Publications by authors named "Aristatile Balakrishnan"

17 Publications

  • Page 1 of 1

Fruit Extract Induces Tp53/Caspase-Mediated Apoptosis in MCF-7 Breast Cancer Cells.

Biomed Res Int 2020 25;2020:3712536. Epub 2020 Jun 25.

Adipocytes and Metabolic Disorders Lab, Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, P.O. Box 2460, Riyadh 11451, Saudi Arabia.

The second most biggest cancer worldwide is breast cancer. There is an increasing need for safer, effective, and affordable drug candidates from natural sources to treat breast cancer. In the present investigation, the anticancer effect of Bouché (. ) fruit extract was tested on the human breast cancer cells such as MCF-7. The cells were exposed with different doses of . , for the assessment of IC concentrations on the MCF-7 cell lines for 24 hs. The effect of . fruit extract on morphological and apoptotic changes were evaluated by specific fluorescence staining techniques and real-time PCR in a time-dependent manner for 24 hs and 48 hs. The IC value for . fruit extract was found to be 90 g/mL. Morphological alteration and apoptotic distinctiveness aspect like chromatin condensation and nuclear fragmentation were noticed in extract exposed breast cancer cells. Further, we observed that . extract-induced programmed cell death in the MCF-7 cells were mediated with the elevated expression of the tumor suppressor gene such as p53 and apoptotic markers such as caspase-8, caspase-9, caspase-3, fatty acid synthase (FAS), Fas-associated protein with death domain (FADD), Bcl-2 homologous antagonist/killer (BAK), and Bcl-2-associated X protein (BAX). These observations established that . significantly concealed the cell division and provoked p53/caspase-mediated programmed cell death. Further, we noticed that this cell death in MCF-7 cells is concentration and time dependent. As evaluated through the comet assay, . induced DNA damage; further upon increasing the duration of the treatment, the DNA damage was higher than before. Thus, our study concludes that . could serve as an effective anticancer agent through vital gene modulation.
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http://dx.doi.org/10.1155/2020/3712536DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335397PMC
April 2021

Pumpkin () extract attenuate the adipogenesis in human mesenchymal stem cells by controlling adipogenic gene expression.

Saudi J Biol Sci 2019 May 2;26(4):744-751. Epub 2018 Oct 2.

Adipocytes and Metabolic Disorders Lab, Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, P.O. Box 2460, Riyadh 11451, Saudi Arabia.

Prevention and management of obesity through dietary modification is one of the top way to trim down its consequences. Development of adipose tissue requires the differentiation of less specialized cells, such as human mesenchymal stem cells (hMSCs), into adipocytes. Since food constituents play a major role in the cell differentiation and proliferation, we sought to determine if various extracts of (), could affect the adipogenic differentiation of hMSCs. Flow cytometry analysis with quantitative and qualitative Nile red, and quantitative PCR methods were employed to evaluate the effect on hMSCs adipogenesis. Results revealed that, chloroform extract exhibits significant adipogenic inhibition than that of hexane and methanol extracts. Chloroform extract treated cells display the down-regulation of ADIPOQ, FABP4, PPARGC1A, CEBPB & LPL and up-regulation of ACACB & CEBPA genes. Further, various phytoconstituents present in the chloroform extract of were analyzed though LC-MS and GC-MS Our results indicates that chloroform extract of might be used as a food supplement to control obesity and its related consequences.
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http://dx.doi.org/10.1016/j.sjbs.2018.10.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6486525PMC
May 2019

Butein protects the nonalcoholic fatty liver through mitochondrial reactive oxygen species attenuation in rats.

Biofactors 2018 May 19;44(3):289-298. Epub 2018 Apr 19.

Adipocytes and Metabolic Disorders Lab, Food Science and Nutrition Department, King Saud University, Riyadh, 11451, Saudi Arabia.

One of the worldwide metabolic health dilemma is nonalcoholic fatty liver diseases (NAFLD). Researchers are searching effective drug to manage NAFLD patients. One of the best way to manage the metabolic imperfection is through natural principal isolated from different sources. Butein, a natural compound known to have numerous pharmacological application. In the current study we assessed the therapeutic effect of butein administration on liver function tests, oxidative stress, antioxidants, lipid abnormalities, serum inflammatory cytokines, and mitochondrial reactive oxygen species levels, in rats with methionine-choline deficient (MCD) diet induced NAFLD. Male Wistar rats were treated with MCD diet with/without butein (200 mg/kg body wt. orally) for 6 weeks. The protective effect of butein, were evident from decreased transaminase activities, restoration of albumin, globulin, albumin/globulin ratio, and oxidants in serum (P < 0.01), further it improved liver antioxidant status (P < 0.01). Butein significantly lowered lipid profile parameters (P < 0.01), suppressed inflammatory cytokines (P < 0.01), and improved liver histology. Further to understand the possible mechanism behind the hepatoprotective and lipid lowering effect of butein, the activities of heme oxygenase (HO1), myeloperoxidase (MPO), and mitochondrial reactive oxygen species (ROS) were measured. We found that butein supplementation significantly decreased the activity of HO1 (P < 0.001), and increased the activity of MPO (P < 0.001). Furthermore butein attenuated mitochondrial ROS produced in NAFLD condition. Present study shows that butein supplementation restore liver function by altering liver oxidative stress, inflammatory markers, vital defensive enzyme activities, and mitochondrial ROS. In summary, butein has remarkable potential to develop effective hepato-protective drug. © 2018 BioFactors, 44(3):289-298, 2018.
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http://dx.doi.org/10.1002/biof.1428DOI Listing
May 2018

Unveiling anticancer potential of glibenclamide: Its synergistic cytotoxicity with doxorubicin on cancer cells.

J Pharm Biomed Anal 2018 May 14;154:294-301. Epub 2018 Mar 14.

Department of Biochemistry and Molecular Biology, Pondicherry University, Puducherry 605 014, India. Electronic address:

Drug repurposing has been an emerging therapeutic strategy, which involves exploration of a new therapeutic approach for the use of an existing drug. Glibenclamide (Gli) is an anti-diabetic sulfonylurea drug extensively used for the treatment of type-2 diabetes, it has also been shown to possess anti-proliferative effect against several types of tumors. The present study was executed to understand the mechanisms underlying the interaction of Gli with DNA under physiological conditions. The binding mechanism of Gli with DNA was scrutinized by UV-vis absorption spectroscopy and fluorescence emission spectroscopy. The conformational changes and electrochemical properties were analyzed by circular dichroism spectroscopy and cyclic voltammetry. Isothermal titration calorimetry was employed to examine the thermodynamic changes and molecular docking technique used to analyze the interaction mode of Gli with DNA. The spectroscopic studies revealed that Gli interacts with DNA through groove binding mode. Further, isothermal titration calorimetry depicted a stronger mode of interaction favorably groove-binding. Recently, systemic combination therapy has shown significant promise in inhibiting multiple targets simultaneously yielding high therapeutic competence with lesser side effects. With this concern, we intended to study the combined cytotoxicity of Gli with doxorubicin (Dox). The results of MTT assay and acridine orange (AO)/ethidium bromide (EtBr) staining showed synergistic cytotoxicity of Gli + Dox combination on HepG2 & A549 cells. The present study documents the intricate mechanism of Gli-DNA interaction and delivers a multifaceted access for chemotherapy by Gli + Dox combination.
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http://dx.doi.org/10.1016/j.jpba.2018.03.025DOI Listing
May 2018

Synthesis and characterisation of arsenic nanoparticles and its interaction with DNA and cytotoxic potential on breast cancer cells.

Chem Biol Interact 2018 Nov 22;295:73-83. Epub 2017 Dec 22.

Department of Biochemistry and Molecular Biology, Pondicherry University, Puducherry 605 014, India. Electronic address:

Therapeutic applications of arsenic trioxide (ATO) are limited due to their severe adverse effects. However, nanoparticles of ATO might possess inimitable biologic effects based on their structure and size which differ from their parent molecules. Based on this conception, AsNPs were synthesized from ATO and comparatively analysed for their interaction mechanism with DNA using spectroscopic & electrochemical techniques. Finally, anti-proliferative activity was assessed against different breast cancer cells (MDA-MB-231 & MCF-7) and normal non-cancerous cells (HEK-293). The DNA interaction study revealed that AsNPs and ATO exhibit binding constant values in the order of 10 which indicates strong binding interaction. Binding of AsNPs did not disturb the structural integrity of DNA, on the other hand an opposing effect was observed with ATO through biophysical techniques. Further, in vitro study, confirms cytotoxicity of ATO and AsNPs against different cells, however at particular concentration ATO exhibits more cytotoxicity than that of AsNPs. Furthermore, cytotoxicity was confirmed through acridine orange and comet assay. In conclusion, AsNPs are safer than ATO with comparable efficacy and might be a suitable candidate for the development of novel therapeutic agent against breast cancer and other solid tumours.
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http://dx.doi.org/10.1016/j.cbi.2017.12.025DOI Listing
November 2018

Nimbolide attenuate the lipid accumulation, oxidative stress and antioxidant in primary hepatocytes.

Mol Biol Rep 2017 Dec 28;44(6):463-474. Epub 2017 Nov 28.

Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, P.O. Box 2460, Riyadh, 11451, Saudi Arabia.

Nimbolide is a bioactive compound found in Azadirachta indica. This work was devised to investigate the potential effects of nimbolide on intracellular lipid deposition and its associated redox modulation in primary hepatocytes (Heps). Lipid accumulation was induced in Heps by supplementing 1 mM oleic acid for 24 h which was marked by significant accumulation of lipids. The results demonstrated that nimbolide can decrease intracellular cholesterol, free fatty acids and triglycerides. Nimbolide may also improve hepatocytes function through its antioxidant effects by inhibiting oxidative DNA damage and lipid peroxidation by curtailing the reactive oxygen species levels. Further it also restore the mitochondrial potential, improving the endogenous antioxidant levels such as GSH and antioxidant enzyme activities. Nimbolide increased (P < 0.05) liver X receptor-α (LXRα), peroxisome proliferator-activated receptor-γ (PPARγ) and sterol regulatory element-binding protein-1c (SREBP1c) gene expression in Heps. The biological significance of nimbolide may involve hypolipidemic effect, lipid peroxidation inhibition, DNA damage inhibition, ROS inhibition, restoring mitochondrial function, increases in GSH and SOD & CAT activities, and direct regulation of LXRα, PPARγ and SREBP1c gene expression. Nimbolide may be used as effective lipid lowering compound and lipid deposition-induced Heps changes.
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http://dx.doi.org/10.1007/s11033-017-4132-1DOI Listing
December 2017

2-Hydroxy-4-methoxy benzoic acid attenuates the carbon tetra chloride-induced hepatotoxicity and its lipid abnormalities in rats via anti-inflammatory and antioxidant mechanism.

Inflamm Res 2017 Sep 30;66(9):753-763. Epub 2017 May 30.

Adipocytes and Metabolic Disorders Lab, Food Science and Nutrition Department, King Saud University, Riyadh, Saudi Arabia.

Background And Aim: Liver inflammation stimulates various inflammatory cytokines and initiates injury through oxidative stress. The aim of this study was to curtaile the liver injury through natural principles such as 2-hydroxy-4-methoxy benzoic acid (HMBA).

Methods: The current study examines the hepatoprotective and lipid lowering effect of HMBA against carbon tetra chloride (CCl)-mediated liver toxicity in male Wistar rats.

Results: The hepatoprotective effects of HMBA against CCl-induced liver damage, were evident from low serum transaminases activities, reduced hepatic lipid peroxidation and collagen content, restoration of total glutathione, and recouping of the inflammatory cytokines, such as TNF-α, IL-1β, IL-10, and IL-6 levels. Further it was found that the treatment of HMBA, significantly lowered (P<0.01) the levels of total cholesterol, triglycerides, free fatty acids and phospholipids in serum and liver. To investigate the mechanism behind the hepatoprotective and lipid lowering effect, the activities of heme oxygenase (HO1), and myeloperoxidase (MPO) were measured and expression levels were quantified through western blot following HMBA administration. The results showed that HMBA administration significantly decreased the activity of HO1 (P<0.001), and increased the activity of MPO (P<0.001); further similar finding was observed in western analysis. The hepatoprotective, lipid lowering and shifting key defensive enzyme activities are similar to that of standard drug such as N-acetylcysteine.

Conclusion: HMBA is competent of shielding liver from CCl-induced hepatotoxicity, and this is associated with the lipid lowering, inflammatory cytokine restoration and induction of defensive enzyme activities.
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http://dx.doi.org/10.1007/s00011-017-1054-2DOI Listing
September 2017

In vitro biocompatibility and proliferative effects of polar and non-polar extracts of cucurbita ficifolia on human mesenchymal stem cells.

Biomed Pharmacother 2017 May 20;89:215-220. Epub 2017 Feb 20.

Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, P.O. Box 2460, Riyadh 11451, Saudi Arabia. Electronic address:

Cucurbita ficifolia (C. ficifolia) has been traditionally known for its medicinal properties as an antioxidant, anti-diabetic and anti-inflammatory agent. However, there has been an enduring attention towards the identification of unique method, to isolate the natural components for therapeutic applications. Our study focuses on different polar and non-polar solvents (methanol, hexane and chloroform) to extract the bioactive components from C. ficifolia (pumpkin) and to study the biocompatibility and cytotoxicity effects on human bone marrow-mesenchymal stem cells (hBM-MSCs). The extracts were screened for their effects on cytotoxicity, cell proliferation and cell cycle on the hBM-MSCs cell line. The assays demonstrated that the chloroform extract was highly biocompatible, with less cytotoxic effect, and enhanced the cell proliferation. The methanol extract did not exhibit significant cytotoxicity when compare to the control. Concordantly, the cell cycle analysis confirmed that chloroform extract enhances the proliferation at lower concentrations. On the other hand, hexane extract showed high level of cytotoxicity with apoptotic and necrotic changes in hBM-MSCs. Collectively, our data revealed that chloroform is a good candidate to extract the bioactive components from C. ficifolia. Furthermore, our results suggest that specific gravity and density of the solvent might play a crucial role in the extraction process, which warrants further investigations.
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http://dx.doi.org/10.1016/j.biopha.2017.02.023DOI Listing
May 2017

Corosolic acid suppresses the expression of inflammatory marker genes in CCL4-induced-hepatotoxic rats.

Pak J Pharm Sci 2016 Jul;29(4):1133-8

Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, Riyadh, Saudi Arabia.

The aim of the study was to asses the anti-inflammatory effects of corosolic acid on the carbon tetrachloride (CCL4) toxicity in rats. Liver toxicity was induced by administered CCL4 (single dose (1:1 in liquid paraffin) orally at 1.25 ml/kg. Rats were pretreated with CRA for 7 days before made CCL(4) toxicity at 20 mg/kg BW. The mRNA levels of TNF-α, IL-6, iNOS, COX-2 and NF-kB were assayed by reverse transcriptase PCR analysis. The mRNA levels of proinflammatory cytokines such as TNF-α, IL-6, and the inflammatory markers such as iNOS, COX-2 and NF-kB were significantly up regulated in CCl(4) induced rats and treatment with corosolic acid significantly reduced the expression of the above indicators. Our results suggest that the inhibition of TNF-α, IL-6, iNOS, COX-2 and NF-κB by corosolic acid, a potential candidate could possess anti-inflammatory activity besides its hepatoprotective effect in CCl4 liver toxicity in rats.
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July 2016

Protective Effect of Carvacrol on Oxidative Stress and Cellular DNA Damage Induced by UVB Irradiation in Human Peripheral Lymphocytes.

J Biochem Mol Toxicol 2015 Nov 21;29(11):497-507. Epub 2010 May 21.

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, 608 002, India.

Exposure to ultraviolet B (UVB; 280-320 nm) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of carvacrol on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular an-tioxidant status in human lymphocytes. A series of in vitro assays (hydroxyl radical, superoxide, nitric oxide, DPPH (2,2-Diphenyl-1-picryl hydrazyl), and ABTS (2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assays) demonstrate antioxidant property of carvacrol in our study. UVB exposure significantly increased thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHPs), % tail DNA and tail moment; decreased % cell viability and antioxidant status in UVB-irradiated lymphocytes. Treatment with carvacrol 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA, and tail moment and increased % cell viability as carvacrol concentration increased. UVB irradiated lymphocytes with carvacrol alone (at 10 μg/mL) gave no significant change in cell viability, TBARS, LHP, % tail DNA, and tail moment when compared with normal lymphocytes. On the basis of our results, we conclude that carvacrol, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced ROS.
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http://dx.doi.org/10.1002/jbt.20355DOI Listing
November 2015

Docking studies on the interaction of flavonoids with fat mass and obesity associated protein.

Pak J Pharm Sci 2015 Sep;28(5):1647-53

Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.

Obesity is the excessive fat accumulation in human body leading to increases a risk of various chronic diseases such as diabetes, cardiovascular diseases, cancer and osteoarthritis. Several flavonoids are known to have lipolytic activity influencing lipolysis and adipogenesis in adipose cells. To explore mechanism of the association of flavonoids in obesity and obesity associated protein (FTO), molecular docking studies were done for FTO with flavonoids, with orlistat (antiobesity drug) as a control. Autodock tools were used for docking flavonoids and orlistat with FTO. The results were visualized by PyMol and Discovery studio visualizer. Upon docking simulation, it was observed that flavonoid quercetin showed highest binding affinity (most negative δG), whereas daidzein was least affinity towards FTO. The binding affinity of other flavonoids was in the order of Exemestane >Kaempherol >Letrozole >Rutin. This study concludes that flavonoids primarily, quercetin ameliorates obesity by establishing a physical interaction with FTO. Interactions were also observed between FTO and other flavonoids and were of not greater inhibition compared to quercetin.
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September 2015

Carvacrol ameliorates the PPAR-A and cytochrome P450 expression on D-galactosamine induced hepatotoxicity rats.

Afr J Tradit Complement Altern Med 2014 3;11(3):118-23. Epub 2014 Apr 3.

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar - 608 002, Tamilnadu, India.

Background: Carvacrol (2-methyl-5-(1-methylethyl)-phenol) is a predominant monoterpenic phenol which occurs in many essential oils of the family Labiatae including Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. It is well known for its anti-inflammatory, antioxidant and antitumor activities. The present study investigates the influence of carvacrol on CYP2E1 and PPAR-α on D-Galactosamine (D-GalN)-induced hepatotoxic rats.

Materials And Methods: The mRNA and protein expression levels of CYP2E1 and PPAR-α have been assayed by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot analysis.

Result: The result demonstrated that the mRNA and protein expressions of CYP2E1(p=0.012; p=0.015) significantly up-regulated while the mRNA and protein expressions of PPAR-α (p=0.026; p=0.03) significantly down-regulated on D-galactosamine induced hepatotoxic rats and treatment with carvacrol significantly suppressed the mRNA and protein (CYP2E1, p=0.010; p=0.011) (PPAR-α, p=0.033; p=0.037) expressions of these genes.

Conclusion: Thus, the present results have shown that carvacrol has the hepatoprotective effect and also alleviates liver damage associated with GalN induced hepatotoxic rats by down-regulating the CYP2E1 and up-regulating the PPAR-α expression.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202429PMC
http://dx.doi.org/10.4314/ajtcam.v11i3.18DOI Listing
July 2015

Carvacrol suppresses the expression of inflammatory marker genes in D-galactosamine-hepatotoxic rats.

Asian Pac J Trop Med 2013 Mar;6(3):205-11

Research and Development Centre Bharathiar University, Coimbatore - 641046, Tamilnadu, India.

Objective: To unravel the mechanism of anti-inflammatory activity of carvacrol in D-galactosamine (D-GalN)-induced hepatotoxic rats.

Methods: The mRNA and protein expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor kappa-B (NF-κB) were assayed by semi-quantitative reverse transcriptase polymerase chain reaction (RTPCR) and western blot analysis.

Results: We found that the mRNA and protein expressions of TNF-α, IL-6, iNOS, COX-2 and NF-κB were significantly up-regulated in D-galactosamine induced hepatotoxic rats and treatment with carvacrol significantly down-regulated the expressions of these genes showing the mechanism behind the anti-inflammatory activity of carvacrol.

Conclusions: All above results reveal that the carvacrol well known anti-inflammatory activities in D-galactosamine induced hepatotoxic rats.
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http://dx.doi.org/10.1016/S1995-7645(13)60024-3DOI Listing
March 2013

Pharmacological effect of carvacrol on D: -galactosamine-induced mitochondrial enzymes and DNA damage by single-cell gel electrophoresis.

J Nat Med 2011 Jul 21;65(3-4):568-77. Epub 2011 May 21.

Department of Food Science and Nutrition, King Saud University, Riyadh, Saudi Arabia.

The present study aimed at investigating the effect of carvacrol on hepatic mitochondrial enzyme activities and DNA damage in D: -galactosamine (D: -GalN)-induced hepatotoxicity in male albino Wistar rats. The activities of hepatic mitochondrial enzymes such as isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADPH dehydrogenase and cytochrome c oxidase significantly decreased in D: -GalN-hepatotoxic rats, and administration of carvacrol brought these parameters towards normality. In D: -GalN-hepatotoxic rats, the hepatic mitochondrial concentration of thiobarbituric acid reactive substances significantly increased, and administration of carvacrol significantly reduced them towards normality. Furthermore, the activities of enzymatic antioxidants such as superoxide dismutase and glutathione peroxidase and the levels of non-enzymatic antioxidants such as vitamin C, vitamin E and reduced glutathione decreased significantly in the liver mitochondria. Administration of carvacrol returned the enzymatic and non-enzymatic antioxidants towards normality. D: -GalN-hepatotoxic rats had increased DNA damage, which administration of carvacrol significantly decreased. These results suggest that carvacrol has liver mitochondrial antioxidant properties and possesses a defensive effect against mitochondrial enzymes and DNA damage in D: -GalN-induced rats.
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http://dx.doi.org/10.1007/s11418-011-0544-8DOI Listing
July 2011

Effects of Melothria maderaspatana leaf extract on antioxidant status in sham-operated and uninephrectomized DOCA-salt hypertensive rats.

Saudi J Biol Sci 2011 Jan 31;18(1):99-105. Epub 2010 May 31.

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608 002, Tamilnadu, India.

The present study was designed to investigate the antihypertensive and antioxidant effect of Melothria maderaspatana leaf extract (MME) on sham-operated and DOCA-salt (deoxycorticosterone acetate) induced hypertensive rats. Administration of DOCA-salt significantly increased the systolic (from 127 to 212 mm Hg) and diastolic (from 91 to 174 mm Hg) blood pressure compared to sham-operated control rats, while treatment with MME significantly reduced the systolic (from 212 to 135 mm Hg) and diastolic (from 174 to 96 mm Hg) blood pressure compared to hypertensive control. In DOCA-salt rats, the plasma and tissue concentration of thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxide (LOOH) significantly increased and administration of MME significantly reduced these parameters towards the levels in sham-operated control. In hypertensive rats, activities of the enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and levels of non-enzymatic antioxidants such as vitamin C, vitamin E and reduced glutathione (GSH) decreased significantly in the plasma and tissues. Administration of MME returned the enzymatic and non-enzymatic antioxidants towards sham-operated control. MME shows both antihypertensive and antioxidant properties in DOCA-salt hypertensive rats and, among the three different doses tested, 200 mg/kg caused the maximum effect.
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http://dx.doi.org/10.1016/j.sjbs.2010.05.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3730574PMC
January 2011

Effect of carvacrol on hepatic marker enzymes and antioxidant status in D-galactosamine-induced hepatotoxicity in rats.

Fundam Clin Pharmacol 2009 Dec 24;23(6):757-65. Epub 2009 Jul 24.

Department of Food Science and Nutrition, College of Food and Agricultural Science, King Saud University, Riyadh, Saudi Arabia.

Carvacrol (2-methyl-5-(1-methylethyl)-phenol) is a predominant monoterpenic phenol which occurs in many essential oils of the family Labiatae including Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. This study was designed to investigate the hepatoprotective and antioxidant properties of carvacrol on D-galactosamine (D-GalN)-induced hepatotoxicity and oxidative damage in male albino Wistar rats. D-GalN hepatotoxic rats exhibited elevation in the activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and lipidperoxidative markers such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides. Activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and the levels of non-enzymatic antioxidants (vitamin C, vitamin E, and reduced glutathione) in the plasma, erythrocytes, liver, and kidney decreased in the hepatotoxic rats. Oral administration of carvacrol for 21 days brought these parameters towards normal. The biochemical observations were supported by histological studies of rat liver and kidney tissues. These results suggest that carvacrol could afford a significant hepatoprotective and antioxidant effect against D-GalN-induced rats.
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http://dx.doi.org/10.1111/j.1472-8206.2009.00721.xDOI Listing
December 2009

Antihyperlipidemic effect of carvacrol on D-galactosamine-induced hepatotoxic rats.

J Basic Clin Physiol Pharmacol 2009 ;20(1):15-27

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar-608 002, Tamilnadu, India.

Carvacrol (2-methyl-5-(1-methylethyl)-phenol) is a predominant monoterpenic phenol occuring in many essential oils of the family Labiatae including, Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. The present study was designed to investigate the effect of carvacrol on D-galactosamine (D-GalN)-induced hepatotoxicity in rats. D-GalN-hepatotoxic rats exhibited elevation in the serum bilirubin level and the activities of the hepatic marker enzymes aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase. In the plasma, increased levels of very low density lipoprotein cholesterol and low density lipoprotein cholesterol and decreased high density lipoprotein cholesterol were observed. Further, an increase in the levels of total cholesterol, phospholipids, triglycerides, and free fatty acids in the plasma and tissues of liver and kidney were observed in hepatotoxic rats. The administration of carvacrol for 21 days prevented and improved these parameters toward normalcy. The results suggest that carvacrol affords a significant hepatoprotective and hypolipidemic effect against D-GalN-induced-rats.
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http://dx.doi.org/10.1515/jbcpp.2009.20.1.15DOI Listing
July 2009
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