of cadmium was also indicated by significantly decreased levels of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C and vitamin E). Administration of Naringenin at a dose of (50mg/kg) significantly reversed the activities of serum hepatic marker enzymes to their near-normal levels when compared to Cd-treated rats. In addition, Naringenin significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. The histopathological studies in the liver of rats also showed that Naringenin (50mg/kg) markedly reduced the toxicity of cadmium and preserved the normal histological architecture of the tissue. The present study suggested that Naringenin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of rats.
Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-kappaB and inhibiting mitogen-activated protein kinases.[Pubmed:22552813]
Int J Mol Med. 2012 Jul;30(1):204-10.
Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, has been reported to exhibit anti-inflammatory and antitumor activities. However, the cellular and molecular mechanisms underlying the Naringenin anti-inflammatory activity are poorly understood. In this study, we conducted an investigation of the inhibitory effects of Naringenin on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators in BV2 microglial cells. We found that pre-treatment with Naringenin prior to treatment with LPS significantly inhibited excessive production of nitric oxide (NO) and prostaglandin E2 (PGE2) in a dose-dependent manner. The inhibition was associated with downregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Naringenin also attenuated the production of pro-inflammatory cytokines and chemokines, including interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) by suppressing expression of mRNAs for these proteins. In addition, the molecular mechanism underlying Naringenin-mediated attenuation in BV2 cells has a close relationship to suppressing translocation of the nuclear factor-kappaB (NF-kappaB) p65 subunit into the nucleus and the phosphorylation of Akt and mitogen-activated protein kinases (MAPKs). These findings suggest that Naringenin may provide neuroprotection through suppression of pro-inflammatory pathways in activated BV2 microglial cells.
Naringenin attenuates cisplatin nephrotoxicity in rats.[Pubmed:15826879]
Life Sci. 2005 Mar 18;76(18):2125-35.
The effect of Naringenin (NAR), a naturally occurring citrus flavanone, on the acute nephrotoxicity produced by cisplatin (7 mg/kg, i.v.) was investigated in the rat. Oral administration of NAR (20 mg/kg/day) for 10 days, starting 5 days before cisplatin single i.v. injection, produced significant protection of renal function. NAR reduced the extent of cisplatin-induced nephrotoxicity, as evidenced by significant reduction in serum urea and creatinine concentrations, decreased polyuria, reduction in body weight loss, marked reduction in urinary fractional sodium excretion and glutathione S-transferase (GST) activity, and increased creatinine clearance. Cisplatin-induced alterations in renal cortex lipid peroxides and GST activity were markedly improved by NAR. Cisplatin-induced alterations in renal cortex antioxidant defense system were greatly prevented by NAR. In cisplatin-NAR combined treatment group, antioxidant enzymes namely superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were significantly increased to 54.5, 30.3 and 35.6%, respectively compared to cisplatin treated group. Platinum renal content was not affected by NAR treatment. The results provide further insight into the mechanisms of cisplatin-induced nephrotoxicity and confirm the antioxidant potential of NAR.