Abstract
We investigated the antioxidant effects of curcumin in an experimental rat model of allergic rhinitis (AR). Female Wistar albino rats (n = 34) were divided randomly into four groups: healthy rats (control group, n = 8), AR with no treatment (AR + NoTr group, n = 10), AR with azelastine HCl treatment (AR + Aze group, n = 8), and AR with curcumin treatment (AR + Curc group, n = 8). On day 28, total blood IgE levels were measured. For measurement of antioxidant activity, the glutathione (GSH) level and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were measured in both inferior turbinate tissue and serum. Malondialdehyde (MDA) levels were measured only in inferior turbinate tissue, and paraoxonase (PON) and arylesterase (ARE) activities were measured only in serum. Statistically significant differences were found for all antioxidant measurements (GSH levels and CAT, SOD, GSH-Px activities in the serum and tissue, MDA levels in the tissue, and PON and ARE activities in the serum) between the four groups. In the curcumin group, serum SOD, ARE, and PON and tissue GSH values were higher than the control group. Moreover, tissue GSH levels and serum GSH-Px activities in the curcumin group were higher than in the AR + NoTr group. In the azelastine group, except MDA, antioxidant measurement values were lower than in the other groups. Curcumin may help to increase antioxidant enzymes and decrease oxidative stress in allergic rhinitis. We recommend curcumin to decrease oxidative stress in allergic rhinitis.
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Introduction
Curcumin (diferuloylmethane) is a natural yellow polyphenolic pigment isolated from the rhizomes of the plant Curcuma longa L. (turmeric). Curcumin can inhibit the antigen-mediated activation of mast cells, IgE production, airway inflammation, and passive cutaneous anaphylaxis in allergy animal models [1]. It is commonly used as a food additive and it shows a wide spectrum of biological and pharmacological effects, such as anti-inflammatory, antioxidant, antimicrobial, antihepatoxic, hypolipidemic, and anticancer properties [2]. Curcumin also has immunomodulatory and anti-allergic activities [1].
Oxidation is a chemical reaction that transfers electrons from one substance to another; the oxidizing agent becomes chemically reduced by taking away the electrons from its reaction partner, which itself is oxidized. Although such reduction/oxidation (redox) reactions are crucial for life, they can also be damaging [3]. Reactive oxygen species (ROS) are defined as strongly oxidizing chemicals, such as hydrogen peroxide (H2O2), ions like hypochlorite (OCI−), most reactive radicals, such as the hydroxyl radical (OH·), and the superoxide anion (O2 −). In vivo, ROS are formed as a by-product of cellular respiration in mitochondria [4].
Oxidative stress is thought to contribute to the development of a wide range of diseases, including cardiovascular and neurodegenerative diseases [5, 6]. Early cell death caused by ROS has also been connected with several pathologies that are associated with a chronically activated immune system, such as human immunodeficiency virus infection and acquired immunodeficiency syndrome, and also malignant tumors and autoimmune pathologies [4, 7].
Many herbal antioxidants have been reported, such as ascorbic acid, vitamin E, hesperidin, diosmin, mangiferin, mangostin, cyanidin, astaxanthin, lutein, lycopene, resveratrol, tetrahydro-curcumin, rosmaric acid, hypericin, ellagic acid, chlorogenic acid, oleuropein, andrographolide, potentilla erecta extract, grape seed extract, pycnogenol, green tea extract, white tea extract, and black tea extract [8]. In curcumin, hydroxyl groups largely contribute to its antioxidant and anti-allergic activities [9].
In this study, we investigated the antioxidant activity of curcumin in an allergic rhinitis (AR) induced rat model. The activities of the antioxidant enzymes glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), paraoxonase (PON), and arylesterase (ARE) and malondialdehyde (MDA) levels were assessed to evaluate antioxidant activity.
Materials and methods
This study was conducted in the Faculty of Medicine, Eskisehir Osmangazi University. Animal adaptation, care, and experimental manipulation were performed at TICAM (the Experimental Studies Center of Eskisehir Osmangazi University). Animals were treated in compliance with relevant principles of the Declaration of Helsinki; and Ethics Committee Approval was also taken from Eskisehir Osmangazi University.
Animals
Healthy albino female Wistar rats (n = 34, weighing 190–220 g) were used in this study. The experimental protocol was reviewed and approved by the Committee of Ethics of Osmangazi University, Center of Medical and Surgical Experiments. All animal procedures were performed in accordance with the approved protocol.
All rats were housed under the same conditions in a room where the temperature and humidity were controlled (20 ± 1 °C, 50 ± 10 % relative humidity) under a 14/10-h to 16/8-h light/dark cycle. Tap water and standard pelleted food were provided ad libitum.
Experimental design
The 34 rats were divided randomly into four groups:
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Group 1: Healthy rats (control group, n = 8).
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Group 2: AR with no treatment (AR + NoTr group, n = 10): AR was induced, but no treatment was given.
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Group 3: AR with azelastine HCl treatment (AR + Aze group, n = 8): AR was induced and azelastine HCl was given on days 21–28.
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Group 4: AR with curcumin treatment (AR + Curc group, n = 8): AR was induced and curcumin was given on days 21–28.
Methods
Induction of AR
The sensitizing solution was prepared by dissolving 0.3 mg ovalbumin (OVA) (Sigma, St. Louis, MO, USA) in 1 mL saline with 30 mg aluminum hydroxide (40 mg/mL) as an adjuvant. Rats in the AR + NoTr, AR + Aze and AR + Curc groups were injected intraperitoneally with this agent every other day for 14 days (on days 1, 3, 5, 7, 9, 11, and 13; total of seven injections per rat). The rats in the control group were given 1 mL saline plus 30 mg aluminum hydroxide intraperitoneally (total of seven injections per rat) on the same days. After 14 days of systemic sensitization, rats in the AR + NoTr, AR + Aze and AR + Curc groups were given 50 µL 2 % (w/v) OVA-saline solution in the form of intranasal drops into each nostril once daily for 14 days. Rats in the control group received saline drops [6–8]. Each nostril received 25 µL 2 % (w/v) OVA-saline solution or saline [10–13].
Measurement of total IgE levels
On day 28, total serum IgE levels were measured in all groups. Blood samples (1 mL) were centrifuged (3000 rpm, 20 min) and the supernatants stored at −20 °C prior to analysis. Serum IgE levels were determined using a commercially available rat IgE ELISA kit (SunReed Biotechnology Co. Ltd., China) according to the manufacturer’s instructions. All results are expressed as kU/L.
Treatment of AR + Aze group
Group 3 rats received azelastine HCl drops in each nostril once daily for 7 days on days 21–28. Drops were given 1 h before intranasal OVA.
Treatment of AR + Curc group
Group 4 rats received curcumin dissolved in distilled water (at 200 mg/mL, 20 µL/nostril) twice daily for 7 days on days 21–28. Drops were given 1 h before intranasal OVA. During curcumin treatment, we did not observe any complications.
Measurement of antioxidant activity
Glutathione (GSH) levels and catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities were measured in both inferior turbinate tissue and serum. Malondialdehyde (MDA) levels were measured only in inferior turbinate tissue, and paraoxonase (PON) and arylesterase (ARE) activities were measured only in serum.
Measurement of MDA levels
Tissue MDA levels were determined by thiobarbituric acid (TBA) reaction according to Yagi’s method [14]. MDA levels for inferior turbinate tissue are expressed as nmol/mL.
Measurement of CAT activity
Serum and tissue CAT activities were determined according to the method of Aebi et al. [15]. Catalase activity is expressed as U/mg protein for tissue and U/mL for serum.
Measurement of SOD activity
Serum and tissue SOD activities were measured on the basis of the inhibition of nitroblue tetrazolium (NBT) reduction by O2 generated by the xanthine/xanthine oxidase system. One unit of SOD activity was defined as the amount of protein causing 50 % inhibition of the NBT reduction rate [16]. SOD activity is expressed as U/mg protein for tissue and U/mL for serum.
Measurement of PON and ARE activities
Serum PON and ARE activities were measured spectrophotometrically as described by Eckerson et al. [17] using a molar extinction coefficient of 18,290 mol/L/cm at 412 nm for p-nitrophenol and 1310 mol/L/cm at 270 nm for phenol, respectively. Their activities were determined through calculation of the rates of hydrolysis of paraoxon and phenyl acetate at 25 °C, respectively. PON and ARE activities are expressed as U/mg protein for tissue and U/mL for serum.
Measurement of GSH levels
GSH in tissue or serum was determined by the method of Ellman [18] modified by Jollow et al. [19]. The method is based on the development of a yellow color when DTNB (5,5′-dithiobis-2-nitrobenzoic acid) was added to compounds containing sulfhydryl groups. Serum or homogenized tissue in phosphate buffer (500 µL) was added to 3 mL of 4 % sulfosalicylic acid. The mixture was centrifuged (3500×g, 10 min). Next, 500 µL of the supernatant were taken and added to Ellman’s reagent. The absorbance was measured at 412 nm after 10 min. Total GSH content is expressed as μg/mg protein for tissue and μg/mL for serum.
Measurement of GSH-Px activity
The activity of GSH-Px in tissue or serum was determined by the Jocelyn method [20]. GSH-Px activity is expressed as U/mg protein for tissue and U/mL for serum.
Total protein content
The protein content of inferior turbinate tissues was measured according to the method of Lowry et al. [21] using bovine serum albumin as a standard.
Statistical analysis
The SPSS software (ver. 16.0) was used for statistical calculations. Kruskal–Wallis variance analysis was used to explore differences among the three groups. If a statistically significant difference was apparent, the Mann–Whitney U test with the Bonferroni correction was used to identify the parameter causing the difference. A p value of <0.05 was considered to indicate statistical significance. If a Bonferroni adjustment was performed, an adjusted p value of <0.0125 was considered to indicate statistical significance.
Results
The total IgE blood levels were 1656.4, 2766.2, 1223.8, and 1804.5 kU/L in Groups 1–4, respectively. The among-group differences were statistically significant by Kruskal–Wallis variance analysis (p < 0.05). The total IgE level of Group 2 was significantly higher than those of Groups 1, 3, and 4 (p adjusted < 0.0125).
Antioxidant measurement results in the four groups are shown in Table 1. For all antioxidant measures (GSH level and CAT, SOD, GSH-Px activities in serum and tissue, MDA level in tissue, and PON and ARE activities in serum), the differences between the four groups (Control, AR + NoTr, and AR + Curc groups) were found as statistically significant (p < 0.05).
SOD (serum and tissue)
In the curcumin group, serum SOD activity was significantly higher than in the control group. In the azelastine group, the tissue SOD level was significantly lower than in the three other groups (adjusted p < 0.0125; Table 2).
CAT (serum and tissue)
Serum and tissue CAT activities in the azelastine group were significantly lower than those in the three other groups (adjusted p < 0.0125; Table 2).
GSH (serum and tissue)
Serum and tissue GSH levels in the azelastine group were significantly lower than those in the three other groups. Additionally, tissue GSH level in the curcumin group was significantly higher than in the control group and AR + NoTr group (adjusted p < 0.0125).
GSH-Px (serum and tissue)
Serum GSH-Px activity in the control and curcumin groups was significantly higher than in the azelastine group. In the curcumin group, serum GSH-Px activity was significantly higher than in the AR + NoTr group (adjusted p < 0.0125). Tissue GSH-Px activity in the azelastine group was significantly lower than in the three other groups (adjusted p < 0.0125; Table 2).
Serum ARE
Serum ARE activity in the curcumin and AR + NoTr groups was significantly higher than in the control group. Serum ARE activity in the azelastine group was significantly lower than in the three other groups (adjusted p < 0.0125; Table 2).
Serum PON
Serum PON activity in the curcumin and AR + NoTr groups was significantly higher than in the control group and azelastine groups (adjusted p < 0.0125; Table 2).
Tissue MDA
Tissue MDA levels in the curcumin and AR + NoTr groups were significantly lower than those in the azelastine group (adjusted p < 0.0125; Table 2).
Discussion
Curcumin (diferuloylmethane) [22], present in the rhizome of the plant Curcuma longa, possesses strong antihepatotoxic [23], antioxidant [24], anti-inflammatory [25] and antitumour [26] activities. It also prevents the initiation of proliferation, invasion, angiogenesis, and metastasis in different cancer cells by interacting with the different cell signaling proteins in mice and rats [27].
Antioxidant compounds are capable of neutralizing ROS, which represents an important aspect of the proinflammatory cascade and Th1-type immunity [28]. To counteract the harmful effects of ROS, cells have a variety of defense strategies, among which are several small molecules that function as antioxidants, as well as two major enzymes, catalase and superoxide dismutase, which are induced to neutralize ROS biochemically [29–31].
Antioxidants also terminate oxidative chain reactions by removing free radical intermediates [31]. Antioxidants may be synthesized in the body or obtained from the diet, as many normal food compounds are antioxidants. They are especially abundant in fruits and vegetables, such as bananas, cranberries, apples, dates, red grapes, potatoes, tomatoes, as well as in beverages, such as coffee, cocoa, and tea. In recent years, glutathione, ascorbic acid (vitamin C), carotenes (vitamin A), melatonin, tocopherols, and tocotrienols (vitamin E) have been under intense investigation with regard to their capacities as antioxidants and in free radical neutralization [32].
Antioxidants may promote health and reduce the effects of aging by cancelling out the cell-damaging effects of free radicals [4]. Various antioxidant compounds have been demonstrated to suppress features of the Th1-type immune response. These agents include not only vitamins, antioxidant phytochemicals, plant extracts, and beverages, but also food preservatives, like sodium sulfite, benzoate, and sorbate, and colorants, like curcumin and beet root extract [33]. Suzuki et al. [34] reported that the hydroxy groups of curcumin play a significant role in exerting both the anti-oxidative and anti-allergic activities, and that most of the compounds develop the anti-allergic activities through mechanisms related to anti-oxidative activities, but some through mechanisms unrelated to anti-oxidation activity.
In this study, we investigated the effects of curcumin in an experimental rat model of AR. Antioxidant measurements were performed in all four groups. Statistically significant differences were found for all antioxidant measurements (GSH level and CAT, SOD, GSH-Px activities in serum and tissue, MDA levels in tissue, and PON and ARE activities in serum) between the four groups. In the curcumin group, serum SOD, ARE, and PON, and tissue GSH values were higher than in the control group. Moreover, tissue GSH level and serum GSH-Px activity in the curcumin group were higher than in the AR + NoTr group. In the azelastine group, except for MDA, antioxidant measurement values were lower than in the other groups.
In a guinea pig model with induced allergic rhinitis, curcumin reduced allergy-related symptoms, such as sneezing, rubbing frequency, lacrimation, and nasal congestion, and reduced inflammatory cell infiltration of the nasal mucosa [35]. Curcumin also inhibited house dust mite-induced lymphocyte proliferation and IL-2, IL-5, granulocyte macrophage-colony stimulating factor (GM-CSF), and IL-4 production in vivo [36]. The antioxidant mechanisms of garlic and curcumin have been attributed to their ability to scavenge ROS through modulation of cellular antioxidant enzyme activity and GSH levels [37–41]. Curcumin has an anti-allergic effect through modulating mast cell-mediated allergic responses in AR. It also inhibited the histopathological changes of nasal mucosa, and decreased the serum levels of histamine, OVA-specific IgE and TNF-α in OVA-induced allergic rhinitis mice. In addition, curcumin suppressed the production of inflammatory cytokines, such as TNF-α, IL-1β, IL-6 and IL-8 [42]. Curcumin also inhibits the arachidonate 5-lipoxygenase (5-LOX) enzyme [43] and cyclooxygenase (COX) enzyme. Two main enzymes of COX and LOX are responsible for the production of eicosanoids. Inhibition of these two enzymes delays tumorigenesis in animals and humans [44].
Curcumin has antioxidant and anti-inflammatory properties [45]. Curcumin inhibits lipid peroxidation and oxidative DNA damage, and reduces the release of arachidonic acid through lipoxygenase and cyclooxygenase inhibition. Curcumin facilitates excretion of many oxygen radicals, particularly superoxide anion, nitrogen dioxide, and hydrogen radicals. Moreover, curcumin shows an anti-inflammatory effect by inhibiting NFκB activation [46, 47]. Curcumin decreased TNF-α and IL-1β levels by preventing inflammation [48]. Curcumin play a vital role against free radical-mediated peroxidation of membrane lipids and oxidative damage of DNA and proteins as an antioxidant activity. The anti-inflammatory effect of curcumin is most likely mediated through its ability to inhibit COX-2, LOX, and inducible nitric oxide synthase (iNOS) whose are important enzymes that mediate inflammatory processes. Upregulation of COX-2 and/or iNOS has been associated with inflammatory disorders [45].
Yarru et al. [49] observed that dietary curcumin increased the expression of hepatic GSH-Px when compared with controls and the expression of the GSH-Px gene was not significantly decreased in birds fed AFB1, where the indirect antioxidant capacity of curcumin was defined by its ability to induce the expression of GSH-Px. Curcumin has relatively low toxicity in human subjects [50]. Large doses of curcumin can cause gastrointestinal problems, including diarrhea and constipation, and in rare cases, contact dermatitis [51, 52]. Curcumin has potential for topical therapy in various allergic diseases, including allergic rhinitis, especially in view of its low toxicity in human subjects [53].
Curcumin, with its antioxidant properties, reduces the oxidative stress that occurs in allergic rhinitis. Because curcumin is an herbal product, and the adverse reactions were limited, it may be suggested for use in people with allergic rhinitis. As an example, curcumin products may be added to yogurt, so it may be used as a nutritional supplement in people with allergic rhinitis. For this purpose, bioavailability should be investigated in detail. These products can be considered as products that will enhance the quality of life. We recommend further research to investigate this issue.
We conclude that curcumin may help to increase antioxidant enzymes and lead to a decrease in oxidative stress in allergic rhinitis. We recommend curcumin for decreasing oxidative stress in allergic rhinitis.
References
Owaga EE, Mponda J, Nyang’inja RA (2014) Nutrigenomic approach in understanding the anti-allergic effects of curcumin. Asian J Biomed Pharm Sci 4(31):1–5. doi:10.15272/ajbps.v4i30.487
Srivastava RM, Singh S, Dubey SK, Misra K, Khar A (2011) Immunomodulatory and therapeutic activity of curcumin. Int Immunopharmacol 11:331–341
Davies K (1995) Oxidative stress, the paradox of aerobic life. Biochem Soc Symp 61:1–31
Zaknun D, Schroecksnadel S, Kurz K, Fuchs D (2012) Potential role of antioxidant food supplements, preservatives and colorants in the pathogenesis of allergy and asthma. Int Arch Allergy Immunol 157(2):113–124
Halliwell B, Gutteridge JMC (2007) Free radicals in biology and medicine, 4th edn. Clarendon, Oxford
Halliwell B (2006) Oxidative stress and neurodegeneration: where are we now? J Neurochem 97:1634–1658
Libby B, Ridker PM, Masari A (2002) Inflammation and atherosclerosis. Circulation 105:1135–1143
Jadhav NR, Powar T, Shinde S, Nadaf S (2014) Herbal nanoparticles: a patent review. Asian J Pharm 8:58–69
Kurup VP, Barrios CS (2008) Immunomodulatory effects of curcumin in allergy. Mol Nutr Food Res 52:1031–1039
Bahekar PC, Shah JH, Ayer UB, Mandhane SN, Thennati R (2008) Validation of guinea pig model of allergic rhinitis by oral and topical drugs. Int Immunopharmacol 8(11):1540–1551
Thakare VN, Osama MM, Naik SR (2013) Therapeutic potential of curcumin in experimentally induced allergic rhinitis in guinea pigs. Int Immunopharmacol 17(1):18–25
Xu YY, Liu X, Dai LB, Zhou SH (2012) Effect of Tong Qiao drops on the expression of eotaxin, IL-13 in the nasal mucosa of rats with allergic rhinitis. J Chin Med Assoc 75(10):524–529. doi:10.1016/j.jcma.2012.07.003 (Epub 2012 Oct 2)
An YF, Wang WH, Zhao CQ, Xue JM, Zhao HL (2007) Preliminary investigation into the allergic rhinitis complicated with acute bacterial sinusitis in mice. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 42:138–142
Yagi K (1998) Simple procedure for specific enzyme of lipid hydroperoxides in serum or plasma. Methods Mol Biol 108:107–110
Aebi H (1984) Catalase in vitro. Methods Enzymol 105:121–126
Sun Y, Oberley LW, Ying L (1988) A simple method for clinical assay of superoxide dismutase. Clin Chem 34(3):497–500
Eckerson HW, Romson J, Wyte C, La Du BN (1983) The human serum paraoxonase polymorphism: identification of phenotypes by their response to salts. Am J Hum Genet 35(2):214–227
Ellman GL (1959) Tissue sulfhydryl groups. Arch Biochem Biophys 82:70–77
Jollow DJ, Mitchell JR, Zampaglione N, Gillette JR (1974) Bromobenzene-induced liver necrosis. Protective role of glutathione and evidence for 3,4-bromobenzene oxide as the hepatotoxic metabolite. Pharmacology 11(3):151–169
Jocelyn PC (1970) The function of subcellular fractions in the oxidation of glutathione in rat liver homogenate. Biochem J 117(5):951–956
Lowry OH, Rosebrough NI, Farr AL, Randall RJ (1961) Protein measurement with the Folin Phenol reagent. J Biol Chem 193:265–275
Maiti M, Chattopadhyay K, Verma M, Chattopadhyay B (2015) Curcumin protects against nicotine-induced stress during protein malnutrition in female rat through immunomodulation with cellular amelioration. Mol Biol Rep 42(12):1623–1637
Aggarwal BB, Kumar A, Bharti AC (2003) Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res 23:363–398
Kalpana C, Sudheer AR, Rajasekharan KN, Menon VP (2007) Comparative effect of curcumin and its synthetic analogue lipid per oxidation on tissue and antioxidant status during nicotine induced toxicity. Singap Med J 48:124–130
Shehzad A, Ha T, Subhan F, Lee YS (2011) New mechanisms and the anti-inflammatory role of curcumin in obesity and obesity-related metabolic diseases. Eur J Nutr 50:151–161
Kunnumakkara AB, Guha S, Krishnan S, Diagaradjane P, Gelovani J, Aggarwal BB (2007) Curcumin potentiates antitumor activity of gemcitabine in an orthotopic model of pancreatic cancer through suppression of proliferation, angiogenesis, and inhibition of nuclear factor-jß-regulated gene products. Can Res 67:3853–3861
Kunnumakkara AB, Anand P, Aggarwal BB (2008) Curcumin inhibits proliferation, invasion, angiogenesis and metastasis of different cancers through interaction with multiple cell signaling proteins. Can Lett 269:199–225
Karin M, Greten FR (2005) NF-κB linking inflammation and immunity to cancer development and progression. Nat Rev Immunol 5:749–759
Halliwell B (1999) Antioxidant defence mechanism: from the beginning to the end (of the beginning). Free Radic Res 31:261–272
Halliwell B, Rafter J, Jenner A (2005) Health promotion by flavonoids, tocopherols, tocotrienols, and other phenols: direct and indirect effects? Antioxidant or not? Am J Clin Nutr 81:268S–276S
Siess H (1997) Oxidative stress: oxidants and antioxidants. Exp Physiol 82:291–295
Balsano C, Alisi A (2009) Antioxidant effects of natural bioactive compounds. Curr Pharm Des 15:3063–3073
Jenny M, Klieber M, Zaknun D, Schroecksnadel S, Kurz K, Ledochowski M et al (2010) In vitro testing for anti-inflammatory properties of compounds employing peripheral blood mononuclear cells freshly isolated from healthy donors. Inflamm Res 60:127–135
Suzuki M, Nakamura T, Iyoki S, Fujiwara A, Watanabe Y, Mohri K, Isobe K et al (2005) Elucidation of anti-allergic activities of curcumin-related compounds with a special reference to their anti-oxidative activities. Biol Pharm Bull 28(8):1438–1443
Thakare VN, Osama M, Naik SR (2013) Therapeutic potential of curcumin in experimentally induced allergic rhinitis in guinea pigs. Int Immunopharmacol 17:18–25
Aggarwal BB, Harikumar KB (2009) Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. Int J Biochem Cell Biol 41:40–59
Ide N, Lau BH (1997) Garlic compounds protect vascular endothelial cells from oxidized low-density lipoproteininduced injury. J Pharm Pharmacol 49:908–911
Ray B, Chauhan NB, Lahiri DK (2011) Oxidative insults to neurons and synapse are prevented by aged garlic extract and Sallyl-l-cysteine treatment in the neuronal culture and APPTg mouse model. J Neurochem 117:388–402
Anoush M, Eghbal MA, Fathiazad F, Hamzeiy H, Kouzehkonani NS (2009) The protective effects of garlic extract against acetaminophen-induced oxidative stress and glutathione depletion. Pak J Biol Sci 12:765–771
Nahdi A, Hammami I, Kouidhi W, Chargui A, Ben Ammar A, Hamdaoui MH et al (2010) Protective effects of crude garlic by reducing iron-mediated oxidative stress, proliferation and autophagy in rats. J Mol Histol 41:233–245
Khanna NM (1999) Turmeric-nature’s precious gift. Curr Sci 76:1351–1356
Zhang N, Li H, Jia J, He M (2015) Anti-inflammatory effect of curcumin on mast cell-mediated allergic responses in ovalbumin-induced allergic rhinitis mouse. Cell Immunol 298(1–2):88–95
Bishayee K, Khuda-Bukhsh AR (2013) 5-lipoxygenase antagonist therapy: a new approach towards targeted cancer chemotherapy. Acta Biochim Biophys Sin (Shanghai) 45(9):709–719
August EM, Nguyen T, Malinowski NM, Cysyk RL (1994) Non-steroidal anti-inflammatory drugs and tumor progression: inhibition of fibroblast hyaluronic acid production by indomethacin and mefenamic acid. Cancer Lett 82:49–54
Menon VP, Sudheer AR (2007) Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol 595:105–125
Epstein J, Sanderson IR, Macdonald TT (2010) Curcumin as a therapeutic agent: the evidence from in vitro, animal and human studies. Br J Nutr 103(11):1545–1557
Thiyagarajan M, Sharma SS (2004) Neuroprotective effect of curcumin in middle cerebral artery occlusion induced focal cerebral ischemia in rats. Life Sci 74(8):969–985
Yılmaz Savcun G, Ozkan E, Dulundu E, Topaloğlu U, Sehirli AO, Tok OE et al (2013) Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury in an experimental sepsis model in rats. Ulus Travma Acil Cerrahi Derg 19(6):507–515. doi:10.5505/tjtes.2013.76390
Yarru LP, Settivari RS, Gowda NK, Antoniou E, Ledoux DR, Rottinghaus GE (2009) Effects of turmeric (Curcuma longa) on the expression of hepatic genes associated with biotransformation, antioxidant, and immune systems in broiler chicks fed aflatoxin. Poult Sci 88:2620–2627
Hsu CH, Cheng AL (2007) Clinical studies with curcumin. Adv Exp Med Biol 595:471–480
Liddle M, Hull C, Liu C, Powell D (2006) Contact urticaria from curcumin. Dermatitis 17:196–197
Thompson DA, Tan BB (2006) Tetrahydracurcumin-related allergic contact dermatitis. Contact Dermatitis 55:254–255
Lee JH, Kim JW, Ko NY, Mun SH, Her E, Kim BK et al (2008) Curcumin, a constituent of curry, suppresses IgE-mediated allergic response and mast cell activation at the levelof Syk. J Allergy Clin Immunol 121(5):1225–1231
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With the exception of data collection, preparation of this paper, including design and planning, was supported by the Continuing Education and Scientific Research Association.
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Author Niyazi Altıntoprak declares that he has no conflict of interest. Author Murat Kar declares that he has no conflict of interest. Author Mustafa Acar declares that he has no conflict of interest. Author Mehmet Berkoz declares that he has no conflict of interest. Author Nuray Bayar Muluk declares that she has no conflict of interest. Author Cemal Cingi declares that he has no conflict of interest.
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Animals were treated in compliance with relevant principles of the Declaration of Helsinki; and Ethics Committee Approval was also taken from Eskisehir Osmangazi University. All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. Article does not contain studies with human participants.
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Altıntoprak, N., Kar, M., Acar, M. et al. Antioxidant activities of curcumin in allergic rhinitis. Eur Arch Otorhinolaryngol 273, 3765–3773 (2016). https://doi.org/10.1007/s00405-016-4076-4
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DOI: https://doi.org/10.1007/s00405-016-4076-4