Artigo_pequi

8/7/2019 Artigo_pequi

1/7

Please cite this article in press as: Saraiva, R.A., et al., Topical anti-inflammatory effect ofCaryocar coriaceum Wittm. (Caryocaraceae) fruit pulpfixed oil on mice ear edema induced by different irritant agents. J. Ethnopharmacol. (2010), doi: 10.1016/j.jep.2010.07.002

ARTICLE IN PRESSGModel

JEP-6201; No.of Pages7

Journal of Ethnopharmacology xxx (2010) xxxxxx

Contents lists available at ScienceDirect

Journal of Ethnopharmacology

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / j e t h p h a r m

Topical anti-inflammatory effect ofCaryocar coriaceum Wittm. (Caryocaraceae)fruit pulp fixed oil on mice ear edema induced by different irritant agents

Rogrio A. Saraiva a,, Mariana K.A. Araruna a, Romagna C. Oliveira a, Kleber D.P. Menezes a,Gerlnia O. Leite a, Marta R. Kerntopfa, Jos G.M. Costa b, Joo B.T. Rocha c, Adriana R. Tom d,Adriana R. Campos e, Irwin R.A. Menezes a

a Universidade Regional do Cariri (URCA), Departamento de Qumica Biolgica, Laboratrio de Farmacologia e Qumica Molecular, 63105-000 Crato, CE, Brazilb Universidade Regional do Cariri (URCA), Departamento de Qumica Biolgica, Laboratrio de Pesquisa em Produtos Naturais, 63105-000 Crato, CE, Brazilc Universidade Federal de Santa Maria (UFSM), Departamento de Qumica, Laboratrio de Bioqumica Toxicolgica, 57900-000 Santa Maria, RS, Brazild Universidade Estadual do Cear (UECE). Campus do Itaperi, 60740-903 Fortaleza, CE, Brazile Universidade de Fortaleza (UNIFOR). 60811-905 Fortaleza, CE, Brazil

a r t i c l e i n f o

Article history:

Received 14 January 2010Received in revised form 6 June 2010Accepted 2 July 2010Available online xxx

Keywords:

Pequi oilCaryocar coriaceumSkin irritantsFatty acidsDermatitis

Natural products

a b s t r a c t

Aimof thestudy: Caryocar coriaceum Wittm.fruitpulp fixed oil(CCFO) hasbeenwidely employed by com-munities from Brazil Northeastern in the treatment of skin inflammation, respiratory affections, woundhealing and muscle pain. In this study, we evaluated the topical effect of CCFO against different irritantagents in vivo, in order to verify its antiedematous effect as well to unravel its tentative mechanisms ofaction.Materials and methods: CCFO was obtained from Caryocar coriaceum fruits using ethyl acetate as solvent.Ear edema provoked by the application of Croton oil (single and multiple applications), arachidonic acid(AA), capsaicin, phenol and histamine to Swiss mice was used to evaluate the topical anti-inflammatoryeffect of CCFO. Histological analysis from mice ears sensitized with Croton oil and AA single applicationwas also performed.Results: Crude CCFO (20L/ear) demonstrated significant topical antiedematous effect against Croton oil

single (inhibition of 32.0%; P< 0.05) and multiple (41.4% after 9 days, P< 0.001) applications, AA (inhibi-tion of 49.7%; P< 0.01) and phenol (inhibition of 38.8%; P< 0.001). In contrast, CCFO did not antagonizethe edema caused by topical treatment with capsaicin and histamine when compared to control group(P> 0.05). Histological analysis also revealed that CCFO was able to reduce the edema and the influx ofinflammatory cells in mice ears sensitized with Croton oil and AA.Conclusions: CCFO exhibited a similar profile of topical anti-inflammatory activity to that of drugs thatclassicallymodulatetheproductionofarachidonicacidmetabolites.Thestudyalsoindicatesthepotentialapplication of CCFO as an important herbal medicine to be used against skin inflammatory diseases.

2010 Elsevier Ireland Ltd. All rights reserved.

1. Introduction

As the principal physical barrier to the external environment,the skin provides an important bodily defense mechanism when

subjected to injury and invasion by pathogens or other exter-nal noxious agents (Freinkel and Woodley, 2000). Normally, thisdefense mechanismaims to repairthe tissuedamage or destroy themicrobial pathogen and do not cause serious damage. However, aninappropriate or misdirected immune activity can implicate in thepathogenesis of a large variety of inflammatory skin disorders, suchas psoriasis and atopic dermatitis (Kupper and Fuhlbrigge, 2004;Maldini et al., 2009).

Corresponding author. Tel.: +55 88 2101 1212.E-mail address: [email protected](R.A. Saraiva).

It is widely recognized that the modulation on production ofinflammatory mediators (cytokines, neuropeptides, arachidonicacid metabolites, etc) may be used therapeutically against skininflammations(Wellsetal.,2004). Forthispropose,glucocorticoids,

antihistaminesandnon-steroidalanti-inflammatorydrugsaregen-erally employed (Davies et al., 2006). However, they can frequentlyexhibit a set of undesirable side effects and are not effective in allcases (Schoepe et al., 2006). As alternative, extracts and isolatedcompounds from herbal medicine have been studied in order todiscover new effective and safe topical anti-inflammatory drugs(Cordell and Colvard, 2005; Khanna et al., 2007; Lee et al., 2009).

Caryocar coriaceum Wittm. (Caryocaraceae), popularly knownin Brazil as pequi, is a common plant found in cerrado (savanna)areas from Araripe plateau, Cear State, Brazil Northeastern (Costaet al., 2004). Pequi fruits contain excellent nutritional sources suchas antioxidant vitamins (A and E) and essential fatty acids (Sena et

0378-8741/$ see front matter 2010 Elsevier Ireland Ltd. All rights reserved.

doi:10.1016/j.jep.2010.07.002
http://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002http://www.sciencedirect.com/science/journal/03788741http://www.elsevier.com/locate/jethpharmmailto:[email protected]://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002mailto:[email protected]://www.elsevier.com/locate/jethpharmhttp://www.sciencedirect.com/science/journal/03788741http://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002


2/7




2 R.A. Saraiva et al. / Journal of Ethnopharmacology xxx (2010) xxxxxx

al., 2010), and are largely appreciated as food by the population ofthe Cariri region, in Cear State, and of neighboring cities of Per-nambuco and Piau States (De Oliveira et al., 2010). Besides beinga nutritional source, the handmade oil extracted from the pulp orthe seed is also popularly employed to treat skin inflammation,respiratory affections, wound healing, ulcers, rheumatism, musclepain and contusions (Braga, 1960; Agra et al., 2007; Matos, 2007).Previous studies from ourgroup have confirmedthat Caryocar cori-aceum fixed oil possesses healing and gastroprotective activities invivo (Leite et al., 2009; Quirino et al., 2009).

Although thepopular useof pequi pulp oilagainst inflammatorydisorders is known in Brazil Northeastern, data about the mecha-nisms of action involved its topical anti-inflammatory activity arenot available in the literature. Thus, we were encouraged to eval-uate the topical effect of pequi pulp oil against different irritantagents in vivo, in order to verify its anti-inflammatory activity aswell to unravel its possible mechanisms of action.

2. Materials and methods

2.1. Plant material

Fruits ofCaryocar coriaceum Wittm. were collected in a cerradoarea from Araripe plateau, Crato, Cear State, Brazil (S 72153,1;W 392842,6)in January 2009. A voucher specimen wasidentifiedby Prof. Dr.LgiaQueiroz Matiasand depositedin thePrisco BezerraHerbariumof the Federal University of Cear under number 44523.

2.2. Chemicals

Croton oil, arachidonic acid, capsaicin, histamine dihydrochlo-ride, indomethacin, and Tween 80 were purchased from SigmaChemical Co. (St. Louis, USA). Dexamethasone (Decadron) waspurchased fromAch (Brazil).Ketamine chloride and xylazinechlo-ride were purchased from Syntec (Brazil). Acetone, ethanol and

ethyl acetate, of analytical grade, were purchased from Dinmica(Brazil).

2.3. Animals

Male and female Swiss mice (Mus musculus), weighting2535 g, were previously housed in standard polypropylene cagesunder controlled conditions of temperature (222 C) and 12-hlight/dark cycle,with free access to water androdent chow (Labina,Purina, Brazil). Mice were allowed to adapt to laboratory forat least1 h before testing. All the procedures were previously approved byResearch Ethics Committee from Faculty of Medicine of Juazeiro doNorte (Brazil), under number 2009 0218.

2.4. Extraction of fixed oil

The fixed oil from Caryocar coriaceum fruit pulp (CCFO) wasobtained through hot-extraction method. The in natura pulp fromCaryocar coriaceum fruits was removed and placed in a Soxhletapparatus in contact with ethyl acetate (solvent) during 3 h (60C).At the end of the process, a yellow solution (oil+ ethyl acetate) andan orange precipitate were obtained. The orange precipitate wasseparated from the yellow solution by decantation, using a separa-tion funnel. Ethyl acetate was removed from the yellow solution ina rotaryevaporator apparatusunderreduced pressure andat a con-trolledtemperature(702 C).Thefinaloilextracthadgold-yellowappearance and a sui generis smell.

2.5. Identification of fatty acids from CCFO

Thefattyacid components were obtained as their methylesters.A sample of 0.2g of the oil was subjected to reflux (30min) withmethanolic potassium hydroxide. The oil was then converted tomethyl esters by methanolysis with acid catalyst. Isolation andesterification of free and total fattyacids wereperformedaccordingto well-knownreported procedures(Hartman andLago,1973). Themethyl esters of fatty acids were analyzed by gas chromatographyon a Hewlett-Packard Model 5971, equipped with capillary columnand FID detector. The operating conditions were oven temperatureprogram start at 35180 C at a rate of 4 C/min, then heated ata rate of 10 C/min to 250 C and held isothermally; injector anddetector temperature of 250 and 200 C, respectively, and H2 as acarrier gas flowing at 0.8ml/min. The identification wascarried outby co-injection of authentic compounds and retention times. Per-centage area values were obtained electronically from the GC-FIDresponse. The oil was then characterized by a high content, 64.9%of unsaturated fatty acids. The two major components identifiedwere oleic acid (55.79%) and palmitic acid (34.18%). Other con-stituents found were palmitoleic acid (0.27%), stearic acid (1.73%),linoleic acid (1.80%), heptadecenoic acid (5.86%) and 11-eicosenoicacid (0.37%).

2.6. Croton oil single application-induced mouse ear edema

Groups of six Swiss mice were previously treated on the innerand outer surfaces of the right ear with 20L ofCCFO diluted in2%Tween 80 at concentrations of 50, 100, 200 and 400 mg/mL (1, 2, 4and 8 mg/ear) orcrude CCFO (20L = 13mg/ear).The negative con-trol received topically 20L of vehicle (2% Tween 80) on right ear.Dexamethasone (0.08mg/ear) was used as positive control. After15 min, the edema was induced on the right ear by topical appli-cation of 20L of Croton oil 5% (v/v) in acetone, while the left earreceived 20L of vehicle acetone. Theear edema was evaluated 6 hafter Croton oil application (Tubaro et al., 1985).

2.7. Croton oil multiple application-induced mouse ear edema

This study was conducted in 9 days (days 08). Croton oil 5%(v/v) in acetone (20L/ear) was applied on the right ears and ace-toneontheleftearsofSwissmice(n = 6/group) witha micropipetteon alternate days. The ear edema was evaluated daily by mea-suring the ear thickness. On days 48, the mice were treated onthe inner and outer surfaces of the right ear with crude CCFO(20L/ear), saline solution (NaCl 0.9%, 20L/ear) or dexametha-sone (0.08 mg/ear) twice a day. On day 8, the mice were killed and6-mm diameter ear punch biopsies were collected and weighted(Stanley et al., 1991).

2.8. Arachidonic acid, capsaicin and phenol-induced mouse ear

edema

Inflammation was induced in mice (n =6/group) by applying onthe inner and outer surfaces of the right ear 20L of the follow-ing irritants: arachidonic acid (AA) 0.1mg/L in acetone; capsaicin0.01mg/L in 90% ethanol and 10% phenol (v/v) in acetone. Fifteenminutes before the application of each irritant agent, the right earswere topically treated with crude CCFO (20L/ear), saline solu-tion (negative control, 20L/ear), indomethacin (positive controlfor AA, 2 mg/ear) or dexamethasone (positive control for capsaicinand phenol, 0.08mg/ear). The ear edema was evaluated 1h afterAA and phenol, and 30 min after capsaicin application (Young etal., 1984; Gbor and Razga, 1992; Gbor, 2000).
http://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002


3/7




R.A. Saraiva et al. / Journal of Ethnopharmacology xxx (2010) xxxxxx 3

2.9. Histamine subcutaneous application-induced mouse ear

edema

Mice (n = 6/group) were previously anesthetized with ketamine20 mg/kg i.p. and xylazine 10 mg/kg i.p. After that, their right earswere treated topicallywith salinesolution(20L/ear), dexametha-sone(0.08mg/ear)orcrudeCCFO(20L/ear). Fifteen minutes later,the edema was induced on the right ear by intradermical applica-tionof5L of histamine dihydrochloride0.1 mg/L using a syringewith a 29G-hypodermical needle, while the left ear received 5 Lof saline solution by the same procedure described(Sham). The earedema was evaluated 2 h after the histamine solution application(Brand et al., 2002).

2.10. Ear edema measurement

Edema was expressed as percentage of the increase in earweight (all models) or as ear thickness variation (Croton oil multi-ple application-inducedear edema) dueto inflammatory challenge.Ear thickness was measured with a digital caliper (Jomarca). Thedigital caliper was applied near the tip of the ear just distalto the cartilaginous ridges and the thickness was recorded in

micrometer (m). To evaluate the ear weight, animals were killedby cervical dislocation, 6-mm diameter ear punch biopsies col-lected using a metal punch, and the biopsies were individuallyweighed on a MettlerToledo (AB204) balance. The extent of theedema was expressed as percentage of increase in the ear tis-sue weight (%), using the following formula: Percentage of edemaweight(%)=[(wRE wLE)100]/wLE, where wRE is thecircle weightobtained from the right ear (inflamed) and wLE is the circle weightobtained from the left ear (non-inflamed). The mean of inhibitionedema percentage (%) was calculated by comparing to negativecontrol group.

2.11. Histology

Ear biopsies from Croton oil and arachidonic acid-induced sin-gle application mouse ear edema were collected and fixed in 70%ethanol for 24h and then preserved in 10% formalin. Subsequently,the ears were dehydrated, blocked in paraffin and then sectionedwith a microtome (5m). The cross-sections were stained withhematoxylin and eosin for the evaluation of leukocyte accumula-tion and edema intensity. A representative area was selected forqualitative light microscope analysis (200 magnification).

2.12. Statistical analysis

The results are expressed as mean standard error of mean(s.e.m.). The comparison between groupswas assessed by one-wayanalysis of variance (ANOVA) followed by StudentNewmanKeuls

test or by two-way ANOVA followed by Bonferroni test (repeatedmeasures) when appropriated. Values ofP< 0.05 were accepted asstatistically significant.

3. Results

Topical application of Croton oil, AA, capsaicin, phenol or his-tamine caused a significant inflammatory response in mice asdetermined by the increase of ear weight, when compared to theears that received only vehicle of its respective irritant agent (ace-tone, 90%ethanol or salinesolution). However, it wasobservedthattheedematous potentialof capsaicinand histaminewas lower thanthat of arachidonic acid, phenol and Croton oil. Further details are

discussed below.

Table 1

Effect of CCFO and dexamethasone on Croton oil single application-induced earedema.

Treatment Croton oil single application

Percentage ofedema weight (%)

Inhibition (%)

2% Tween 80 (Control group) 167.39.6 CCFO 1 mg/ear 145.318.7 13.2

2 mg/ear 143.210.1 14.44 mg/ear 149.89.7 10.58 mg/ear 119.79.5* 28.5*

Crude CCFO 13 mg/ear 113.814.4* 32.0*

Dexamethasone 0.08 mg/ear 24.52.7*** 85.4***

Data expressed as mean s.e.m.*P


4/7




4 R.A. Saraiva et al. / Journal of Ethnopharmacology xxx (2010) xxxxxx

Fig. 1. Effect of CCFO on Croton oil multiple application-induced ear edema. In (A)is showing the timeresponse curve of effect from days 0 to 8. The Croton oil inacetone wasapplied onalternate days. Thethicknessof theear wasmeasured daily,using a digital caliper. On days 47, the ear of the animals received saline solution,dexamethasone (DEX) or crudeCCFO (arrows indicate the dayswhen the treatmentoccurred). The effect of the compounds was examined by varying the thickness ofthe ear, calculated as the difference between the initial and final thickness. Thepoints represent the mean of 6 animals and vertical bars s.e.m (two-way ANOVAfollowed by Bonferroni test). In (B) is showing the percentage of edema weight of

each group on day 8 (one-way ANOVA followed by StudentNewmanKeuls test).*P


5/7





Fig.2. Effect of crudeCCFO,dexamethasone (DEX) or indomethacin(IND) on miceear edema induced by differentirritantsubstances.(A) Arachidonic acid(AA); (B)capsaicin;(C) histamine; and (D) phenol. The control group received saline solution as treatment. Each point represents the mean s.e.m. of 6 mice. *P


6/7


7/7

Please cite this article in press as: Saraiva, R.A., et al., Topical anti-inflammatory effect ofCaryocar coriaceum Wittm. (Caryocaraceae) fruit pulpfixed oil on mice ear edema induced by different irritant agents J Ethnopharmacol (2010) doi: 10 1016/j jep 2010 07 002




de Queiroz Farias (Universidade Federal do Cear) for identifyingthe voucher specimen and to Faculty of Medicine of Juazeiro doNorte, for providing animals to this research.

References

Agra, M.F., Freitas, P.F., Barbosa Filho, J.M., 2007. Synopsis of the plants known asmedicinal and poisonous in Northeast of Brazil. Revista Brasileira de Farmacog-nosia 17, 114140.

Blazs, G., Gbor, M., 1995. Effects of prostaglandin antagonist phloretin derivateson mouse ear edema induced with different skin irritants. Prostaglandins 50,161168.

Braga, R.,1960. Plantasdo Nordeste,especialmente do Cear, 2a ed.ImprensaOficial,Fortaleza, Brazil, 540 pp.

Brand, C., Townley, S.L., Finlay-Jones, J.J., Hart, P.H., 2002. Tea tree oil reduceshistamine-inducedoedemain murineears. InflammationResearch51, 283289.

Calder, P.C., 2005. Polyunsaturated fatty acids and inflammation. Biochemical Soci-ety Transactions 33, 423427.

Carlson, R., ONeill-Davis, L., Chang, J., Lewis, A.J., 1985. Modulation of mouse earedema by cycloxygenase and lipoxygenase inhibitors and other pharmacologicagents. Agents Actions 17, 197204.

Cordell, G.A., Colvard, M.D., 2005. Some thoughts on the future of ethnopharmacol-ogy. Journal of Ethnopharmacology 100, 514.

Costa, I.R., Araujo, F.S., Lima-Verde, L.W., 2004. Flora e aspectos auto-ecolgicos deumencravede cerrado na chapada doAraripe,Nordeste do Brasil. Acta BotanicaBrasilica 18, 759770.

Crummey, A., Harper, G.P., Boyle, E.A., Mangan, F.R., 1987. Inhibition of arachidonicacid-induced ear oedema as a model for assessing topical anti-inflammatory

compounds. Agents Actions 20, 6976.Das,U.N., 2006.Essential fattyacids a review. Current PharmaceuticalBiotechnol-ogy 7, 467482.

Davies, N.M., Reynolds, J.K., Underberg, M.R., Gates, B.J., Ohgami, Y., Vega-Villa, K.R.,2006. Minimizing risks of NSAIDs: cardiovascular, gastrointestinal and renal.Expert Review of Neurotherapeutics 6, 16431655.

De Oliveira, M.E.B., Guerra, N.B., Maia, A.D.N., Alves, R.E., Matos, N.M.D., Sampaio,F.G.M., Lopes, M.M.T., 2010. Chemical and physicalchemical characteristics inpequi from the chapada do Araripe, Ceara, Brazil. Revista Brasileira de Fruticul-tura 32, 114125.

Ferrandiz, M.L., Gil, B., Sanz, M.J., Ubeda, A., Erazo, S., Gonzlez, E., Negrete, R.,Pacheco,S.,Paya,M.,Alcaraz,M.J.,1996.Effectofbakuchiolonleucoytefunctionsand some inflammatory responses in mice. Journal of Pharmacy and Pharma-cology 48, 975980.

Freinkel, R.K., Woodley, D.T., 2000. The Biology of the Skin. Parthenon, New York,pp. 1519.

Fritsche, K. L., 2008. Too much linoleic acid promotes inflammation doesnt it?Prostaglandins, Leukotrienes and Essential Fatty Acids 79, 173175.

Gbor, M., 2000. Mouse Ear Inflammation Models and their Pharmacological Appli-

cations. Akadmiai Kiad, Budapest.Gbor,M.,Razga,Z.,1992.Developmentandinhibitionofmouseearoedemainduced

with capsaicin. Agents Actions 36, 8386.Green, C.A., Shuster, S., 1987. Lack of effect of topical indomethacin on psoriasis.

British Journal of Clinical Pharmacology 24, 381384.Hartman, L., Lago, R.C.A., 1973. Rapid preparation of fatty acid methyl esters from

lipids. Laboratory Practice 22, 475477.Henry, G.E., Momin, R.A., Nair, M.G., Dewitt, D.L., 2002. Antioxidant and cyclooxy-

genase activities of fatty acids found in food. Journal of Agricultural and FoodChemistry 50, 22312234.

Inoue, H., Nagata, N., Koshihara, Y., 1993. Profile of capsaicin-induced mouse earoedema as neurogenic inflammatory model: comparisonwith arachidonic acid-induced ear oedema. British Journal of Pharmacology 110, 16141620.

Inoue, H., Nagata, N., Koshihara, Y., 1995. Participation of serotonin in capsaicin-induced mouse ear edema. Japanese Journal of Pharmacology 69, 6168.

Khanna, D.,Sethi,G., Ahn,K.S.,Pandey,M.K.,Kunnumakkara, A.B., Sung, B.,Aggarwal,A., Aggarwal, B.B., 2007. Natural products as a gold mine for arthritis treatment.Current Opinion in Pharmacology 7, 344351.

Kupper, T.S., Fuhlbrigge, R.C., 2004. Immune surveillance in the skin: mechanismsand clinical consequences. Nature Reviews Immunology 4, 211222.

Lawrence, T., Willoughby, D.A., Gilroy, D.W., 2002. Anti-inflammatory lipid medi-ators and insights into the resolution of inflammation. Nature ReviewsImmunology 2, 787795.

Lee, D.Y., Choo, B.K., Yoon, T., Cheon, M.S., Lee, H.W., Lee, A.Y., Kim, H.K., 2009. Anti-inflammatory effects ofAsparagus cochinchinensis extract in acute and chroniccutaneous inflammation. Journal of Ethnopharmacology 121, 2834.

Leite, G.O., Penha, A.R.S., Quirino, G.S., Colares, A.V., Rodrigues, F.F.G., Costa, J.G.M.,Cardoso, A.L.H., Campos, A.R., 2009. Gastroprotective effect of medicinal plantsfrom Chapada do Araripe, Brazil. Journal of Young Pharmacists 1, 5456.

Lim, H., Park, H., Kim, H.P., 2004. Inhibition of contact dermatitis in animalmodels and suppression of proinflammatory gene expression by topi-

cally applied flavonoid, wogonin. Archives of Pharmacological Research 27,442448.Maldini, M., Sosa, S., Montoro, P., Giangaspero, A., Balick, M.J., Pizza, C., Della-Logia,

R., 2009.Screening of thetopical anti-inflammatory activity of thebark ofAcaciacornigera Willdenow, Brysonima crassifolia Kunth, Sweetia panamensis Yakowlevand the leaves ofSphagneticola trilobata Hitchcock. Journal of Ethnopharmacol-ogy 122, 430433.

Mantione, C.R., Rodriguez, R., 1990. A bradykinin (BK)1 receptor antagonist blockscapsaicin-induced ear inflammation in mice. British Journal of Pharmacology99, 516518.

Matos, F.J.A., 2007.PlantasMedicinais:Guia de Seleco e Emprego de Plantas Usadasem Fitoterapia no Nordeste do Brasil, 3a ed. Imprensa Universitria, Fortaleza,Brazil, 394 pp.

Murakawa, M., Yamaoka, K., Tanaka, Y., Fukuda, Y., 2006. Involvement of necrosisfactor (TNF)- in phorbol ester 12-o-tetradecaoylphorbol-13-acetate (TPA)-induced skin edema in mice. Biochemical Pharmacology 71, 13311336.

Murray, A.R., Kisin, E., Castranova, V., Kommineni, C., Gunther, M.R., Shvedova, A.A.,2007. Phenol-induced in vivo oxidative stress in skin: evidence for enhancedfree radical generation, thiol oxidation, and antioxidant depletion. Chemical

Research Toxicology 20, 17691777.Quirino,G.S.,Leite,G.O.,Rebelo,L.M.,Tom,A.R.,Costa,J.G.M.,Cardoso,A.H.,Campos,

A.R., 2009. Healing potential of pequi (Caryocar coriaceum Wittm.) fruit pulp oil.Phytochemistry Letters 2, 179183.

Ringbom, T.,Huss, U.,Stenholm, .,Flock, S.,Skattebl,L., Perera, P.,Bohlin,L., 2001.COX-2inhibitory effects of naturally occurring and modified fattyacids. Journalof Natural Products 64, 745749.

SenaJr.,D.M.,Rodrigues,F.F.G.,Freire,P.T.C., deLima, S.G.,Coutinho,H.D.M.,Carvajal,J.C.L., Costa, J.G.M., 2010. Physicochemical and spectroscopical investigation ofPequi (Caryocar coriaceum Wittm.) pulp oil. Grasas y Aceites 61, 191196.

Schoepe,S., Schcke,H., May,E., Asadullah,K., 2006.Glucocorticoid therapy-inducedskin atrophy. Experimental Dermatology 15, 406420.

Stanley, P.L., Steiner, S., Havens, M., Transposch, K.M., 1991. Mouse skin inflamma-tion induced by multiple topical application of 12-O-tetradecanoylphorbol-13-acetate. Journal of Pharmacological and Biophysiological Research 4, 262271.

Tubaro, A., Dri, P., Delbello, G., Zilli, C., Della-Loggia, R., 1985. The croton oil testrevisited. Agents Actions 17, 347349.

Wang, H.Q., Kim, M.P., Tiano, H.F., Langenbach, R., Smart, R.C., 2001. Protein kinase

C-alpha coordinately regulates cytosolic phospholipase A2 activity and theexpression of ciclooxygenase-2 trought differtent mechanism in mouse ker-atinocytes. Molecular Pharmacology 59, 860866.

Wells, T., Basketter, D., Schrder, K.R., 2004. In vitro skin irritation: facts and future.State of the art review of mechanisms and models. Toxicology In Vitro 18,231243.

Wilmer, J.L., Burleson, F.G., Kayama, F., Kauno, J., Luster, M.I., 1994. Cytokine induc-tion in human epidermal keratinocytes exposed to contact irritants and itsrelation to chemical-induced inflammation in mouse skin. Journal of Investiga-tive Dermatology 102, 915922.

Young, J.M., Spires, D.A., Bedord, C.J., Wagner, B., Ballaron, S.J., De Young, L.M., 1984.The mouse ear inflammatory response to topical arachidonic acid. The Journalof Investigative Dermatology 82, 367371.

Zhao, G., Etherton, T.D., Martin, K.R., Heuvel, J.P.V., Gillies, P.J., West, S.G., Kris-Etherton, P.M., 2005. Anti-inflammatory effects of polyunsaturated fatty acidsin THP-1 cells. Biochemical and Biophysical Research Communications 336,909917.

Ziboh, V.A., Miller, C.C., Cho, Y., 2000. Metabolism of polyunsaturated fatty acids byskin epidermal enzymes: generation of antiinflammatory and antiproliferative

metabolites. American Journal of Clinical Nutrition 71, 361S366S.
http://dx.doi.org/10.1016/j.jep.2010.07.002http://dx.doi.org/10.1016/j.jep.2010.07.002

Artigo_pequi

Documents

Transcript of Artigo_pequi