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  1. Fulltext Hepatoprotective activity of methanol extract of Melastoma malabathricum leaf in rats
    Kamisan FH, Yahya F, Ismail NA, Din SS, Mamat SS, Zabidi Z, et al.
    J Acupunct Meridian Stud, 2013 Feb;6(1):52-5.
    PMID: 23433055 DOI: 10.1016/j.jams.2012.08.002
    The present study aimed to determine the hepatoprotective activity of a methanol extract of Melastoma malabathricum leaves (MEMM) using two established rat models. Ten groups of rats (n=6) were given a once-daily administration of 10% dimethyl sulfoxide (negative control), 200 mg/kg silymarin (positive control), or MEMM (50, 250, or 500 mg/kg) for 7 days followed by induction of hepatotoxicity either using paracetamol or carbon tetrachloride. Blood samples and livers were collected for biochemical and microscopic analysis. Based on the results obtained, MEMM exhibited a significant (p<0.05) hepatoprotective activity against both inducers, as indicated by an improvement in the liver function test. These observations were supported by the histologic findings. In conclusion, M. malabathricum leaves possessed hepatoprotective activity, which could be linked to their phytochemical constituents and antioxidant activity; this therefore requires further in-depth studies.
    Matched MeSH terms: Protective Agents/administration & dosage*
  2. Fulltext Cytoprotective Role of Omentin Against Oxidative Stress-Induced Vascular Endothelial Cells Injury
    Binti Kamaruddin NA, Fong LY, Tan JJ, Abdullah MNH, Singh Cheema M, Bin Yakop F, et al.
    Molecules, 2020 May 29;25(11).
    PMID: 32485974 DOI: 10.3390/molecules25112534
    Endothelial cell injury caused by reactive oxygen species (ROS) plays a critical role in the pathogenesis of cardiovascular diseases. Omentin, an adipocytokine that is abundantly expressed in visceral fat tissue, has been reported to possess anti-inflammatory and antidiabetic properties. However, endothelial protective effects of omentin against oxidative stress remain unclear. This study aimed to evaluate the protective effect of omentin against hydrogen peroxide (H2O2)-induced cell injury in human umbilical vein endothelial cells (HUVECs). Cytotoxicity and cytoprotective effects of omentin were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptotic activity of HUVECs was detected using Annexin-V/PI and Hoechst 33258 staining methods. Antioxidant activity of omentin was evaluated by measuring both reactive oxygen species (ROS) levels and glutathione peroxidase (GPx) activity. No cytotoxicity effect was observed in HUVECs treated with omentin alone at concentrations of 150 to 450 ng/ml. MTT assay showed that omentin significantly prevented the cell death induced by H2O2 (p < 0.001). Hoechst staining and flow cytometry also revealed that omentin markedly prevented H2O2-induced apoptosis. Moreover, omentin not only significantly inhibited ROS production (p < 0.01) but also significantly (p < 0.01) increased GPx activity in HUVECs. In conclusion, our data suggest that omentin may protect HUVECs from injury induced by H2O2.
    Matched MeSH terms: Protective Agents/pharmacology
  3. Protective effect of apple mangrove Sonneratia caseolaris extract in Edwardsiella tarda-infected African catfish, Clarias gariepinus
    Aznan AS, Lee KL, Low CF, Iberahim NA, Wan Ibrahim WN, Musa N, et al.
    Fish Shellfish Immunol, 2018 Jul;78:338-345.
    PMID: 29684603 DOI: 10.1016/j.fsi.2018.04.033
    Outbreaks of edwardsiellosis have severe impact on the aquaculture production of African catfish Clarias gariepinus. In this study, feed supplemented with apple mangrove Sonneratia caseolaris extract was evaluated for its protective effect against Edwardsiella tarda infection in African catfish. Results showed an increase in growth performance and higher survival rate in the treatment groups in a dose dependent manner. Haematological analyses showed an increase in white blood cell count in the treatment groups. Histopathological analysis revealed degenerative changes and regeneration of liver tissue architecture in both the control and treatment groups. However, the presence of inflammatory cells was found exclusively in the kidney of T3 treatment group that was supplemented with the highest dose of extract at 3.17 mg/ml, which inferred the activation of immune response in the fish. Contrast to the deteriorative alteration observed in the kidney of the control group due to E. tarda infection, treatment group exhibited tissue regeneration and well-defined kidney tissue architecture at 3 dpi. Taken together, these results demonstrated that supplementation with the methanol extract of S. caseolaris possesses protective effect in African catfish against the infection of E. tarda.
    Matched MeSH terms: Protective Agents/pharmacology*
  4. Fulltext Molecular Characterization and Gene Expression of Glutathione Peroxidase 1 in Tor tambroides Exposed to Temperature Stress
    Do TD, Thi Mai N, Duy Khoa TN, Abol-Munafi AB, Liew HJ, Kim CB, et al.
    Evol Bioinform Online, 2019;15:1176934319853580.
    PMID: 31236006 DOI: 10.1177/1176934319853580
    Temperature is an abiotic factor that affects various biological and physiological processes in fish. Temperature stress is known to increase the production of reactive oxygen species (ROS) that subsequently cause oxidative stress. Fish is known to evolve a system of antioxidant enzymes to reduce ROS toxicology. Glutathione peroxidase (GPx) family consists of key enzymes that protect fish from oxidative stress. In this study, full-length GPx1 cDNA (GenBank accession no. KY984468) of Tor tambroides was cloned and characterized by rapid amplification of cDNA ends (RACE). The 899-base-pair (bp) GPx1 cDNA includes a 576-bp open reading frame encoding for 191 amino acids, plus 28 bp of 5'-untranslated region (UTR) and 295 bp of 3'-UTR. Homology analysis revealed that GPx1 of T tambroides (Tor-GPx1) shared high similarity with GPx1 sequences of other fish species. The phylogenetic construction based on the amino acid sequence showed that Tor-GPx1 formed a clade with GPx1 sequences of various fish species. Real-time polymerase chain reaction (PCR) was performed to assess the levels of GPx1 gene expression in the liver and muscle of T tambroides under thermal stress. The results indicated that GPx1 gene expression was down-regulated under decreased temperature. However, there was no significant difference between GPx1 gene expression in fish exposed to high temperature and control. Our study provides the first data regarding GPx gene expression in T tambroides under thermal stress.
    Matched MeSH terms: Protective Agents
  5. Protective potential of cerium oxide nanoparticles in diabetes mellitus
    Chai WF, Tang KS
    J Trace Elem Med Biol, 2021 Jul;66:126742.
    PMID: 33773280 DOI: 10.1016/j.jtemb.2021.126742
    BACKGROUND: Diabetes mellitus (DM) is a non-communicable metabolic disease which is closely related to excessive oxidative stress after constant exposure to high plasma glucose. Although the current antidiabetic medications are effective in lowering blood glucose, these medications do not prevent or reverse the disease progression. Thus, there is a crucial need to explore new therapeutic interventions that could address this shortcoming. As cerium oxide nanoparticles (CONPs) possess antioxidant property, this agent may be used as a treatment option for the management of DM.

    PURPOSE: This review aims to provide a critical evaluation of the pharmacological and antidiabetic effects of CONPs in cell and animal models. The roles of CONPs in attenuating DM complications are also presented in this report.

    METHODS: We conducted a literature search in the PubMed database using the keywords "cerium oxide", "cerous oxide", "ceria", "nanoceria", and "diabetes" from inception to December 2020. The inclusion criteria were primary source articles that investigated the role of CONPs in DM and diabetic complications.

    RESULTS: We identified 47 articles from the initial search. After the thorough screening, only 31 articles were included in this study. We found that CONPs can attenuate parameters that are related to DM and diabetic complications in various animals and cell culture models.

    CONCLUSION: CONPs could potentially be used in the treatment of those with DM and complications caused by the disease.

    Matched MeSH terms: Protective Agents/pharmacology*; Protective Agents/chemistry
  6. Glycyrrhizic acid (GCA) as 11β-hydroxysteroid dehydrogenase inhibitor exerts protective effect against glucocorticoid-induced osteoporosis
    Ramli ES, Suhaimi F, Asri SF, Ahmad F, Soelaiman IN
    J. Bone Miner. Metab., 2013 May;31(3):262-73.
    PMID: 23274351 DOI: 10.1007/s00774-012-0413-x
    Rapid onset of bone loss is a frequent complication of systemic glucocorticoid therapy which may lead to fragility fractures. Glucocorticoid action in bone depends upon the activity of 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). Regulations of 11β-HSD1 activity may protect the bone against bone loss due to excess glucocorticoids. Glycyrrhizic acid (GCA) is a potent inhibitor of 11β-HSD. Treatment with GCA led to significant reduction in bone resorption markers. In this study we determined the effect of GCA on 11β-HSD1 activity in bones of glucocorticoid-induced osteoporotic rats. Thirty-six male Sprague-Dawley rats (aged 3 months and weighing 250-300 g) were divided randomly into groups of ten. (1) G1, sham operated group; (2) G2, adrenalectomized rats administered with intramuscular dexamethasone 120 μg/kg/day and oral vehicle normal saline vehicle; and (3) G3, adrenalectomized rats administered with intramuscular dexamethasone 120 μg/kg/day and oral GCA 120 mg/kg/day The results showed that GCA reduced plasma corticosterone concentration. GCA also reduced serum concentration of the bone resorption marker, pyridinoline and induced 11β-HSD1 dehydrogenase activity in the bone. GCA improved bone structure, which contributed to stronger bone. Therefore, GCA has the potential to be used as an agent to protect the bone against glucocorticoid induced osteoporosis.
    Matched MeSH terms: Protective Agents/pharmacology; Protective Agents/therapeutic use*
  7. Comparative angioprotective effects of magnesium compounds
    Kharitonova M, Iezhitsa I, Zheltova A, Ozerov A, Spasov A, Skalny A
    J Trace Elem Med Biol, 2015 Jan;29:227-34.
    PMID: 25127069 DOI: 10.1016/j.jtemb.2014.06.026
    Magnesium (Mg) deficiency is implicated in the development of numerous disorders of the cardiovascular system. Moreover, the data regarding the efficacy of different magnesium compounds in the correction of impaired functions due to low magnesium intake are often fragmentary and inconsistent. The aim of this study was to compare the effects of the most bioavailable Mg compounds (Mg l-aspartate, Mg N-acetyltaurate, Mg chloride, Mg sulphate and Mg oxybutyrate) on systemic inflammation and endothelial dysfunction in rats fed a low Mg diet for 74 days. A low Mg diet decreased the Mg concentration in the plasma and erythrocytes, which was accompanied by a reduced concentration of eNOs and increased levels of endothelin-1 level in the serum and impaired endothelium-dependent vasodilatation. These effects increased the concentration of proinflammatory molecules, such as VCAM-1, TNF-α, IL-6 and CRP, indicating the development of systemic inflammation and endothelial dysfunction. The increased total NO level, which estimated from the sum of the nitrate and nitrite concentrations in the serum, may also be considered to be a proinflammatory marker. Two weeks of Mg supplementation partially or fully normalised the ability of the vascular wall to effect adequate endothelium-dependent vasodilatation and reversed the levels of most endothelial dysfunction and inflammatory markers (except CRP) to the mean values of the control group. Mg sulphate had the smallest effect on the endothelin-1, TNF-α and VCAM-1 levels. Mg N-acetyltaurate was significantly more effective in restoring the level of eNOS compared to all other studied compounds, except for Mg oxybutyrate. Taken together, the present findings demonstrate that all Mg compounds equally alleviate endothelial dysfunction and inflammation caused by Mg deficiency. Mg sulphate tended to be the least effective compound.
    Matched MeSH terms: Protective Agents/pharmacology*
  8. Ursodeoxycholic acid protects cardiomyocytes against cobalt chloride induced hypoxia by regulating transcriptional mediator of cells stress hypoxia inducible factor 1α and p53 protein
    Mohamed AS, Hanafi NI, Sheikh Abdul Kadir SH, Md Noor J, Abdul Hamid Hasani N, Ab Rahim S, et al.
    Cell Biochem Funct, 2017 Oct;35(7):453-463.
    PMID: 29027248 DOI: 10.1002/cbf.3303
    In hepatocytes, ursodeoxycholic acid (UDCA) activates cell signalling pathways such as p53, intracellular calcium ([Ca2+ ]i ), and sphingosine-1-phosphate (S1P)-receptor via Gαi -coupled-receptor. Recently, UDCA has been shown to protect the heart against hypoxia-reoxygenation injury. However, it is not clear whether UDCA cardioprotection against hypoxia acts through a transcriptional mediator of cells stress, HIF-1α and p53. Therefore, in here, we aimed to investigate whether UDCA could protect cardiomyocytes (CMs) against hypoxia by regulating expression of HIF-1α, p53, [Ca2+ ]i , and S1P-Gαi -coupled-receptor. Cardiomyocytes were isolated from newborn rats (0-2 days), and hypoxia was induced by using cobalt chloride (CoCl2 ). Cardiomyocytes were treated with UDCA and cotreated with either FTY720 (S1P-receptor agonist) or pertussis toxin (PTX; Gαi inhibitor). Cells were subjected for proliferation assay, beating frequency, QuantiGene Plex assay, western blot, immunofluorescence, and calcium imaging. Our findings showed that UDCA counteracted the effects of CoCl2 on cell viability, beating frequency, HIF-1α, and p53 protein expression. We found that these cardioprotection effects of UDCA were similar to FTY720, S1P agonist. Furthermore, we observed that UDCA protects CMs against CoCl2 -induced [Ca2+ ]i dynamic alteration. Pharmacological inhibition of the Gαi -sensitive receptor did not abolish the cardioprotection of UDCA against CoCl2 detrimental effects, except for cell viability and [Ca2+ ]i . Pertussis toxin is partially effective in inhibiting UDCA protection against CoCl2 effects on CM cell viability. Interestingly, PTX fully inhibits UDCA cardioprotection on CoCl2 -induced [Ca2+ ]i dynamic changes. We conclude that UDCA cardioprotection against CoCl2 -induced hypoxia is similar to FTY720, and its actions are not fully mediated by the Gαi -coupled protein sensitive pathways. Ursodeoxycholic acid is the most hydrophilic bile acid and is currently used to treat liver diseases. Recently, UDCA is shown to have a cardioprotection effects; however, the mechanism of UDCA cardioprotection is still poorly understood. The current data generated were the first to show that UDCA is able to inhibit the activation of HIF-1α and p53 protein during CoCl2 -induced hypoxia in cardiomyocytes. This study provides an insight of UDCA mechanism in protecting cardiomyocytes against hypoxia.
    Matched MeSH terms: Protective Agents/pharmacology*
  9. Fulltext Antioxidant protective effect of honey in cigarette smoke-induced testicular damage in rats
    Mohamed M, Sulaiman SA, Jaafar H, Sirajudeen KN
    Int J Mol Sci, 2011;12(9):5508-21.
    PMID: 22016605 DOI: 10.3390/ijms12095508
    Cigarette smoke (CS) can cause testicular damage and we investigated the possible protective effect of honey against CS-induced testicular damage and oxidative stress in rats. CS exposure (8 min, 3 times daily) and honey supplementation (1.2 g/kg daily) were given for 13 weeks. Rats exposed to CS significantly had smaller seminiferous tubules diameter and epithelial height, lower Leydig cell count and increased percentage of tubules with germ cell loss. CS also produced increased lipid peroxidation (TBARS) and glutathione peroxidase (GPx) activity, as well as reduced total antioxidant status (TAS) and activities of superoxide dismutase (SOD) and catalase (CAT). However, supplementation of honey significantly reduced histological changes and TBARS level, increased TAS level, as well as significantly restored activities of GPx, SOD and CAT in rat testis. These findings may suggest that honey has a protective effect against damage and oxidative stress induced by CS in rat testis.
    Matched MeSH terms: Protective Agents/pharmacology
  10. Protective effect of honey against cigarette smoke induced-impaired sexual behavior and fertility of male rats
    Mohamed M, Sulaiman SA, Sirajudeen KN
    Toxicol Ind Health, 2013 Apr;29(3):264-71.
    PMID: 22275383 DOI: 10.1177/0748233711432568
    Cigarette smoking is associated with sexual dysfunction and impaired fertility in males. The aim of this study was to determine the potential protective effect of honey against the toxic effect of cigarette smoke (CS) on sexual behavior and fertility of male rats. Thirty-two adult Sprague-Dawley rats were randomly divided into four groups (8 rats/group) as control, honey (H), CS and H plus CS (H + CS) groups. Rats in control and CS groups received oral administration of distilled water daily while rats in H and H + CS groups received honey (1.2 g/kg body weight/day) by oral gavage. Rats in CS and H + CS groups were also exposed to CS for 8 min 3 times/day. From 10 to 13 weeks of treatment, each male rat was cohabited with 3 untreated female rats for sexual behavioral and reproductive performance studies. Honey significantly increased the percentages of rats achieving intromission and ejaculation as well as increased mating and fertility indexes of male rats exposed to CS. Thus, honey has a protective effect against CS-induced impaired sexual behavior and fertility in male rats.
    Matched MeSH terms: Protective Agents/pharmacology*
  11. Fulltext Effects of nerol on paracetamol-induced liver damage in Wistar albino rats
    Islam MT, Quispe C, Islam MA, Ali ES, Saha S, Asha UH, et al.
    Biomed Pharmacother, 2021 Aug;140:111732.
    PMID: 34130201 DOI: 10.1016/j.biopha.2021.111732
    Nerol, a monoterpene is evident to possess diverse biological activities, including antioxidant, anti-microbial, anti-spasmodic, anthelmintic, and anti-arrhythmias. This study aims to evaluate its hepatoprotective effect against paracetamol-induced liver toxicity in a rat model. Five groups of rats (n = 7) were orally treated (once daily) with 0.05% tween 80 dissolved in 0.9% NaCl solution (vehicle), paracetamol 640 mg/kg (negative control), 50 mg/kg silymarin (positive control), or nerol (50 and 100 mg/kg) for 14 days, followed by the hepatotoxicity induction using paracetamol (PCM). The blood samples and livers of the animals were collected and subjected to biochemical and microscopical analysis. The histological findings suggest that paracetamol caused lymphocyte infiltration and marked necrosis, whereas maintenance of the normal hepatic structural was observed in group pre-treated with silymarin and nerol. The rats pre-treated with nerol significantly and dose-dependently reduced the hepatotoxic markers in animals. Nerol at 100 mg/kg significantly reversed the paracetamol-induced altered situations, including the liver enzymes, plasma proteins, antioxidant enzymes and serum bilirubin, lipid peroxidation (LPO) and cholesterol [e.g., total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c)] levels in animals. Taken together, nerol exerted significant hepatoprotective activity in rats in a dose-dependent manner. PCM-induced toxicity and nerol induced hepatoprotective effects based on expression of inflammatory and apoptosis factors will be future line of work for establishing the precise mechanism of action of nerol in Wistar albino rats.
    Matched MeSH terms: Protective Agents/pharmacology; Protective Agents/therapeutic use*
  12. Protective effects of zinc L-carnosine against hydrogen peroxide-induced DNA damage and micronucleus formation in CCD-18co human colon fibroblast cells
    Ooi TC, Chan KM, Sharif R
    Free Radic Res, 2020 May;54(5):330-340.
    PMID: 32366187 DOI: 10.1080/10715762.2020.1763333
    Zinc L-carnosine (ZnC) is a chelated compound of zinc and L-carnosine. The present study aims to determine the protective effects of ZnC against hydrogen peroxide (H2O2)-induced oxidative stress and genomic damage in CCD-18co human normal colon fibroblast cells. Generally, cells were pretreated with ZnC (0-100 µM) for 24 h before challenged with 20 µM of H2O2 for 1 h to induce oxidative damage. Results showed that pretreatment with ZnC was able to reduce the intracellular ROS level in CCD-18co cells after being challenged with H2O2. Moreover, pretreatment with ZnC demonstrated protection from H2O2-induced DNA strand breaks and micronucleus formation. Our current findings revealed that pretreatment with ZnC could induce the activation of MTF-1 signaling pathway and expression of metallothionein (MT) in a dose-dependent manner. However, ZnC did not have any effects on Nrf2 signaling pathway and the expression of glutathione, superoxide dismutase 1, and glutamate-cysteine ligase catalytic subunit (GCLC). Furthermore, pretreatment with ZnC did not induce the expression of OGG1 and PARP-1 in CCD-18co cells, suggesting that these two DNA repairing enzymes are not related to the genoprotective effects of ZnC. Since the expression of MT has been demonstrated to protect cells from oxidative DNA damage induced by various genotoxic agents, the genoprotective effects of ZnC might be due to the ability of ZnC to induce the expression of MT. In conclusion, ZnC pretreatment was able to protect CCD-18co cells from H2O2-induced genomic damage via the activation of the MTF-1 signalling pathway and the induction of MT expression.
    Matched MeSH terms: Protective Agents/pharmacology*
  13. Fulltext Cytoprotective effect of palm kernel cake phenolics against aflatoxin B1-induced cell damage and its underlying mechanism of action
    Oskoueian E, Abdullah N, Zulkifli I, Ebrahimi M, Karimi E, Goh YM, et al.
    BMC Complement Altern Med, 2015 Oct 30;15:392.
    PMID: 26518905 DOI: 10.1186/s12906-015-0921-z
    BACKGROUND: Palm kernel cake (PKC), a by-product of the palm oil industry is abundantly available in many tropical and subtropical countries. The product is known to contain high levels of phenolic compounds that may impede the deleterious effects of fungal mycotoxins. This study focused on the evaluation of PKC phenolics as a potential cytoprotective agent towards aflatoxin B1 (AFB1)-induced cell damage.

    METHODS: The phenolic compounds of PKC were obtained by solvent extraction and the product rich in phenolic compounds was labeled as phenolic-enriched fraction (PEF). This fraction was evaluated for its phenolic compounds composition. The antioxidant activity of PEF was determined by using 1,1-diphenyl-2-picryl-hydrazil scavenging activity, ferric reducing antioxidant power, inhibition of ß-carotene bleaching, and thiobarbituric acid reactive substances assays. The cytotoxicity assay and molecular biomarkers analyses were performed to evaluate the cytoprotective effects of PEF towards aflatoxin B1 (AFB1)-induced cell damage.

    RESULTS: The results showed that PEF contained gallic acid, pyrogallol, vanillic acid, caffeic acid, syringic acid, epicatechin, catechin and ferulic acid. The PEF exhibited free radical scavenging activity, ferric reducing antioxidant power, ß-carotene bleaching inhibition and thiobarbituric acid reactive substances inhibition. The PEF demonstrated cytoprotective effects in AFB1-treated chicken hepatocytes by reducing the cellular lipid peroxidation and enhancing antioxidant enzymes production. The viability of AFB1-treated hepatocytes was improved by PEF through up-regulation of oxidative stress tolerance genes and down-regulation of pro-inflammatory and apoptosis associated genes.

    CONCLUSIONS: The present findings supported the proposition that the phenolic compounds present in PKC could be a potential cytoprotective agent towards AFB1 cytotoxicity.

    Matched MeSH terms: Protective Agents/pharmacology*
  14. Fulltext Urinary metabolomics study on the protective role of Orthosiphon stamineus in Streptozotocin induced diabetes mellitus in rats via (1)H NMR spectroscopy
    Azam AA, Pariyani R, Ismail IS, Ismail A, Khatib A, Abas F, et al.
    BMC Complement Altern Med, 2017 May 25;17(1):278.
    PMID: 28545435 DOI: 10.1186/s12906-017-1777-1
    BACKGROUND: Orthosiphon stamineus (OS) is a herb known in ethnomedicine for treating diabetes mellitus (DM). In this study, a (1)H NMR based urine metabolomics tool has been used for the first time to identify the metabolic protective mechanism of OS in DM using Streptozotocin (STZ) induced experimental model in rats.

    METHODS: Four different solvent extracts of OS, namely aqueous, ethanolic, 50% aqueous ethanolic and methanolic, at a dose of 500 mg/kg body weight (bw) were orally administered for 14 days to diabetic rats induced via intraperitoneal injection of 60 mg/kg bw STZ. NMR metabolomics approach using pattern recognition combined with multivariate statistical analysis was applied in the rat urine to study the resulted metabolic perturbations.

    RESULTS: OS aqueous extract (OSAE) caused a reversal of DM comparable to that of 10 mg/kg bw glibenclamide. A total of 15 urinary metabolites, which levels changed significantly upon treatment were identified as the biomarkers of OSAE in diabetes. A systematic metabolic pathways analysis identified that OSAE contributed to the antidiabetic activity mainly through regulating the tricarboxylic acid cycle, glycolysis/gluconeogenesis, lipid and amino acid metabolism.

    CONCLUSIONS: The results of this study validated the ethnopharmacological use of OS in diabetes and unveiled the biochemical and metabolic mechanisms involved.

    Matched MeSH terms: Protective Agents/administration & dosage*; Protective Agents/chemistry
  15. Potential protective effect of sunitinib after administration of diclofenac: biochemical and histopathological drug-drug interaction assessment in a mouse model
    Tan JR, Chakravarthi S, Judson JP, Haleagrahara N, Segarra I
    Naunyn Schmiedebergs Arch Pharmacol, 2013 Jul;386(7):619-33.
    PMID: 23552887 DOI: 10.1007/s00210-013-0861-4
    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.
    Matched MeSH terms: Protective Agents/administration & dosage*
  16. Dietary UKMR-1 roselle supplementation prevents nicotine-induced cardiac injury by inhibiting myocardial oxidative stress
    Ramalingam A, Siti Balkis Budin, Lim Yc, Lislivia Si Yn, Satirah Zainalabidin
    Sains Malaysiana, 2016;45:1131-1137.
    UKMR-1, a local variant of mutant Roselle strain (Hibiscus sabdariffa) is enriched with free radical scavenging polyphenols
    such as anthocyanin, vitamin C and hydroxycitric acid. However, pharmacological actions of UKMR-1 are not fully known.
    This study was conducted to determine whether supplementation of aqueous UKMR-1 calyx extract was able to protect
    against nicotine-induced cardiac injury in rats. In this experimental study, healthy male albino rats were randomly
    allotted into three groups (n=7 per group): control, nicotine and UKMR-1+Nicotine groups. Nicotine (0.6 mg/kg, i.p.)
    was administered to both nicotine and UKMR-1+Nicotine groups for 28 consecutive days. UKMR-1+Nicotine group also
    received 100 mg/kg UKMR-1 extract orally via gavage 30 min prior to nicotine injection, daily. UKMR-1+Nicotine group
    had significantly (p<0.05) higher lactate dehydrogenase (LDH) activity, as well as lower malondialdehyde content in
    heart tissue homogenate than nicotine group, suggesting its cardio protective activity by inhibition of lipid peroxidation.
    UKMR-1 also lowered (p<0.05) the blood pressure in nicotine-administered rats. In addition, UKMR-1 significantly (p<0.05)
    restored activities of cytosolic superoxide dismutase, glutathione peroxidase and glutathione-S-transferase as well as
    redox balance ratio (GSH:GSSG). In conclusion, UKMR-1 was a
    Matched MeSH terms: Protective Agents
  17. MicroRNAs: association with radioresistant and potential uses of natural remedies as green gene therapeutic approaches
    Jothy SL, Chen Y, Vijayarathna S, Kanwar JR, Sasidharan S
    Curr Gene Ther, 2015;15(1):15-20.
    PMID: 25478696
    Radiotherapy plays an essential primary role in cancer patients. Regardless of its significant advances in treatment options, tumor recurrence and radio-resistance in cancer cells still occur in a high percentage of patients. Furthermore, the over expression of miRNAs accompanies the development of radio-resistant cancer cells. Consequently, miRNAs might serve as therapeutic targets for the treatment of radio-resistance in cancer cells. The findings of the current research also signify that the use of a natural anti-miRNA substance could inhibit specific miRNAs, and, concurrently, these natural remedies could exhibit radioprotective activity against the healthy cells during radiotherapy. Therefore, in this review, we have reported the association of miRNAs with radio-resistance and the potential uses of natural remedies as green gene therapeutic approaches, as well as radioprotectors against the adverse effects of irradiation on healthy cells during radiotherapy.
    Matched MeSH terms: Radiation-Protective Agents/pharmacology
  18. Herbal remedies for combating irradiation: a green anti-irradiation approach
    Lachumy SJ, Oon CE, Deivanai S, Saravanan D, Vijayarathna S, Choong YS, et al.
    Asian Pac J Cancer Prev, 2013;14(10):5553-65.
    PMID: 24289545
    Plants play important roles in human life not only as suppliers of oxygen but also as a fundamental resource to sustain the human race on this earthly plane. Plants also play a major role in our nutrition by converting energy from the sun during photosynthesis. In addition, plants have been used extensively in traditional medicine since time immemorial. Information in the biomedical literature has indicated that many natural herbs have been investigated for their efficacy against lethal irradiation. Pharmacological studies by various groups of investigators have shown that natural herbs possess significant radioprotective activity. In view of the immense medicinal importance of natural product based radioprotective agents, this review aims at compiling all currently available information on radioprotective agents from medicinal plants and herbs, especially the evaluation methods and mechanisms of action. In this review we particularly emphasize on ethnomedicinal uses, botany, phytochemistry, mechanisms of action and toxicology. We also describe modern techniques for evaluating herbal samples as radioprotective agents. The usage of herbal remedies for combating lethal irradiation is a green anti- irradiation approach for the betterment of human beings without high cost, side effects and toxicity.
    Matched MeSH terms: Radiation-Protective Agents/pharmacology*; Radiation-Protective Agents/therapeutic use*
  19. Fulltext Hepatoprotective potential of Clitoria ternatea leaf extract against paracetamol induced damage in mice
    Nithianantham K, Shyamala M, Chen Y, Latha LY, Jothy SL, Sasidharan S
    Molecules, 2011 Dec 06;16(12):10134-45.
    PMID: 22146374 DOI: 10.3390/molecules161210134
    BACKGROUND AND AIM: Clitoria ternatea, a medicinal herb native to tropical equatorial Asia, is commonly used in folk medicine to treat various diseases. The aim of the present study is to evaluate the hepatoprotective and antioxidant activity of C. ternatea against experimentally induced liver injury.

    METHODS: The antioxidant property of methanolic extract (ME) of C. ternatea leaf was investigated by employing an established in vitro antioxidant assay. The hepatoprotective effect against paracetamol-induced liver toxicity in mice of ME of C. ternatea leaf was also studied. Activity was measured by monitoring the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and billirubin along with histopathological analysis.

    RESULTS: The amount of total phenolics and flavonoids were estimated to be 358.99 ± 6.21 mg/g gallic acid equivalent and 123.75 ± 2.84 mg/g catechin equivalent, respectively. The antioxidant activity of C. ternatea leaf extract was 67.85% at a concentration of 1 mg/mL and was also concentration dependant, with an IC(50) value of 420.00 µg/mL. The results of the paracetamol-induced liver toxicity experiments showed that mice treated with the ME of C. ternatea leaf (200 mg/kg) showed a significant decrease in ALT, AST, and bilirubin levels, which were all elevated in the paracetamol group (p < 0.01). C. ternatea leaf extract therapy also protective effects against histopathological alterations. Histological studies supported the biochemical findings and a maximum improvement in the histoarchitecture was seen.

    CONCLUSIONS: The current study confirmed the hepatoprotective effect of C. ternatea leaf extract against the model hepatotoxicant paracetamol. The hepatoprotective action is likely related to its potent antioxidative activity.

    Matched MeSH terms: Protective Agents/pharmacology; Protective Agents/therapeutic use*
  20. Fulltext Evaluation of the hepatoprotective Effects of Lantadene A, a pentacyclic triterpenoid of Lantana plants against acetaminophen-induced liver damage
    Grace-Lynn C, Chen Y, Latha LY, Kanwar JR, Jothy SL, Vijayarathna S, et al.
    Molecules, 2012 Nov 23;17(12):13937-47.
    PMID: 23178309 DOI: 10.3390/molecules171213937
    The aim of the present study was to evaluate the hepatoprotective activity of lantadene A against acetaminophen-induced liver toxicity in mice was studied. Activity was measured by monitoring the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and bilirubin, along with histo-pathological analysis. Silymarin was used as positive control. A bimodal pattern of behavioural toxicity was exhibited by the lantadene A-treated group at the beginning of the treatment. However, treatment with lantadene A and silymarin resulted in an increase in the liver weight compared with the acetaminophen treated group. The results of the acetaminophen-induced liver toxicity experiments showed that mice treated with lantadene A (500 mg/kg) showed a significant decrease in the activity of ALT, AST and ALP and the level of bilirubin, which were all elevated in the acetaminophen treated group (p < 0.05). Histological studies supported the biochemical findings and a maximum improvement in the histoarchitecture was seen. The lantadene A-treated group showed remarkable protective effects against histopathological alterations, with comparable results to the silymarin treated group. The current study confirmed the hepatoprotective effects of lantadene A against the model hepatotoxicant acetaminophen, which is likely related to its potent antioxidative activity.
    Matched MeSH terms: Protective Agents/administration & dosage
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