• Users Online: 517
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2021  |  Volume : 10  |  Issue : 1  |  Page : 60-65

Anti-inflammatory effects of memantine in carrageenan-induced paw edema model in rats

1 Department of Pharmacology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran
2 Department of Comparative Biomedical Sciences, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran

Date of Submission11-Apr-2020
Date of Acceptance30-Aug-2020
Date of Web Publication31-May-2021

Correspondence Address:
Dr. Hamid Soraya
Department of Pharmacology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrptps.JRPTPS_37_20

Rights and Permissions

Background: The anti-inflammatory effect of memantine (MEM) was investigated using carrageenan-induced hind paw edema model in rats. Materials and Methods: Thirty male Wistar rats were randomly assigned to five groups (n = 6). Group 1 received 0.1 mL of 1% carrageenan at the right hind paw. Group 2 received dexamethasone (10 mg/kg) and Groups 3, 4, and 5 received 5, 10, and 20 mg/kg MEM intraperitoneally (ip), 20 min after injection of carrageenan into the right hind paw, respectively. Animals’ paw thickness was measured at 0, 1, 2, 3, 4, and 5 h after carrageenan injection. Then, animals were euthanized and myeloperoxidase (MPO) and malondialdehyde (MDA) levels were measured in the paw tissues. The tissue samples were further examined histopathologically using light microscopy. One-way ANOVA and Tukey post hoc test was used to compare the mean values between the groups. Results: Treating with MEM at all doses significantly decreased hind paw thickness at 2 (P < 0.05 and P < 0.01 at MEM 10 mg/kg and MEM 5 and 20 mg/kg, respectively), 3 (P < 0.001), and 4 (P < 0.001 at 5 mg/kg and P < 0.01 at MEM 10 and 20 mg/kg) hours after carrageenan injection in comparison to the carrageenan group. There was a significant (P < 0.05 and P < 0.001, respectively) reduction in MPO activity and MDA levels in MEM-treated groups when compared with the carrageenan group. Conclusion: This study showed that MEM decreased paw edema, leukocyte infiltration, MPO activity, and MDA levels, and MEM can be considered as an effective anti-inflammatory agent.

Keywords: Carrageenan, inflammation, lipid peroxidation, memantine, myeloperoxidase

How to cite this article:
Azarbaijani M, Kian M, Soraya H. Anti-inflammatory effects of memantine in carrageenan-induced paw edema model in rats. J Rep Pharma Sci 2021;10:60-5

How to cite this URL:
Azarbaijani M, Kian M, Soraya H. Anti-inflammatory effects of memantine in carrageenan-induced paw edema model in rats. J Rep Pharma Sci [serial online] 2021 [cited 2021 Dec 8];10:60-5. Available from: https://www.jrpsjournal.com/text.asp?2021/10/1/60/317248

  Introduction Top

Inflammation is a normal adaptive physiological response of the immune system to the invasion of pathogenic agents and/or tissue injury.[1] Although inflammation is a defensive response, hyperactivation of the immune system causes secondary complications in the body.[2]N-methyl-d-aspartate receptors (NMDARs) are one of the subclasses of ionotropic glutamate receptors that play a role in many neurophysiological functions such as learning, neurogenesis, and synaptic plasticity.[3] In addition to central nervous system, these receptors are present in various peripheral tissues.[4] Some studies have suggested NMDARs’ participation in inflammatory processes.[5],[6] It has been proposed that activation of NMDARs is directly associated with the onset of the inflammatory cascade which results in cellular generation of free radicals.[6] NMDARs express in leukocytes such as neutrophils, monocytes, and macrophages. Activation of NMDARs modulates migration of these cells and increases secretion of their products. Considering that, blockade of NMDARs may lead to suppression of inflammatory response. It has been reported that some of the NMDAR antagonists possess anti-inflammatory activities. Some studies have shown that ketamine attenuates pro-inflammatory mediators and regulates inflammatory response.[2],[7],[8] MK-801 (dizocilpine), an uncompetitive NMDAR antagonist, downregulates expression of inflammatory genes.[9] Moreover, administration of dizocilpine decreased cardiovascular inflammation following Mg2+ deficiency in rats.[6] Another NMDAR antagonist, dextromethorphan, attenuated lung inflammation induced by heat in rats.[10] However, many NMDAR antagonists such as dizocilpine could not be used in human patients because they have shown highly undesirable adverse effects in clinical trials.[11]

Memantine (MEM) is an uncompetitive NMDAR antagonist that is clinically well tolerated.[12] MEM is used for the treatment of Alzheimer’s disease and its suppressive effects on neuroinflammation have been reported in some studies.[13],[14],[15],[16] It has been demonstrated that MEM attenuated neuroinflammation in streptozotocin (STZ)-induced memory impairment in rats.[13] A study by Wu et al. showed that MEM decreased the release of pro-inflammatory factors in neuron-glia cultures exposed to lipopolysaccharide.[15] A reduction in the level of inflammatory cytokines by MEM has been reported in rats addicted to morphine.[14] Rajasekar et al.[16] reported that MEM inhibits neuroinflammation induced by STZ in astrocytes. In addition, recent studies have shown that MEM attenuates cardiac, pulmonary, and colonic inflammation in experimental models.[5],[17],[18],[19]

The carrageenan-induced-rat paw edema is an appropriate model to assess the effects of anti-inflammatory drugs.[20] Inflammatory response due to carrageenan injection constitutes three phases that mediate by pro-inflammatory agents, including histamine, serotonin (primary phase), kinins (secondary phase), and prostaglandins, particularly E series (final phase). This response is quantified by an increase in hind paw thickness (edema).[21],[22] The maximum level of edema in the hind paw appears about 3 h after injection of carrageenan.[23] Neutrophil’s migration into the hind paw causes generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS).[21] Also, myeloperoxidase (MPO) secreted by neutrophils, initiates lipid peroxidation in the inflamed site.[24] Heretofore, no study was conducted on the effects of MEM against acute inflammation in the hind paw induced by carrageenan. In the present study, the effects of MEM on paw edema, histopathology, MPO activity, and malondialdehyde (MDA) levels were evaluated in carrageenan-induced inflammation in the hind paw of rats.

  Materials and Methods Top

Drugs and chemicals

Carrageenan was purchased from Sigma-Aldrich Co. (St. Louis, MO, USA). MEM was purchased from Sobhan Darou Co. (Rasht, Iran). The other reagents were of a commercial analytical grade.


Thirty male Wistar rats with a weight range of 250 ± 30 and the age of 8–10 weeks were used in this study. Animals were maintained under standard conditions (12-h light/dark cycle, temperature 22 ± 1°C and 50 ± 10% humidity) with free access to water and standard laboratory animals’ food. All experiments on animals were carried out following the Guide for the Care and Use of Laboratory Animals published by the US National Institute of Health (NIH Publication, 8th edition, 2011) and approved by the Ethics Committee of the University (IR.UMSU.RES.1396.140; 2017-07-19).

Experimental design

The rats were randomly divided into five groups of six animals per group. Group 1 (carrageenan) received 0.1 mL of 1% carrageenan by subplantar injection into the right hind paw of the animals. Group 2 (DEXA) received 10 mg/kg of dexamethasone ip 20 min after injection of 0.1 mL of 1% carrageenan. Groups 3–5 served as MEM groups and received 5, 10, and 20 mg/kg of MEM ip, respectively, 20 min after injection of 0.1 mL of 1% carrageenan.

Assessing hind paw thickness

The inflammation was quantified by measuring the right hind paw thickness of animals using a digital caliper at 0, 1, 2, 3, 4, and 5 h after carrageenan injection.

Histopathological studies

The right hind paw of each rat was excised after euthanasia with pentobarbital and fixed in 10% formalin. Then, hematoxylin and Eosin (H&E) staining was used to evaluate the degree of inflammation and neutrophil infiltration. Histopathological changes such as edema and necrosis were scored by two pathologists in a single-blind fashion as 0, 1, 2, 3, and 4 for absent, mild (slight degree of inflammation), moderate (edema with degeneration of muscle fibers), moderate to severe (edema with myofibrillar degeneration and/or diffuse inflammation), and sever (edema with extensive myofibrillar degeneration and necrosis) pathological changes, respectively.[25],[26]

Determination of MPO activity

MPO activity was considered as neutrophils activities according to the Bradley method.[27] In brief, Right animals’ hind paws were homogenized in 50mM potassium-phosphate-buffered solution (pH = 6.0) which contained hexadecyltrimethylammonium bromide (HTAB), then centrifuged at 4°C and 10,000 rpm and supernatant was collected. Thereafter, the absorbance was measured by a spectrophotometer (Cecil 9000, UK) at 460 nm and concentration was calculated by using the calibration curve (y = 0.00616x − 0.0085). The results were expressed as units of MPO in 100 mg weight of wet tissue (U/100 mg tissue).[27]

Measurement of tissue lipid peroxidation

Malondialdehyde (MDA) levels were measured in the right animals’ hind paws by using the thiobarbituric acid reacting substance method.[28] Briefly, the hind paws of animals were homogenized in Tris–HCl buffer (0.1 M, pH = 7.4). Then samples were centrifuged at 4°C and 10,000 rpm and supernatant was collected. The tissue samples were reacted with thiobarbituric acid at acidic pH at high temperature in a boiling bath for 45 min. The absorbance of samples was determined at 532 nm by using a spectrophotometer (Cecil 9000, UK). N-Butyl alcohol was used as a blank. The results were presented as nanomoles per milligram protein.

Statistical analysis

All values are presented as mean ± SEM. Data were analyzed by one-way analysis of variance (ANOVA). When the ANOVA analysis indicated significant differences, the Tukey post hoc test was performed to compare the mean values between the groups. Differences between means were considered significant at P < 0.05.

  Results Top

Effects of MEM on paw thickness in carrageenan-induced hind paw edema

As shown in [Figure 1], at the first hour after injection of carrageenan hind paw thickness of animals had no significant difference between the groups. At 2nd h, hind paw thickness in treated groups with MEM significantly (P < 0.05 and P < 0.01 at MEM 10 mg/kg and MEM 5 and 20 mg/kg, respectively) decreased in comparison to the carrageenan group. At 3rd h, MEM- and DEXA-treated groups showed a significant (P < 0.001 and P < 0.01, respectively) decrease in comparison to the carrageenan group. Also, at 4th h after injection of carrageenan, hind paw thickness significantly reduced in MEM (P < 0.001 at 5 mg/kg and P < 0.01 at MEM 10 and 20 mg/kg) and DEXA (P < 0.01) groups in comparison to the carrageenan group. After that, at 5th h, hind paw thickness of animals in all groups were similar to each other and no significant difference was observed.
Figure 1: Effects of MEM on carrageenan-induced paw edema in rats at different times. Values are present as mean ± SEM (n = 6). Different letters (a–c) show significant differences (a: P < 0.05, b: P < 0.01 and c: P < 0.001) in comparison with the carrageenan group using one-way ANOVA with Tukey post hoc test

Click here to view

Effects of MEM on histopathology

The histological sections of the hind paw obtained from the carrageenan group showed a high number of leukocyte accumulation in the tissue with significant degeneration of muscle fibers. MEM treatment at all doses considerably decreased edema, leukocyte infiltration, and myofibril degeneration in comparison to the carrageenan group (P < 0.05 at 5 mg/kg and P < 0.01 at MEM 10 and 20 mg/kg). Also, administration of DEXA as a positive control markedly reduced leukocyte infiltration in the tissue (P < 0.001) [Figure 2].
Figure 2: (A) Photomicrographs of sections of rat hind paws after H&E staining. (B) Grading of histopathological changes in the rats’ hind paw tissues. Grades 1, 2, 3, and 4 represent low, moderate, high, and intensive pathological changes, respectively. Values are mean ± SEM. *P < 0.05, **P < 0.01, and *** P < 0.001 as compared to the carrageenan group using one-way ANOVA with Tukey post hoc test

Click here to view

Effects of MEM on MPO activity

[Figure 3] indicates that administration of MEM at all doses significantly (MEM 5 mg/kg P < 0.01 and MEM 10, 20 mg/kg P < 0.001) decreased MPO activity in the hind paw of animals in comparison to the carrageenan group.
Figure 3: The effect of MEM on MPO activity in hind paws of rats injected with carrageenan. Values are present as mean ± SEM (n = 6). **P < 0.01 and ***P < 0.001 as compared to the carrageenan group using one-way ANOVA with Tukey post hoc test

Click here to view

Effects of MEM on lipid peroxidation

Obviously, treating with MEM at all doses significantly (P < 0.001) reduced MDA levels in hind paw tissue [Figure 4].
Figure 4: The effect of MEM on MDA levels in hind paws of rats injected with carrageenan. Values are present as mean ± SEM (n = 6). ***P < 0.001 as compared to the carrageenan group using one-way ANOVA with Tukey post hoc test

Click here to view

  Discussion Top

As mentioned earlier, NMDARs are participated in triggering inflammatory responses. In this study, MEM, an uncompetitive NMDAR antagonist, was administered to treat inflammation induced by carrageenan. Our results revealed that treatment with MEM significantly reduced hind paw thickness, leukocyte infiltration, MPO activity, and MDA levels.

As expected, injection of carrageenan induced hind paw inflammation that is characterized by increasing hind paw thickness and edema. The maximum amount of edema was observed at 3 h after carrageenan injection. The edema is one of the typical signs of inflammation following carrageenan injection which occurred due to action of pro-inflammatory agents generated by tissue or infiltrating cells in the inflamed site.[21],[22],[29]

Administration of MEM significantly reduced hind paw edema in animals. Similar to our findings, a study indicated that systemic administration of NMDAR antagonists decreased paw swelling induced by formalin.[30],[31] As previously mentioned, histamine, serotonin, and prostaglandin mediate inflammatory response phases following carrageenan injection which induce hind paw edema.[21] MEM competitively inhibits human organic cation transporter 2 (hOCT2), a monoamine transporter that can translocate histamine and serotonin.[32] Therefore, it can be a reason for edema reduction by MEM. Moreover, another reason may relate to prostaglandin production. These bio-compounds sensitized by arachidonic acid and cyclooxygenase (COX) enzymes are catalysts of this reaction.[33] Evidence have indicated that MEM decreased the COX-2 level.[16] Wu et al.[15] showed that pre-treatment with MEM decreased PGE2. Thereby, a reduction in prostaglandin synthesis may be a reason for the anti-inflammatory effect of MEM and reduction of edema. On the other hand, MEM decreases the production of nitric oxide (NO)[13],[15] that has a key role in the mediation of inflammation following carrageenan injection.[29]

MPO is a heme enzymatic protein that presents in neutrophil granulocytes. This enzyme is one of the local mediators of tissue injury and results from occurring inflammation in the damaged site.[24],[34] Therefore, assessment of MPO activity is a dependable indicator of granulocytes infiltration and inflammation in different tissues.[35],[36] MPO through formation of reactive oxygen and nitrogen intermediates which results in lipid peroxidation can cause host tissue damage.[24],[34] Hence, a reduction in MPO activity is a good therapeutic strategy to treat inflammation.[34] Our study indicated that treatment with MEM decreased MPO activity in the carrageenan-injected hind paw of animals. These findings confirmed that MEM has anti-inflammatory effects. In line with our results, previous studies showed that MEM reduced MPO activity in various inflammatory conditions in different organs.[5],[17],[18]

Lipid peroxidation is one of the pathophysiologic consequences of acute inflammatory conditions.[24] Administration of MEM in the present study decreased lipid peroxidation which is similar to other researchers’ findings.[17],[18] Reduction of lipid peroxidation may be related to a decrease in MPO activity, because MPO function is the main factor in the initiation of lipid peroxidation in the inflamed site.[24] Also, it may be associated with a reduction of ROS and RNS due to MEM treatment which can be inferred from previous studies.[13],[15] To the best of our knowledge, this is the first study showing the anti-inflammatory effects of MEM in the carrageenan-induced hind paw edema, as an inflammation model in rats.

  Conclusions Top

The present study demonstrated that MEM decreased paw edema, leukocyte infiltration, MPO activity, and MDA levels, and MEM can be considered as an effective anti-inflammatory agent.

Financial support and sponsorship

This study was financially supported by the Urmia University of Medical Sciences.

Conflict of interest

None declared.

  References Top

Medzhitov R. Origin and physiological roles of inflammation. Nature 2008;454:428-35.  Back to cited text no. 1
Loix S, De Kock M, Henin P. The anti-inflammatory effects of ketamine: State of the art. Acta Anaesthesiol Belg 2011;62:47-58.  Back to cited text no. 2
Zhu S, Gouaux E. Structure and symmetry inform gating principles of ionotropic glutamate receptors. Neuropharmacology 2017;112:11-5.  Back to cited text no. 3
Hogan-Cann AD, Anderson CM. Physiological roles of non-neuronal NMDA receptors. Trends Pharmacol Sci 2016;37:750-67.  Back to cited text no. 4
Motaghi E, Hajhashemi V, Mahzouni P, Minaiyan M. The effect of memantine on trinitrobenzene sulfonic acid-induced ulcerative colitis in mice. Eur J Pharmacol 2016;793:28-34.  Back to cited text no. 5
Tejero-Taldo MI, Chmielinska JJ, Gonzalez G, Mak IT, Weglicki WB. N-methyl-D-aspartate receptor blockade inhibits cardiac inflammation in the Mg2+-deficient rat. J Pharmacol Exp Ther 2004;311:8-13.  Back to cited text no. 6
do Vale EM, Xavier CC, Nogueira BG, Campos BC, de Aquino PE, da Costa RO, et al. Antinociceptive and anti-inflammatory effects of ketamine and the relationship to its antidepressant action and GSK3 inhibition. Basic Clin Pharmacol Toxicol 2016;119:562-73.  Back to cited text no. 7
De Kock M, Loix S, Lavand'homme P. Ketamine and peripheral inflammation. CNS Neurosci Ther2013;19:403-10.  Back to cited text no. 8
Jander S, Schroeter M, Stoll G. Role of NMDA receptor signaling in the regulation of inflammatory gene expression after focal brain ischemia. J Neuroimmunol 2000;109:181-7.  Back to cited text no. 9
Yang HH, Hou CC, Lin MT, Chang CP. Attenuating heat-induced acute lung inflammation and injury by dextromethorphan in rats. Am J Respir Cell Mol Biol 2012;46:407-13.  Back to cited text no. 10
Lipton SA. Failures and successes of NMDA receptor antagonists: Molecular basis for the use of open-channel blockers like memantine in the treatment of acute and chronic neurologic insults. NeuroRx 2004;1:101-10.  Back to cited text no. 11
Parsons CG, Danysz W, Quack G. Memantine is a clinically well tolerated N-methyl-D-aspartate (NMDA) receptor antagonist—A review of preclinical data. Neuropharmacology 1999;38:735-67.  Back to cited text no. 12
Rai S, Kamat PK, Nath C, Shukla R. A study on neuroinflammation and NMDA receptor function in STZ (ICV) induced memory impaired rats. J Neuroimmunol 2013;254:1-9.  Back to cited text no. 13
Chen SL, Tao PL, Chu CH, Chen SH, Wu HE, Tseng LF, et al. Low-dose memantine attenuated morphine addictive behavior through its anti-inflammation and neurotrophic effects in rats. J Neuroimmune Pharmacol 2012;7:444-53.  Back to cited text no. 14
Wu HM, Tzeng NS, Qian L, Wei SJ, Hu X, Chen SH, et al. Novel neuroprotective mechanisms of memantine: Increase in neurotrophic factor release from astroglia and anti-inflammation by preventing microglial activation. Neuropsychopharmacology 2009;34:2344-57.  Back to cited text no. 15
Rajasekar N, Nath C, Hanif K, Shukla R. Inhibitory effect of memantine on streptozotocin-induced insulin receptor dysfunction, neuroinflammation, amyloidogenesis, and neurotrophic factor decline in astrocytes. Mol Neurobiol 2016;53:6730-44.  Back to cited text no. 16
Abbaszadeh S, Javidmehr A, Askari B, Janssen PML, Soraya H. Memantine, an NMDA receptor antagonist, attenuates cardiac remodeling, lipid peroxidation and neutrophil recruitment in heart failure: A cardioprotective agent? Biomed Pharmacother 2018;108:1237-43.  Back to cited text no. 17
Li Y, Liu Y, Peng XP, Liu W, Zhao FY, Feng DD, et al. NMDA receptor antagonist attenuates bleomycin-induced acute lung injury. PLoS One 2015;10:1-14.  Back to cited text no. 18
Cheng Q, Fang L, Feng D, Tang S, Yue S, Huang Y, et al. Memantine ameliorates pulmonary inflammation in a mice model of COPD induced by cigarette smoke combined with LPS. Biomed Pharmacother 2019;109:2005-13.  Back to cited text no. 19
Winter CA, Risley EA, Nuss GW. Carrageenin-induced edema in hind paw of the rat as an assay for antiinflammatory drugs. Exp Biol Med. 1962;111:544-7.  Back to cited text no. 20
Morris CJ. Carrageenan-induced paw edema in the rat and mouse. Methods Mol Biol 2003;225:115-21.  Back to cited text no. 21
Vinegar R, Schreiber W, Hugo R. Biphasic development of carrageenin edema in rats. J Pharmacol Exp Ther 1969;166:96-103.  Back to cited text no. 22
Matsumoto K, Obara S, Kuroda Y, Kizu J. Anti-inflammatory effects of linezolid on carrageenan-induced paw edema in rats. J Infect Chemother 2015;21:889-91.  Back to cited text no. 23
Zhang R, Brennan ML, Shen Z, MacPherson JC, Schmitt D, Molenda CE, et al. Myeloperoxidase functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. J Biol Chem 2002;277:46116-22.  Back to cited text no. 24
Soraya H, Rameshrad M, Mokarizadeh A, Garjani A. Metformin attenuates myocardial remodeling and neutrophil recruitment after myocardial infarction in rat. Bioimpacts 2015;5:3-8.  Back to cited text no. 25
Hussein SZ, Mohd Yusoff K, Makpol S, Mohd Yusof YA. Gelam honey attenuates carrageenan-induced rat paw inflammation via NF-κb pathway. PLoSs One 2013;8:e72365.  Back to cited text no. 26
Mullane KM, Kraemer R, Smith B. Myeloperoxidase activity as a quantitative assessment of neutrophil infiltration into ischemic myocardium. J Pharmacol Methods 1985;14:157-67.  Back to cited text no. 27
Yousefi K, Soraya H, Fathiazad F, Khorrami A, Hamedeyazdan S, Maleki-Dizaji N, et al. Cardioprotective effect of methanolic extract of Marrubium vulgare L. on isoproterenol-induced acute myocardial infarction in rats. Indian J Exp Biol 2013;51:653-60.  Back to cited text no. 28
Salvemini D, Wang ZQ, Wyatt PS, Bourdon DM, Marino MH, Manning PT, et al. Nitric oxide: A key mediator in the early and late phase of carrageenan-induced rat paw inflammation. Br J Pharmacol 1996;118:829-38.  Back to cited text no. 29
Sluka KA, Jordan HH, Westlund KN. Reduction in joint swelling and hyperalgesia following post-treatment with a non-NMDA glutamate receptor antagonist. Pain 1994;59:95-100.  Back to cited text no. 30
Sawynok J, Reid A. Modulation of formalin-induced behaviors and edema by local and systemic administration of dextromethorphan, memantine and ketamine. Eur J Pharmacol 2002;450:153-62.  Back to cited text no. 31
Busch AE, Karbach U, Miska D, Gorboulev V, Akhoundova A, Volk C, et al. Human neurons express the polyspecific cation transporter HOCT2, which translocates monoamine neurotransmitters, amantadine, and memantine. Mol Pharmacol 1998;54:342-52.  Back to cited text no. 32
Ricciotti E, FitzGerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vasc Biol 2011;31:986-1000.  Back to cited text no. 33
Aratani Y. Myeloperoxidase: Its role for host defense, inflammation, and neutrophil function. Arch Biochem Biophys 2018;640: 47-52.  Back to cited text no. 34
Werner U, Szelenyi I. Measurement of MPO activity as model for detection of granulocyte infiltration in different tissues. Agents Actions1992;36:C101-3.  Back to cited text no. 35
Faith M, Sukumaran A, Pulimood AB, Jacob M. How reliable an indicator of inflammation is myeloperoxidase activity? Clin Chim Acta 2008;396:23-5.  Back to cited text no. 36


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

This article has been cited by
1 Memantine and its benefits for cancer, cardiovascular and neurological disorders
Vahid Shafiei-Irannejad,Samin Abbaszadeh,Paul M.L. Janssen,Hamid Soraya
European Journal of Pharmacology. 2021; : 174455
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Materials and Me...
Article Figures

 Article Access Statistics
    PDF Downloaded105    
    Comments [Add]    
    Cited by others 1    

Recommend this journal