Publications by authors named "Nagaraja Haleagrahara"

44 Publications

Usefulness of Procalcitonin in Diagnosing Diabetic Foot Osteomyelitis: A Pilot Study.

Wounds 2021 07;33(7):192-196

Translational Research in Endocrinology and Diabetes, College of Medicine and Dentistry, James Cook University, Douglas, Queensland, Australia; Department of Endocrinology and Diabetes, Townsville University Hospital, Douglas, Queensland, Australia.

Introduction: Infected diabetic foot is the leading cause of hospital admissions for people with diabetes mellitus. Diabetic foot osteomyelitis (DFO) causes high morbidity and significant mortality. Current diagnostic tests for DFO are either expensive, invasive, or of low diagnostic yield.

Objective: The objective of the study was to determine whether serum levels of procalcitonin (PCT), an inflammatory marker, differ between DFO and diabetic foot ulcers without osteomyelitis (ie, cellulitis) as controls. The authors also aimed to assess the usefulness of PCT in diagnosing DFO.

Methods: A case-control study was designed comparing DFO with diabetic foot cellulitis as the control. Patients were classified as having osteomyelitis and cellulitis based on the International Working Group on the Diabetic Foot diagnostic criteria. Serum inflammatory markers PCT, adiponectin, C-reactive protein-1, osteoprotegerin (OPG), osteopontin (OPN), and interleukin 6 (IL-6) were analyzed in patients with DFO and controls.

Results: The median serum procalcitonin was significantly higher in the DFO group 108.5 pg/mL (range, 65.0-124.0 pg/mL) compared with 57.0 pg/mL (range, 37.2-77.0 pg/mL) controls (P = .02). Procalcitonin had a sensitivity of 79% compared with 50%, 63%, 66%, and 75% for adiponectin, OPG, OPN, and IL-6, respectively. Procalcitonin had a specificity of 70% compared with 50%, 71%, 70%, and 64%. Receiver operator characteristic curves showed a value of area under the curve of 0.73 and 0.77 for PCT and IL-6 compared with 0.4, 0.6, and 0.6 for adiponectin, OPG, and OPN, respectively.

Conclusions: In this study, procalcitonin was a useful diagnostic test for DFOs and provided distinct diagnostic discrimination between DFO from cellulitis. It may serve as a useful marker for diagnosing DFO. Further studies in a larger population are needed to verify the findings.
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http://dx.doi.org/10.25270/wnds/2021.192196DOI Listing
July 2021

Tocotrienols Ameliorate Neurodegeneration and Motor Deficits in the 6-OHDA-Induced Rat Model of Parkinsonism: Behavioural and Immunohistochemistry Analysis.

Nutrients 2021 May 10;13(5). Epub 2021 May 10.

College of Medicine and Dentistry, James Cook University, Townsville, QLD 4811, Australia.

Parkinson's disease (PD) is a debilitating neurodegenerative disease, which progresses over time, causing pathological depigmentation of the substantia nigra (SN) in the midbrain due to loss of dopaminergic neurons. Emerging studies revealed the promising effects of some nutrient compounds in reducing the risk of PD. One such nutrient compound that possess neuroprotective effects and prevents neurodegeneration is tocotrienol (T3), a vitamin E family member. In the present study, a single dose intracisternal injection of 250 µg 6-hydroxydopamine (6-OHDA) was used to induce parkinsonism in male Sprague Dawley (SD) rats. Forty-eight hours post injection, the SD rats were orally supplemented with alpha (α)- and gamma (γ)-T3 for 28 days. The neuroprotective effects of α- and γ-T3 were evaluated using behavioural studies and immunohistochemistry (IHC). The findings from this study revealed that supplementation of α- and γ-T3 was able to ameliorate the motor deficits induced by 6-OHDA and improve the neuronal functions by reducing inflammation, reversing the neuronal degradation, and preventing further reduction of dopaminergic neurons in the SN and striatum (STR) fibre density.
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http://dx.doi.org/10.3390/nu13051583DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8150907PMC
May 2021

Influence of serum concentration in retinoic acid and phorbol ester induced differentiation of SH-SY5Y human neuroblastoma cell line.

Mol Biol Rep 2020 Nov 23;47(11):8775-8788. Epub 2020 Oct 23.

School of Postgraduate Studies, International Medical University, Kuala Lumpur, Malaysia.

Numerous protocols to establish dopaminergic phenotype in SH-SY5Y cells have been reported. In most of these protocols there are variations in concentration of serum used. In this paper, we compared the effects of high (10%), low (3%) and descending (2.5%/1%) serum concentration in differentiation medium containing different proportion of retinoic acid (RA) and 12-O-Tetradecanoylphorbol-13-acetate (TPA) or RA-only on the undifferentiated SH-SY5Y cells with regards to cell morphology, biochemical and gene expression alterations. Cells differentiated in culture medium containing low and descending serum concentrations showed increased number of neurite projections and reduced proliferation rates when compared to undifferentiated cells. The SH-SY5Y cells differentiated in culture medium containing 3% RA and low serum or descending (2.5%/1% RA/TPA) were found to be more susceptible to 6-hydroxydopamine (6-OHDA) induced cytotoxicity. Cells differentiated with RA/TPA or RA differentiated showed increased production of the α-synuclein (SNCA) neuroprotein and dopamine neurotransmitter compared to undifferentiated cells, regardless serum concentrations used. There was no significant difference in the expression of tyrosine hydroxylase (TH) gene between undifferentiated and differentiated SH-SY5Y cells. However, the expression of dopamine receptor D2 (DRD2) gene was markedly increased (p<0.05) in differentiated cells with 3% serum and RA only when compared to undifferentiated cells. In conclusion, to terminally differentiate SH-SY5Y cells to be used as a cell-based model to study Parkinson's disease (PD) to investigate molecular mechanisms and drug discovery, the optimal differentiation medium should contain 3% serum in RA-only.
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http://dx.doi.org/10.1007/s11033-020-05925-2DOI Listing
November 2020

Factors Influencing Medical Students' Experiences and Satisfaction with Blended Integrated E-Learning.

Med Princ Pract 2020 5;29(4):396-402. Epub 2019 Dec 5.

Division of Tropical Health and Medicine, College of Medicine and Dentistry, James Cook University, Townsville, Queensland, Australia,

Objectives: Blended learning has been presented as a promising learner-centred model that emphasises the learning outcome rather than the process of education, but it can negatively affect learners' engagement with learning.

Subject And Methods: Using a mixed-methods approach, this study aimed to determine the significant predictors of learning satisfaction and to evaluate the experiences of medical students with the different domains of an introduced blended integrated learning approach.

Results: The survey was administered to 92 respondents with a mean age of 20.5 years. Male students had significantly higher computer self-efficacy and overall learner satisfaction ratings than their female counterparts. Multiple regression analysis showed that gender (student characteristics), performance expectations (cognitive factors), and learning climate (social environment) were predictors of the perceived satisfaction of learners.

Conclusion: Wider integration of blended learning into pre-clinical undergraduate medical education could enhance the shift towards competency-based education and life-long learning among medical students. However, effective implementation would depend largely on student characteristics, as well as environmental and cognitive components of the delivery method.
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http://dx.doi.org/10.1159/000505210DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445668PMC
July 2021

Helminth-based therapies for rheumatoid arthritis: A systematic review and meta-analysis.

Int Immunopharmacol 2019 Jan 4;66:366-372. Epub 2018 Dec 4.

College of Public Health, Medicine and Veterinary Sciences, James Cook University, Douglas, 4814 Townsville, Australia. Electronic address:

Objective: Proteins from parasitic worms have been posed as novel therapies for rheumatoid arthritis (RA) and other auto-inflammatory diseases. However, with so many potential therapeutics, it is important that drug discovery be based on the specific phyla or species which show the most promising effects. Therefore, the aim of this systematic review and meta-analysis was to evaluate the reported effects of helminthic secretory proteins and derivative therapy on RA in an animal model.

Methods: Medline, Scopus and Web of Science were searched to identify studies evaluating helminthic therapy in the collagen-induced arthritis model of RA. A meta-analysis was undertaken to determine the overall effect of the proteins. Subgroup analyses were also undertaken to investigate individual treatments.

Results: Seven articles were included in the analysis. Overall, helminthic therapy significantly reduced arthritis score (SMD -1.193, 95% CI -1.525, -0.860). Subgroup analyses found a significant reduction in arthritis score following treatment with helminth protein ES-62 (SMD -1.186, 95% CI -1.633, -0.738) and phosphorylcholine-based treatment (SMD -0.997, 95% CI -1.423, -0.571). Subgroup analyses found ES-62 treatment significantly decreased IFN-γ levels (SMD -1.611, 95% CI -2.734, -0.487) and significantly increased levels of IL-10 (SMD 0.946, 95% CI 0.127, 1.765).

Conclusions: Therapeutics from parasitic worms are a promising avenue for drug discovery, especially with all included studies reporting a significant improvement in arthritis score. Based on pooled data presented in this study, the nematode Acanthocheilonema viteae seems to be of particular interest for therapeutics.
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http://dx.doi.org/10.1016/j.intimp.2018.11.034DOI Listing
January 2019

Regulatory T-cell dynamics with abatacept treatment in rheumatoid arthritis.

Int Rev Immunol 2018 14;37(4):206-214. Epub 2018 May 14.

b College of Public Health, Medicine and Veterinary Sciences , James Cook University , Douglas , Townsville , Australia.

The progressive damage in rheumatoid arthritis (RA) has been linked to an increase in inflammatory Th1/Th17 cells and a decrease in number or function of immunomodulatory regulatory T cells (Tregs). Many therapies that are effective in RA are shown to affect Th1/Th17 cells and/or Tregs. One such therapy, abatacept, utilizes a physiologic immunomodulatory molecule called cytotoxic lymphocyte antigen-4 (CTLA-4) which causes contact-dependent inhibition of inflammatory T-cell activation. Recent advances in CTLA-4 research has uncovered the method by which this occurs physiologically but the actions of the CTLA-4Ig fusion protein are still not fully understood. The reported effects of the drug on Treg population number and suppressor function have been very mixed. In this review, we will discuss the current literature surrounding the effects of abatacept in rheumatoid arthritis and explore potential explanations for the differences in results. Future opportunities in this area include contributions to a unified definition for different immune cell populations, LAG3 Tregs which may pose an avenue for further study or the stratification of patients with regards to their specific disease characteristics, resulting in optimized treatment for disease remission.
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http://dx.doi.org/10.1080/08830185.2018.1465943DOI Listing
April 2019

Current Concepts of Neurodegenerative Mechanisms in Alzheimer's Disease.

Biomed Res Int 2018 8;2018:3740461. Epub 2018 Mar 8.

College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD, Australia.

Neurodegenerative diseases are hereditary or sporadic conditions that result in the progressive loss of the structure and function of neurons as well as neuronal death. Although a range of diseases lie under this umbrella term, Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases that affect a large population around the globe. Alzheimer's disease is characterized by the abnormal accumulation of extracellular amyloid- plaques and intraneuronal neurofibrillary tangles in brain regions and manifests as a type of dementia in aged individuals that results in memory loss, multiple cognitive abnormalities, and intellectual disabilities that interfere with quality of life. Since the discovery of AD, a wealth of new information has emerged that delineates the causes, mechanisms of disease, and potential therapeutic agents, but an effective remedy to cure the diseases has not been identified yet. This could be because of the complexity of the disease process, as it involves various contributing factors that include environmental factors and genetic predispositions. This review summarizes the current understanding on neurodegenerative mechanisms that lead to the emergence of the pathology of AD.
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http://dx.doi.org/10.1155/2018/3740461DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5863339PMC
September 2018

Flavonoid quercetin-methotrexate combination inhibits inflammatory mediators and matrix metalloproteinase expression, providing protection to joints in collagen-induced arthritis.

Inflammopharmacology 2018 Oct 3;26(5):1219-1232. Epub 2018 Apr 3.

School of Science and Technology, University of New England, Armidale, NSW, 2351, Australia.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of synovial tissues in joints, leading to progressive destruction of cartilage and joints. The disease-modifying anti-rheumatic drugs currently in use have side-effects. Thus, there is an urgent need for safe anti-inflammatory therapies for RA. This study aimed to evaluate the therapeutic effect of the flavonoid quercetin on arthritis in mice immunized with type II collagen (CII). An arthritis model was established in C57/BL6 mice by intradermal administration of chicken CII mixed with Freund's complete adjuvant. Quercetin (30 mg/kg orally) and methotrexate (0.75 mg intraperitoneally twice a week) were administered to investigate their protective effects against collagen-induced arthritis (CIA). Levels of tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, and the matrix metalloproteinases (MMP), 3, and 9 were detected to assess the anti-inflammatory effect of quercetin. The mRNA expression of MMP3, MMP9, CCL2, and TNF-α was also measured by quantitative real-time PCR. Quercetin significantly alleviated joint inflammation by reducing the levels of circulating cytokines and MMPs. There was a significant decrease in the expression of TNFα and MMP genes in the ankle joints of arthritic mice. A significant reduction in the levels of knee-joint inflammatory mediators were observed with combined quercetin and methotrexate treatment. Thus, quercetin has the potential to prevent joint inflammation and could be used as an adjunct therapy for RA patients who have an inadequate response to anti-rheumatic monotherapy.
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http://dx.doi.org/10.1007/s10787-018-0464-2DOI Listing
October 2018

Redox-sensitive transcription factors play a significant role in the development of rheumatoid arthritis.

Int Rev Immunol 2018 05 12;37(3):129-143. Epub 2017 Sep 12.

b Biomedicine, College of Public Health, Medical and Veterinary Sciences , James Cook University , Townsville , Queensland , Australia.

Rheumatoid arthritis (RA) is a chronic autoimmune disease which is associated with significant morbidity. Redox sensitive transcription factors including NF-κB, HIF, AP-1, and Nrf2 are intimately involved in the pathogenesis of RA. The treatment of this disease is limited by the elusive nature of the pathogenesis of RA. NF-κB is crucial for the maturation of immune cells as well as production of TNFα and MMPs, which escalate RA. HIF is essential for activation of inflammatory cells, angiogenesis and pannus formation in RA. AP-1 regulates cytokine and MMP production as well as synovial hyperplasia which are key processes in RA. Nrf2 is involved with chondrogenesis, osteoblastogenesis, prostaglandin secretion and ROS production in RA. Targeting two or more of these transcription factors may result in increased efficacy than either therapy in isolation. This review will highlight the control specific mediators on these transcription factors, the subsequent effect of these transcription factors once activated, and then mesh this with the pathogenesis of RA. The elucidation of key transcription factor regulation in the pathogenesis of RA may highlight the novel therapy interventions which may prove to have a greater efficacy than those therapies currently available.
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http://dx.doi.org/10.1080/08830185.2017.1363198DOI Listing
May 2018

Therapeutic effect of quercetin in collagen-induced arthritis.

Biomed Pharmacother 2017 Jun 22;90:38-46. Epub 2017 Mar 22.

College of Public Health, Medical and Veterinary Sciences, James Cook University, James Cook Drive, Townsville, Queensland 4811, Australia; Australian Institute of Tropical Health and Medicine, James Cook University, James Cook Drive, Townsville, Queensland 4811, Australia.

Quercetin, a bioactive flavonoid with anti-inflammatory, immunosuppressive, and protective properties, is a potential agent for the treatment of rheumatoid arthritis (RA). Collagen-induced arthritis (CIA) is the most commonly used animal model for studying the pathogenesis of RA. This study analysed the therapeutic role of quercetin in collagen-induced arthritis in C57BL/6 mice. The animals were allocated into five groups that were subjected to the following treatments: negative (untreated) control, positive control (arthritis-induced), arthritis+methotrexate, arthritis+quercetin, and arthritis+methotrexate+quercetin. Assessments of weight, oedema, joint damage, and cytokine production were used to determine the therapeutic effect of quercetin. This study demonstrated for the first time the anti-inflammatory and protective effects of quercetin in vivo in CIA. The results also showed that the concurrent administration of quercetin and methotrexate did not offer greater protection than the administration of a single agent. The use of quercetin as a monotherapeutic agent resulted in the lowest degree of joint inflammation and the highest protection. The reduced severity of the disease in animals treated with quercetin was associated with decreased levels of TNF-α, IL-1β, IL-17, and MCP-1. In conclusion, this study determined that quercetin, which was non-toxic, produced better results than methotrexate for the protection of joints from arthritic inflammation in mice. Quercetin may be an alternative treatment for RA because it modulates the main pathogenic pathways of RA.
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http://dx.doi.org/10.1016/j.biopha.2017.03.026DOI Listing
June 2017

The therapeutic potential of plant flavonoids on rheumatoid arthritis.

Crit Rev Food Sci Nutr 2017 Nov;57(17):3601-3613

a Biomedicine, College of Public Health , Medical & Veterinary Sciences, James Cook University , Townsville , Australia.

Rheumatoid arthritis (RA) is an autoimmune condition that mainly affects peripheral joints. Although immunosuppressive drugs and non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat this condition, these drugs have severe side effects. Flavonoids are the most abundant phenolic compounds which exhibit anti-oxidant, anti-inflammatory and immunomodulatory properties. Many bioactive flavonoids have powerful anti-inflammatory effects. However, a very few have reached clinical use. Dietary flavonoids have been reported to control joint inflammation and alleviate arthritis symptoms in both human RA and animal models of arthritis. There is little scientific evidence about their mechanism of actions in RA. We review the therapeutic effects of different groups of flavonoids belonging to the most common and abundant groups on RA. In particular, the probable mechanisms of major flavonoids on cells and chemical messengers involved in the inflammatory signaling components of RA are discussed in detail.
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http://dx.doi.org/10.1080/10408398.2016.1246413DOI Listing
November 2017

Protective Mechanisms of Flavonoids in Parkinson's Disease.

Oxid Med Cell Longev 2015 20;2015:314560. Epub 2015 Oct 20.

Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD 4811, Australia.

Parkinson's disease is a chronic, debilitating neurodegenerative movement disorder characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta region in human midbrain. To date, oxidative stress is the well accepted concept in the etiology and progression of Parkinson's disease. Hence, the therapeutic agent is targeted against suppressing and alleviating the oxidative stress-induced cellular damage. Within the past decades, an explosion of research discoveries has reported on the protective mechanisms of flavonoids, which are plant-based polyphenols, in the treatment of neurodegenerative disease using both in vitro and in vivo models. In this paper, we have reviewed the literature on the neuroprotective mechanisms of flavonoids in protecting the dopaminergic neurons hence reducing the symptoms of this movement disorder. The mechanism reviewed includes effect of flavonoids in activation of endogenous antioxidant enzymes, suppressing the lipid peroxidation, inhibition of inflammatory mediators, flavonoids as a mitochondrial target therapy, and modulation of gene expression in neuronal cells.
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http://dx.doi.org/10.1155/2015/314560DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4630416PMC
July 2016

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells.

Int J Immunopathol Pharmacol 2016 Mar 5;29(1):30-9. Epub 2015 Nov 5.

Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD, Australia

There is increasing evidence that free radicals induced oxidative stress is a major causative agent in the pathogenesis of neurodegenerative diseases, particularly Parkinson's disease. Quercetin glycosides, namely rutin and isoquercitrin, are flavonoid polyphenol compounds found ubiquitously in fruits and vegetables and have been known to possess antioxidant effects. This study was designed to compare the neuroprotective effects of quercetin glycosides rutin and isoquercitrin in 6-OHDA-induced rat pheochromocytoma (PC-12) cells. The results showed that both rutin and isoquercitrin significantly increased antioxidant enzymes, catalase, superoxide dismutase, glutathione peroxidase, and glutathione level that were attenuated by 6-OHDA in PC-12 cells. There was no significant difference in the activation of glutathione and glutathione peroxidase enzymes between rutin and isoquercitrin. These two glycosides were equally effective in suppressing lipid peroxidation in 6-OHDA-induced PC-12 cells as both compounds suppressed the malondialdehyde generation and prevented cell damage. In conclusion, quercetin glycosides rutin and isoquercetrin are having a significant neuroprotective effect against 6-OHDA toxicity in PC-12 cells.
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http://dx.doi.org/10.1177/0394632015613039DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806739PMC
March 2016

Prolonged Subcutaneous Administration of Oxytocin Accelerates Angiotensin II-Induced Hypertension and Renal Damage in Male Rats.

PLoS One 2015 22;10(9):e0138048. Epub 2015 Sep 22.

College of Public Health, Medical & Veterinary Sciences, James Cook University, Townsville, Queensland 4811 Australia; Centre for Biodiscovery & Molecular Development of Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Townsville Queensland 4811, Australia.

Oxytocin and its receptor are synthesised in the heart and blood vessels but effects of chronic activation of this peripheral oxytocinergic system on cardiovascular function are not known. In acute studies, systemic administration of low dose oxytocin exerted a protective, preconditioning effect in experimental models of myocardial ischemia and infarction. In this study, we investigated the effects of chronic administration of low dose oxytocin following angiotensin II-induced hypertension, cardiac hypertrophy and renal damage. Angiotensin II (40 μg/Kg/h) only, oxytocin only (20 or 100 ng/Kg/h), or angiotensin II combined with oxytocin (20 or 100 ng/Kg/h) were infused subcutaneously in adult male Sprague-Dawley rats for 28 days. At day 7, oxytocin or angiotensin-II only did not change hemodynamic parameters, but animals that received a combination of oxytocin and angiotensin-II had significantly elevated systolic, diastolic and mean arterial pressure compared to controls (P < 0.01). Hemodynamic changes were accompanied by significant left ventricular cardiac hypertrophy and renal damage at day 28 in animals treated with angiotensin II (P < 0.05) or both oxytocin and angiotensin II, compared to controls (P < 0.01). Prolonged oxytocin administration did not affect plasma concentrations of renin and atrial natriuretic peptide, but was associated with the activation of calcium-dependent protein phosphatase calcineurin, a canonical signalling mechanism in pressure overload-induced cardiovascular disease. These data demonstrate that oxytocin accelerated angiotensin-II induced hypertension and end-organ renal damage, suggesting caution should be exercised in the chronic use of oxytocin in individuals with hypertension.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0138048PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4579129PMC
May 2016

Quercetin glycosides induced neuroprotection by changes in the gene expression in a cellular model of Parkinson's disease.

J Mol Neurosci 2015 Mar 17;55(3):609-17. Epub 2014 Aug 17.

Department of Pathology, Faculty of Medicine, International Medical University, Kuala Lumpur, Malaysia.

Quercetin glycosides, rutin and isoquercitrin, are potent antioxidants that have been found to possess neuroprotective effect in diseases like Parkinson's and Alzheimer's disease. In the present study, we have examined the gene expression changes with rutin and isoquercitrin pretreatment on 6-hydroxydopamine (6-OHDA)-treated toxicity in rat pheochromocytoma (PC12) cells. PC12 cells were pretreated with rutin or isoquercitrin and subsequently exposed to 6-OHDA. Rutin-pretreated PC12 attenuated the Park2, Park5, Park7, Casp3, and Casp7 genes which were expressed significantly in the 6-OHDA-treated PC12 cells. Rutin upregulated the TH gene which is important in dopamine biosynthesis, but isoquercitrin pretreatment did not affect the expression of this gene. Both rutin and isoquercitrin pretreatments upregulated the ion transport and antiapoptotic genes (NSF and Opa1). The qPCR array data were further validated by qRT-PCR using four primers, Park5, Park7, Casp3, and TH. This finding suggests that changes in the expression levels of transcripts encoded by genes that participate in ubiquitin pathway and dopamine biosynthesis may be involved in Parkinson's disease.
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http://dx.doi.org/10.1007/s12031-014-0400-xDOI Listing
March 2015

Therapeutic efficacy of vitamin E δ-tocotrienol in collagen-induced rat model of arthritis.

Biomed Res Int 2014 10;2014:539540. Epub 2014 Jul 10.

Department of Pathology, Faculty of Medicine, International Medical University, 57000 Kuala Lumpur, Malaysia.

Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disease primarily involving inflammation of the joints. Although the management of the disease has advanced significantly in the past three decades, there is still no cure for RA. The aim of this study was to determine the therapeutic efficacy of δ-tocotrienol, in the rat model of collagen-induced arthritis (CIA). Arthritis was induced by intradermal injection of collagen type II emulsified in complete Freund's adjuvant. CIA rats were orally treated with δ-tocotrienol (10 mg/kg) or glucosamine hydrochloride (300 mg/kg) from day 25 to 50. Efficacy was assessed based on the ability to reduce paw edema, histopathological changes, suppression of collagen-specific T-cells, and a reduction in C-reactive protein (CRP) levels. It was established that δ-tocotrienol had the most significant impact in lowering paw edema when compared to glucosamine treatment. Paw edema changes correlated well with histopathological analysis where there was a significant reversal of changes in groups treated with δ-tocotrienol. The results suggest that δ-tocotrienol is efficient in amelioration of collagen-induced arthritis. Vitamin E delta-tocotrienol may be of therapeutic value against rheumatoid arthritis.
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http://dx.doi.org/10.1155/2014/539540DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119727PMC
April 2015

Effects of vitamin E supplementation on exercise-induced oxidative stress: a meta-analysis.

Appl Physiol Nutr Metab 2014 Sep 26;39(9):1029-37. Epub 2014 May 26.

a Institute of Sport and Exercise Science, School of Public Health, Tropical Medicine and Rehabilitation Sciences, James Cook University, 4811, Australia.

Tocopherols (commonly referred to as "vitamin E") are frequently studied antioxidants in exercise research. However, the studies are highly heterogeneous, which has resulted in contradicting opinions. The aim of this review is to identify similar studies investigating the effects of tocopherol supplementation on exercise performance and oxidative stress and to perform minimally biased qualitative comparisons and meta-analysis. The literature search and study selection were performed according to Cochrane guidelines. A 2-dimensional study execution process was developed to enable selection of similar and comparable studies. Twenty relevant studies were identified. The high variability of study designs resulted in final selection of 6 maximally relevant studies. Markers of lipid peroxidation (malondialdehyde) and muscle damage (creatine kinase) were the 2 most frequently and similarly measured variables. Meta comparison showed that tocopherol supplementation did not result in significant protection against either exercise-induced lipid peroxidation or muscle damage. The complex antioxidant nature of tocopherols and low accumulation rates in muscle tissues could underlie an absence of protective effects.
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http://dx.doi.org/10.1139/apnm-2013-0566DOI Listing
September 2014

Effect of γ-tocotrienol in counteracting oxidative stress and joint damage in collagen-induced arthritis in rats.

Exp Ther Med 2014 May 28;7(5):1408-1414. Epub 2014 Feb 28.

Discipline of Physiology and Pharmacology, School of Veterinary and Biomedical Sciences, James Cook University, Townsville, Queensland 4811, Australia.

Tocotrienols exhibit a significant anti-inflammatory and antioxidant effect in numerous human diseases. However, the anti-inflammatory and antioxidant effects of tocotrienols in arthritic conditions are not well documented. Therefore, the effect of γ-tocotrienol supplementation against oxidative stress and joint pathology in collagen-induced arthritis in rats was investigated in the present study. Adult female Dark Agouti rats were randomly divided into groups: Control, γ-tocotrienol alone, arthritis alone and arthritis with γ-tocotrienol. Arthritis was induced using 4 mg/kg body weight collagen in complete Freund's adjuvant. The rats were treated orally with 5 mg/kg body weight of γ-tocotrienol between day 21 and day 45. After 45 days, serum C-reactive protein (CRP), tumor necrosis factor (TNF)-α, superoxide dismutase (SOD) and total glutathione (GSH) assays were conducted. γ-tocotrienol significantly reduced the arthritis-induced changes in body weight, CRP, TNF-α, SOD and the total GSH levels. There was a significant reduction in the arthritis-induced histopathological changes in the γ-tocotrienol treatment group. The data indicated that administration of γ-tocotrienol resulted in a significant antioxidant and anti-inflammatory effect on collagen-induced arthritis; therefore, γ-tocotrienol may have therapeutic potential as a long-term anti-arthritic agent in rheumatoid arthritis therapy.
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http://dx.doi.org/10.3892/etm.2014.1592DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991526PMC
May 2014

Hypoxia-inducible factor-1α as a predictive marker in pre-eclampsia.

Biomed Rep 2013 Mar 30;1(2):257-258. Epub 2012 Nov 30.

Faculty of Medicine, Health and Molecular Sciences, James Cook University, Townsville 4811, Australia.

The aim of this study was to determine whether or not the increased levels of hypoxia-inducible factor-1α (HIF-1α) could be used to demonstrate failed placentation in pre-eclamptic mothers. Twenty pregnant females with (pre-eclampsia group) or without pre-eclampsia (control group) were included in the present study. Antenatal and post-delivery HIF-1α transcription factor levels were measured. A significant increase was observed in the HIF-1α levels in the pre- and post-natal pre-eclampsia mothers. The findings suggest that the levels of HIF-1α in the blood of mothers with pre-eclampsia decrease after delivery of the placenta. The results confirm that there is increased HIF-1α in pre-eclampsia and a steady increase in the levels of HIF-1α could be commensurate with the possibility of a patient developing pre-eclampsia at a later trimester.
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http://dx.doi.org/10.3892/br.2012.44DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956219PMC
March 2013

Protective effects of flavonol isoquercitrin, against 6-hydroxy dopamine (6-OHDA)-induced toxicity in PC12 cells.

BMC Res Notes 2014 Jan 21;7:49. Epub 2014 Jan 21.

Discipline of Physiology and Pharmacology, School of Veterinary and Biomedical Sciences, Faculty of Medicine, Health and Molecular Sciences, James Cook University, Townsville 4811, Australia.

Background: Free radicals-induced neurodegeneration is one of the many causes of Parkinson's disease (PD). This study investigated the neuroprotective effects of flavonol isoquercitrin against toxicity induced by 6-hydroxy-dopamine (6-OHDA) in rat pheochromocytoma (PC12) cells.

Methods: PC12 cells were pretreated with different concentrations of isoquercitrin for 4, 8 and 12 hours and incubated with 6-OHDA for 24 hours to induce oxidative cell damage.

Results: A significant cytoprotective activity was observed in isoquercitrin pre-treated cells in a dose-dependent manner. There was a significant increase (P < 0.01) in the antioxidant enzymes namely superoxide dismutase, catalase, glutathione peroxidase, and glutathione in isoquercitrin pretreated cells compared to cells incubated with 6-OHDA alone. Isoquercitrin significantly reduced (P < 0.01) lipid peroxidation in 6-OHDA treated cells. These results suggested that isoquercitrin protects PC 12 cells against 6-OHDA-induced oxidative stress.

Conclusions: The present study suggests the protective role of isoquercitrin on 6-hydroxydopamine-induced toxicity by virtue of its antioxidant potential. Isoquercitrin could be a potential therapeutic agent against neurodegeneration in Parkinson's disease.
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http://dx.doi.org/10.1186/1756-0500-7-49DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3910241PMC
January 2014

Rutin, a bioflavonoid antioxidant protects rat pheochromocytoma (PC-12) cells against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity.

Int J Mol Med 2013 Jul 10;32(1):235-40. Epub 2013 May 10.

Department of Pathology, Faculty of Medicine, International Medical University, Kuala Lumpur 57000, Malaysia.

Free radicals are widely known to be the major cause of human diseases such as neurodegenerative diseases, cancer, allergy and autoimmune diseases. Human cells are equipped with a powerful natural antioxidant enzyme network. However, antioxidants, particularly those originating from natural sources such as fruits and vegetables, are still considered essential. Rutin, a quercetin glycoside, has been proven to possess antioxidant potential. However, the neuroprotective effect of rutin in pheochromocytoma (PC-12) cells has not been studied extensively. Therefore, the present study was designed to establish the neuroprotective role of rutin as well as to elucidate the antioxidant mechanism of rutin in 6-hydroxydopamine (6-OHDA)-induced toxicity in PC-12 neuronal cells. PC-12 cells were pretreated with different concentrations of rutin for 4, 8 and 12 h and subsequently incubated with 6-OHDA for 24 h to induce oxidative stress. A significant cytoprotective activity was observed in rutin pretreated cells in a dose-dependent manner. Furthermore, there was marked activation of antioxidant enzymes including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and total glutathione (GSH) in rutin pretreated cells compared to cells incubated with 6-OHDA alone. Rutin significantly reduced lipid peroxidation in 6-OHDA-induced PC-12 cells. On the basis of these observations, it was concluded that the bioflavonoid rutin inhibited 6-OHDA-induced neurotoxicity in PC-12 cells by improving antioxidant enzyme levels and inhibiting lipid peroxidation.
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http://dx.doi.org/10.3892/ijmm.2013.1375DOI Listing
July 2013

Potential protective effect of sunitinib after administration of diclofenac: biochemical and histopathological drug-drug interaction assessment in a mouse model.

Naunyn Schmiedebergs Arch Pharmacol 2013 Jul 5;386(7):619-33. Epub 2013 Apr 5.

Department of Human Biology, School of Medicine, International Medical University, Jalan 19/155B, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.

Sunitinib is a tyrosine kinase inhibitor for GIST and advanced renal cell carcinoma. Diclofenac is used in cancer pain management. Coadministration may mediate P450 toxicity. We evaluate their interaction, assessing biomarkers ALT, AST, BUN, creatinine, and histopathological changes in the liver, kidney, heart, brain, and spleen. ICR mice (male, n = 6 per group/dose) were administered saline (group A) or 30 mg/kg diclofenac ip (group B), or sunitinib po at 25, 50, 80, 100, 140 mg/kg (group C) or combination of diclofenac (30 mg/kg, ip) and sunitinib (25, 50, 80, 100, 140 mg/kg po). Diclofenac was administered 15 min before sunitinib, mice were euthanized 4 h post-sunitinib dose, and biomarkers and tissue histopathology were assessed. AST was 92.2 ± 8.0 U/L in group A and 159.7 ± 14.6 U/L in group B (p < 0.05); in group C, it the range was 105.1-152.6 U/L, and in group D, it was 156.0-209.5 U/L (p < 0.05). ALT was 48.9 ± 1.6 U/L (group A), 95.1 ± 4.5 U/L (p < 0.05) in group B, and 50.5-77.5 U/L in group C and 82.3-115.6 U/L after coadministration (p < 0.05). Renal function biomarker BUN was 16.3 ± 0.6 mg/dl (group A) and increased to 29.9 ± 2.6 mg/dl in group B (p < 0.05) and it the range was 19.1-33.3 mg/dl (p < 0.05) and 26.9-40.8 mg/dl in groups C and D, respectively. Creatinine was 5.9 pmol/ml in group A; 6.2 pmol/ml in group B (p < 0.01), and the range was 6.0-6.2 and 6.2-6.4 pmol/ml in groups C and D, respectively (p < 0.05 for D). Histopathological assessment (vascular and inflammation damages) showed toxicity in group B (p < 0.05) and mild toxicity in group C. Damage was significantly lesser in group D than group B (p < 0.05). Spleen only showed toxicity after coadministration. These results suggest vascular and inflammation protective effects of sunitinib, not shown after biomarker analysis.
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http://dx.doi.org/10.1007/s00210-013-0861-4DOI Listing
July 2013

Amelioration of collagen-induced arthritis in female dark agouti rats by glucosamine treatment.

ISRN Pharmacol 2013 14;2013:562905. Epub 2013 Feb 14.

School of Veterinary and Biomedical Sciences, James Cook University, Townsville, QLD 4811, Australia.

The present study assessed the therapeutic efficacy of glucosamine hydrochloride against collagen-induced arthritis in female Dark Agouti rats (DA). Arthritis was induced by intradermaly injecting a collagen and complete Freund's adjuvant suspension at multiple sites in the rat at a dose of 4 mg/kg of body weight and thereafter followed by two more boosters of the same dose, after the 1st week and 2nd week of primary immunization. After 21 days from the day of primary immunization, the arthritic group rats were given oral supplementation of glucosamine hydrochloride at a dose of 300 mg/kg of body weight until day 45. The arthritic group treated with glucosamine hydrochloride from day 21 to day 45 showed significant reduction in arthritic histopathological changes of the joints, reduction in paw thickness and also a significant decrease in C-reactive protein and TNF-alpha in the serum. Treatment with 300 mg/kg of glucosamine hydrochloride was able to reverse the arthritic changes, hence suggesting that glucosamine has a therapeutic effect against collagen-induced arthritis.
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http://dx.doi.org/10.1155/2013/562905DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3586518PMC
March 2013

Morphological study of bone marrow to assess the effects of lead acetate on haemopoiesis and aplasia and the ameliorating role of Carica papaya extract.

Exp Ther Med 2013 Feb 5;5(2):648-652. Epub 2012 Dec 5.

Faculty of Medicine, University of Queensland, Brisbane, Australia ;

Lead causes damage to the body by inducing oxidative stress. The sites of damage include the bone marrow, where marrow hypoplasia and osteosclerosis may be observed. Leaves of Carica papaya, which have antioxidant and haemopoietic properties, were tested against the effect of lead acetate in experimental rats. The rats were divided into 8 groups; control, lead acetate only, Carica papaya (50 mg and 200 mg), post-treatment with Carica papaya (50 mg and 200 mg) following lead acetate administration and pre-treatment with Carica papaya (50 mg and 200 mg) followed by lead acetate administration. The substances were administered for 14 days. The effects were evaluated by measuring protein carbonyl content (PCC) and glutathione content (GC) in the bone marrow. Histological changes in the bone marrow were also observed. The results showed that Carica papaya induced a significant reduction in the PCC activity and significantly increased the GC in the bone marrow. Carica papaya also improved the histology of the bone marrow compared with that of the lead acetate-treated group. In summary, Carica papaya was effective against the oxidative damage caused by lead acetate in the bone marrow and had a stimulatory effect on haemopoiesis.
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http://dx.doi.org/10.3892/etm.2012.851DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570158PMC
February 2013

Effect of quercetin and desferrioxamine on 6-hydroxydopamine (6-OHDA) induced neurotoxicity in striatum of rats.

J Toxicol Sci 2013 Feb;38(1):25-33

School of Veterinary and Biomedical Sciences, James Cook University, Australia.

The catecholaminergic neurotoxin 6-hydroxydopamine is used to lesion dopaminergic pathways in the experimental animal models of Parkinson's disease. The present study was aimed to evaluate the combined treatment with bioflavonoid quercetin (QN) and desferrioxamine (DFO) on 6-hydroxydopamine (6-OHDA) - induced neurotoxicity in the striatum of rats. Adult, male Sprague - Dawley rats were divided into control, sham lesion, 6-OHDA treated (300 µg, intracisternal), 6-OHDA with QN (50 mg/kg) treated, 6-OHDA with DFO (50 mg/kg) treated and 6-OHDA with QN and DFO treated groups. Striatal dopamine, protein carbonyl content (PCC), glutathione (GSH) and superoxide dismutase (SOD) were estimated. There was a significant increase (p < 0.05) in PCC and decrease in dopamine, GSH and SOD level and striatal neuronal number with 6-OHDA treatment. QN and DFO treatment significantly (p < 0.05) reduced these changes showing a significant neuronal protection. Combined treatment has a more significant effect (p < 0.05) in protecting the neurons and increasing the antioxidant enzymes in the striatum. In conclusion, an antioxidant with iron chelator treatment showed a significant neuroprotective effect against 6-hydroxydopamine (6-OHDA) by preventing dopaminergic neuronal loss and maintaining the striatal dopamine level.
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http://dx.doi.org/10.2131/jts.38.25DOI Listing
February 2013

Colostrum supplementation protects against exercise-induced oxidative stress in skeletal muscle in mice.

BMC Res Notes 2012 Nov 22;5:649. Epub 2012 Nov 22.

Faculty of Sports Science & Recreation, University Technology Mara, Shah Alam 40450, Kuala Lumpur, Malaysia.

Background: This study examined the effects of bovine colostrum on exercise -induced modulation of antioxidant parameters in skeletal muscle in mice. Adult male BALB/c mice were randomly divided into four groups (control, colostrum alone, exercise and exercise with colostrum) and each group had three subgroups (day 0, 21 and 42). Colostrum groups of mice were given a daily oral supplement of 50 mg/kg body weight of bovine colostrum and the exercise group of mice were made to exercise on the treadmill for 30 minutes per day. Total antioxidants, lipid hydroperoxides, xanthine oxidase and super oxide dismutase level was assayed from the homogenate of hind limb skeletal muscle.

Results: Exercise-induced a significant oxidative stress in skeletal muscles as evidenced by the elevated lipid hydroperoxides and xanthine oxidase levels. There was a significant decrease in skeletal muscle total antioxidants and superoxide dismutase levels. Daily colostrum supplement significantly reduced the lipid hydroperoxides and xanthine oxidase enzyme level and increased the total antioxidant levels in the leg muscle.

Conclusion: Thus, the findings of this study showed that daily bovine colostrum supplementation was beneficial to skeletal muscle to reduce the oxidant-induced damage during muscular exercise.
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http://dx.doi.org/10.1186/1756-0500-5-649DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3571863PMC
November 2012

Effects of Etlingera elatior extracts on lead acetate-induced testicular damage: A morphological and biochemical study.

Exp Ther Med 2012 Jan 21;3(1):99-104. Epub 2011 Sep 21.

Department of Post Graduate Studies, Research Laboratory;

Lead causes damage to the whole body by inducing oxidative stress. This includes the testis, in which spermatogenesis is affected. Etlingera elatior, a consumable plant that is being extensively studied for its high anti-oxidant properties, was tested against the effect of lead acetate in experimental rats. Rats were divided into groups consisting of a control, lead acetate only, Etlingera elatior treatment only, concurrent treatment of lead acetate and Etlingera elatior, post-treatment of lead acetate followed by Etlingera elatior and preventive group of Etlingera elatior followed by lead acetate. The substances were administered for 14 days and the effects were measured by protein carbonyl content (PCC), superoxide dismutase (SOD) activity, glutathione peroxidase (GPx) activity in the testis, as well as the testosterone level in the serum. Histological changes in the testis were also observed. Results showed that Etlingera elatior induced a significant reduction in the testis PCC activity, while at the same time it significantly increased the activities of SOD and GPx in the testis, and the testosterone level in the serum. Etlingera elatior also improved the histology of the testis when compared to the lead acetate-treated group. On the whole, Etlingera elatior is effective against oxidative damage caused by lead acetate in the testis.
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http://dx.doi.org/10.3892/etm.2011.355DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438827PMC
January 2012

Insulin like growth factor-1 (IGF-1) causes overproduction of IL-8, an angiogenic cytokine and stimulates neovascularization in isoproterenol-induced myocardial infarction in rats.

Int J Mol Sci 2011 29;12(12):8562-74. Epub 2011 Nov 29.

Faculty of Medicine, Health and Molecular Sciences, James Cook University, Townsville 4811, Queensland, Australia.

Angiogenesis factors are produced in response to hypoxic or ischemic insult at the site of pathology, which will cause neovascularization. Insulin like growth factor-1 (IGF-1) exerts potent proliferative, angiogenic and anti-apoptotic effects in target tissues. The present study was aimed to evaluate the effects of IGF-1 on circulating level of angiogenic cytokine interleukin-8 (IL-8), in experimentally-induced myocardial ischemia in rats. Male Sprague-Dawley rats were divided into control, IGF-1 treated (2 μg/kg/day subcutaneously, for 5 and 10 days), isoproterenol (ISO) treated (85 mg/kg, subcutaneously for two days) and ISO with IGF-1 treated (for 5 and 10 days). Heart weight, serum IGF-1, IL-8 and cardiac marker enzymes (CK-MB and LDH) were recorded after 5 and 10 days of treatment. Histopathological analyses of the myocardium were also done. There was a significant increase in serum cardiac markers with ISO treatment indicating myocardial infarction in rats. IGF-1 level increased significantly in ISO treated groups and the level of IGF-1 was significantly higher after 10 days of treatment. IL-8 level increased significantly after ISO treatment after 5 and 10 days and IGF-1 concurrent treatment to ISO rats had significantly increased IL-8 levels. Histopathologically, myocyte necrosis and nuclear pyknosis were reduced significantly in IGF-1 treated group and there were numerous areas of capillary sprouting suggestive of neovascularization in the myocardium. Thus, IGF-1 protects the ischemic myocardium with increased production of circulating angiogenic cytokine, IL-8 and increased angiogenesis.
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http://dx.doi.org/10.3390/ijms12128562DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257088PMC
January 2015

Cardioprotective effects of glycyrrhizic acid against isoproterenol-induced myocardial ischemia in rats.

Int J Mol Sci 2011 21;12(10):7100-13. Epub 2011 Oct 21.

Human Biology Division, School of Medicine, International Medical University, Kuala Lumpur 57000, Malaysia.

The aim of the present study was to look into the possible protective effects of glycyrrhizic acid (GA) against isoproterenol-induced acute myocardial infarction in Sprague-Dawley rats. The effect of three doses of glycyrrhizic acid in response to isoproterenol (ISO)-induced changes in 8-isoprostane, lipid hydroperoxides, super oxide dismutase and total glutathione were evaluated. Male Sprague-Dawley rats were divided into control, ISO-control, glycyrrhizic acid alone (in three doses-5, 10 and 20 mg/kg BW) and ISO with glycyrrhizic acid (in three doses) groups. ISO was administered at 85 mg/kg BW at two consecutive days and glycyrrhizic acid was administered intraperitoneally for 14 days. There was a significant increase in 8-isoprostane (IP) and lipid hydroperoxide (LPO) level in ISO-control group. A significant decrease in total superoxide dismutase (SOD) and total glutathione (GSH) was seen with ISO-induced acute myocardial infarction. Treatment with GA significantly increased SOD and GSH levels and decreased myocardial LPO and IP levels. Histopathologically, severe myocardial necrosis and nuclear pyknosis and hypertrophy were seen in ISO-control group, which was significantly reduced with GA treatment. Gycyrrhizic acid treatment proved to be effective against isoproterenol-induced acute myocardial infarction in rats and GA acts as a powerful antioxidant and reduces the myocardial lipid hydroperoxide and 8-isoprostane level.
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http://dx.doi.org/10.3390/ijms12107100DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3211029PMC
November 2014
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