ORIGINAL_ARTICLE
Chemical and Biological Approaches for the Synthesis of Silver Nanoparticles; A mini Review
Since ancient time silver and silver based compound have been used as a powerful antimicrobial agent in medicine. Discovery of antibiotics pushes the silver away from medicine and pharmaceutical sciences. By emerging resistance strains and reducing the efficiency of antibiotics, silver became point of attentions again, but in a novel form of silver nanoparticles (AgNPs). AgNPs are the most effective and powerful novel antimicrobial with ancient roots. Chemical synthesis is one of the first techniques for synthesis of AgNPs. In this technique silver ions reduced to AgNPs by using chemical reducing agents such as sodium borohydride (NaBH4) and sodium citrate (Na3C6H5O7). Later investigations have shown that biological molecules from living organisms such as bacteria, fungi, algae, and plants can also be used as more safe and in some cases sheep reducing agent for biosynthesis of AgNPs.
https://tips.sums.ac.ir/article_42220_74d28d424bc7422b91f0ca3703025314.pdf
2017-06-01
55
62
Alireza
Ebrahiminezhad
a_ebrahimi@sums.ac.ir
1
LEAD_AUTHOR
Seyedeh-Masoumeh
Taghizadeh
2
AUTHOR
Saeed
Taghizadeh
3
AUTHOR
Younes
Ghasemi
ghasemiy@sums.ac.ir
4
AUTHOR
ORIGINAL_ARTICLE
Valproic Acid-Induced Hepatotoxicity and the Protective Role of Thiol Reductants
Valproic acid (VPA) is a widely administered drug against epilepsy and several other neurological disorders. On the other hand, liver injury is a deleterious side effect associated with VPA. Oxidative stress seems to play a critical role in VPA-induced hepatotoxicity. The current investigation was designed to evaluate if N-acetylcysteine (NAC) and dithiothreitol (DTT) as thiol reducing agents have any protective effects against VPA-induced liver injury. Isolated rat hepatocytes (in vitro) were exposed to increasing concentrations of VPA (25, 50, 100, 150, and 250 µM) and markers of cytotoxicity were evaluated. Furthermore, animals received VPA (250 and 500 mg/kg, i.p for 15 consecutive days) (in vivo) and markers of liver injury were monitored. It was found that 250 µM of VPA caused marked cytotoxicity toward isolated hepatocytes as judged by trypan blue exclusion test. Moreover, markers of oxidative stress including glutathione depletion and lipid peroxidation were detected in VPA-treated hepatocytes. On the other hand, VPA caused a significant increase in plasma markers of hepatotoxicity in drug-treated group. Liver histopathological changes and markers of oxidative stress were also detected in VPA-treated animals. It was found that administration of NAC (1 mM), and DTT (1 mM) significantly alleviated VPA-induced cytotoxicity (In vitro). NAC (250 and 500 mg/kg) and DTT (15 and 30 mg/kg) also significantly mitigated VPA hepatotoxicity (In vivo). The data obtained from the current investigation indicate potential therapeutic properties of thiol reductants against VPA-induced liver injury.
https://tips.sums.ac.ir/article_42221_fd59e891c3819c642384d805a3ecd897.pdf
2017-06-01
63
70
glutathione
Hepatoprotective
Hepatotoxicity
Oxidative stress
Sodium Valproate
Nahid
Najafi
rheidari@sums.ac.ir
1
AUTHOR
Akram
Jamshidzadeh
ajamshid@sums.ac.ir
2
AUTHOR
Hamideh
Fallahzadeh
3
AUTHOR
Mahmoud
Omidi
m_omidi@sums.ac.ir
4
AUTHOR
Narges
Abdoli
5
AUTHOR
Asma
Najibi
6
AUTHOR
Negar
Azarpira
7
AUTHOR
Reza
Heidari
rezaheidari@hotmail.com
8
Shiraz University of Medical Sciences, Pharmaceutical Sciences Research Center
AUTHOR
Hossein
Niknahad
niknahadh@sums.ac.ir
9
LEAD_AUTHOR
Davies JA, Valproic Acid, in xPharm: The Comprehensive Pharmacology Reference2007, Elsevier: New York. p. 1-5.
1
Bryant AE, Dreifuss FE. Valproic acid hepatic fatalities. III. U.S. experience since 1986. Neurology. 1996;46;465-469.
2
Chateauvieux S, Morceau F, Diederich M, Valproic Acid, in Encyclopedia of Toxicology (Third Edition), P. Wexler, Editor 2014, Academic Press: Oxford. p. 905-908.
3
Nanau RM, Neuman MG. Adverse drug reactions induced by valproic acid. Clin Biochem. 2013;46;1323-1338.
4
Heidari R, Jafari F, Khodaei F, Shirazi Yeganeh B, Niknahad H. The Mechanism of Valproic Acid-Induced Fanconi Syndrome Involves Mitochondrial Dysfunction and Oxidative Stress in Rat Kidney. Nephrology (Carlton, Vic). 2017;In-Press.
5
Li S, Guo J, Ying Z, Chen S, Yang L, Chen K, Long Q, Qin D, Pei D, Liu X. Valproic acidâinduced hepatotoxicity in alpers syndrome is associated with mitochondrial permeability transition pore openingâdependent apoptotic sensitivity in an induced pluripotent stem cell model. Hepatology. 2015;61;1730-1739.
6
Vitins AP, Kienhuis AS, Speksnijder EN, Roodbergen M, Luijten M, Ven LTMvd. Mechanisms of amiodarone and valproic acid induced liver steatosis in mouse in vivo act as a template for other hepatotoxicity models. Arch Toxicol. 2014;88;1573-1588.
7
Gezginci-Oktayoglu S, Turkyilmaz IB, Ercin M, Yanardag R, Bolkent S. Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties. Protoplasma. 2015.
8
Ahangar N, Naderi M, Noroozi A, Ghasemi M, Zamani E, Shaki F. Zinc Deficiency and Oxidative Stress Involved in Valproic Acid Induced Hepatotoxicity: Protection by Zinc and Selenium Supplementation. Biol Trace Element Res. 2017;1-8.
9
Chang TKH, Abbott FS. Oxidative stress as a mechanism of valproic acid-associated hepatotoxicity. Drug Metab Rev. 2006;38;627-639.
10
Michoulas A, Tong V, Teng XW, Chang TKH, Abbott FS, Farrell K. Oxidative stress in children receiving valproic acid. J Pediatric. 2006;149;692-696.
11
Fisher R, Nau H, Gandolfi AJ, Putnam CW, Brendel K. Valproic Acid Hepatotoxicity in Human Liver Slices. Drug Chem Toxicol. 1991;14;375-394.
12
Heidari R, Babaei H, Eghbal MA. Amodiaquine-induced toxicity in isolated rat hepatocytes and the cytoprotective effects of taurine and/or N-acetyl cysteine. Res Pharm Sci. 2014;9;97-105.
13
Khan S, O'Brien PJ. 1-bromoalkanes as new potent nontoxic glutathione depletors in isolated rat hepatocytes. Biochem Biophy Res Commun. 1991;179;436-41.
14
Heidari R, Babaei H, Eghbal MA. Cytoprotective Effects of Taurine Against Toxicity Induced by Isoniazid and Hydrazine in Isolated Rat Hepatocytes. Arch Indust Hyg Toxicol. 2013;64;201-210.
15
Jamshidzadeh A, Niknahad H, Kashafi H. Cytotoxicity of chloroquine in isolated rat hepatocytes. J Appl Toxicol. 2007;27;322-6.
16
Abdoli N, Heidari R, Azarmi Y, Eghbal MA. Mechanisms of the Statins Cytotoxicity in Freshly Isolated Rat Hepatocytes. J Biochem Mol Toxicol. 2013;n/a-n/a.
17
Heidari R, Babaei H, Eghbal M. Mechanisms of methimazole cytotoxicity in isolated rat hepatocytes. Drug Chem Toxicol. 2013;36;403-411.
18
Heidari R, Babaei H, Eghbal MA. Ameliorative effects of taurine against methimazole-induced cytotoxicity in isolated rat hepatocytes. Scientia pharmaceutica. 2012;80;987.
19
Sokmen BB, Tunali S, Yanardag R. Effects of vitamin U (S-methyl methionine sulphonium chloride) on valproic acid induced liver injury in rats. Food Chem Toxicol. 2012;50;3562-3566.
20
Gezginci-Oktayoglu S, Turkyilmaz IB, Ercin M, Yanardag R, Bolkent S. Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties. Protoplasma. 2015;253;127-135.
21
Jamshidzadeh A, Heidari R, Mohammadi-Samani S, Azarpira N, Najbi A, Jahani P, Abdoli N. A Comparison between the Nephrotoxic Profile of Gentamicin and Gentamicin Nanoparticles in Mice. J Biochem Mol Toxicol. 2015;29;57-62.
22
Heidari R, Taheri V, Rahimi HR, Yeganeh BS, Niknahad H, Najibi A. Sulfasalazine-induced renal injury in rats and the protective role of thiol-reductants. Renal Failure. 2016;38;137-141.
23
Jamshidzadeh A, Heidari R, Golzar T, Derakhshanfar A. Effect of Eisenia foetida Extract against Cisplatin-Induced Kidney Injury in Rats. J Diet Suppl. 2016;13;551-559.
24
Jamshidzadeh A, Heidari R, Abazari F, Ramezani M, Khodaei F, Ommati MM, Ayarzadeh M, Firuzi R, Saeedi A, Azarpira N, others. Antimalarial Drugs-Induced Hepatic Injury in Rats and the Protective Role of Carnosine. Pharm Sci. 2016;22.
25
Niknahad H, Heidari R, Firuzi R, Abazari F, Ramezani M, Azarpira N, Hosseinzadeh M, Najibi A, Saeedi A. Concurrent Inflammation Augments Antimalarial Drugs-Induced Liver Injury in Rats. Adv Pharm Bull. 2016;6.
26
Moezi L, Heidari R, Amirghofran Z, Nekooeian AA, Monabati A, Dehpour AR. Enhanced anti-ulcer effect of pioglitazone on gastric ulcers in cirrhotic rats: The role of nitric oxide and IL-1b. Pharmacol Report. 2013;65;134-143.
27
Heidari R, Jamshidzadeh A, Niknahad H, Mardani E, Ommati MM, Azarpira N, Khodaei F, Zarei A, Ayarzadeh M, Mousavi S, Abdoli N, Yeganeh BS, Saeedi A, Najibi A. Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia. Toxicol Report. 2016;3;870-879.
28
Heidari R, Niknahad H, Jamshidzadeh A, Azarpira N, Bazyari M, Najibi A. Carbonyl Traps as Potential Protective Agents against Methimazole-Induced Liver Injury. J Biochem Mol Toxicol. 2014;29;173-181.
29
Niknahad H, Heidari R, Mokhtebaz T, Mansouri S, Dehshahri S, Abdoli N, Najibi A. Evaluating the effects of different fractions obtained from Gundelia tournefortii extract against carbon tetrachloride-induced liver injury in rats. Trend Pharm Sci. 2016;2;25-34.
30
Sedlak J, Lindsay RH. Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman's reagent. Analyt Bioch. 1968;25;192-205.
31
Heidari R, Jamshidzadeh A, Niknahad H, Safari F, Azizi H, Abdoli N, Ommati MM, Khodaei F, Saeedi A, Najibi A. The Hepatoprotection Provided by Taurine and Glycine against Antineoplastic Drugs Induced Liver Injury in an Ex Vivo Model of Normothermic Recirculating Isolated Perfused Rat Liver. Trend Pharm Sci. 2016;2;59-76.
32
Heidari R, Babaei H, Roshangar L, Eghbal MA. Effects of Enzyme Induction and/or Glutathione Depletion on Methimazole-Induced Hepatotoxicity in Mice and the Protective Role of N-Acetylcysteine. Adv Pharm Bull. 2014;4;21-28.
33
Tong V, Teng XW, Chang TKH, Abbott FS. Valproic acid II: effects on oxidative stress, mitochondrial membrane potential, and cytotoxicity in glutathione-depleted rat hepatocytes. Toxicol Sci. 2005;86;436-443.
34
Labbe G, Pessayre D, Fromenty B. Drug-induced liver injury through mitochondrial dysfunction: mechanisms and detection during preclinical safety studies. Fundament Clin Pharmacol. 2008;22;335-353.
35
Heidari R, Niknahad H, Jamshidzadeh A, Eghbal MA, Abdoli N. An Overview on the Proposed Mechanisms of Antithyroid Drugs-Induced Liver Injury. Adv Pharm Bull. 2015;5;1-11.
36
Silva MFB, Aires CCP, Luis PBM, Ruiter JPN, Ijlst L, Duran M, Wanders RJA, Almeida ITd. Valproic acid metabolism and its effects on mitochondrial fatty acid oxidation: A review. J Inherit Metab Dis. 2008;31;205-216.
37
Banaclocha MMn, Hernandez AI, MartıÌnez N, Ferrandiz MaL. N-Acetylcysteine protects against age-related increase in oxidized proteins in mouse synaptic mitochondria. Brain Res. 1997;762;256-258.
38
Kamboj SS, Sandhir R. Protective effect of N-acetylcysteine supplementation on mitochondrial oxidative stress and mitochondrial enzymes in cerebral cortex of streptozotocin-treated diabetic rats. Mitochondrion. 2011;11;214-222.
39
ORIGINAL_ARTICLE
Analysis of the expression level of aquaporins under acetylene treatment and pathogen attack
Fusarium wilt disease and Sigatoka leaf spots threaten global market of Musa sp. Major Intrinsic Proteins (MIP) consisting aquaporins (AQPs) facilitate the transport of water and molecules like H2O2, CO2, silicon, boron, urea, and ammonia. Biotic and abiotic stresses affect the expression level of MIPs and influence the transportation of water and nutrients, which results in the susceptibility of plants to diseases. Expression level of MIP genes in Musa acuminata (MaMIPs) fruits during development and under acetylene treatment; expression of MaMIPs in the corms of banana infected with Fusarium oxysporum cubense (Foc), and the expression of MaMIP genes in the leaves treated with Mycosphaerella fijiensis were retrieved from the banana genome hub database. Expression data of roots, treated with virulent Focs at 3, 27, and 51 hours post-inoculation (hpi) were downloaded from Gene Expression Omnibus. The expression data were analyzed using MeV 4.9 program. Expression level of MaMIPs was mainly suppressed by acetylene and biotic treatments. Twenty seven and 51 hpi of roots with Foc, 88% and 63% of MaMIPs were down-regulated. However, MaNIP2-1 expression showed a significant up-regulation in all conditions. Infection of banana corms resulted in the suppression of MaMIPs. A low decrease in the expression of MaMIPs was observed, when the leaves were under Mycosphaerella fijiensis attack. Suppression of MaMIPs might be in line with repression of plant defense by banana pathogens as an approach for infection progression. Identification of the MIPs influenced by stresses provides the opportunity for the production of transgenic resistant cultivars.
https://tips.sums.ac.ir/article_42222_8db4fd30a6709e2ef2c05f6da9115811.pdf
2017-06-01
71
82
aquaporin
Banana
Biotic stress
Expression profile
Fusarium
Mycosphaerella
Shiva
Hemmati
hemmatish@sums.ac.ir
1
LEAD_AUTHOR
ORIGINAL_ARTICLE
N-Phenyl Ureidobenzenesulfonate derivatives as novel anticancer agents: QSAR and Molecular docking studies
DNA double strand-breaks (DSBs) are the most deleterious lesions that can affect the genome of living beings and are lethal if not quickly and properly repaired. Recently, N-phenyl ureidobenzenesulfonates (PUB-SOs) as tubulin inhibitors that are blocking the cells cycle progression in S-phase and inducing DNA DSBs is discovered. Here, a set of PUB-SOs derivatives were applied to quantitative structural activity relationship (QSAR) analysis. A series of chemometrics methods like MLR, FA- MLR, PCR and partial least squared included in variable selection genetic algorithm (GA-PLS) were used for relations between structural features of these compounds and their anti-proliferative activity against MCF-7 cell line. New potent lead compounds were also designed based on new structural patterns using in silico-screening study. Molecular docking studies of these compounds on DNA and tubulin were conducted. The results obtained from validated docking protocol indicate that the important amino acids inside the active site cavity that are in charge of essential interactions with tubulin are Ala30, Lys B254, Asn B258, Met B259, Asn A101, Glu A183, Thr A179, Leu B255, Ser A178 and Gln B247. And the most important base pairs inside the minor groove of DNA being responsible for essential interclation with DNA are G2, G4, G10, G12, A5, A6, C9 and C11 base pairs.
https://tips.sums.ac.ir/article_42223_cf91fffa662a36654a3d3e7737405753.pdf
2017-06-01
83
104
QSAR
molecular docking
N-phenyl ureidobenzenesulfonates
in silico-screening
Masood
Fereidoonnezhad
fereidoonnezhad-m@ajums.ac.ir
1
Department of Medicinal Chemistry, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
LEAD_AUTHOR
Azar
Mostoufi
azarmostoufi@yahoo.com
2
1 Department of Medicinal Chemistry, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
2 Research Center of Marine Pharmaceutical Science, Ahvaz Jundishahpour University of Medical Science, P.O. Code 61357-73135, Iran
AUTHOR
Fariba
Aliyan
fariba.aliyan20@gmail.com
3
Department of Medicinal Chemistry, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
ORIGINAL_ARTICLE
Formulation and evaluation of an Aloe vera -Licorice combination topical gel: a potential choice for wound healing
Wound healing is a natural body response to injury and consists of three steps; Inflammation, proliferation and remodeling. Natural products have always been attractive in pharmacy and drug delivery and have shown higher patient compliance in some treatments. Aloe vera and licorice extract have each been used to improve and accelerate wound healing. It seems that combination of these two natural products may show better and effective results. Aloe vera gel and licorice extract powder were standardized with their major and important components, Glycyrrhizin and Glucomannan, respectively. Three different polymers in three different concentrations were used to prepare topical gels containing Aloe vera gel and licorice extract powder. Gels were examined for different properties such as appearance, pH, viscosity, spreadability, drug content and in vitro release. Optimized formulations contained carbopol 2% (F3) and CMC 3% (F5) with pH (5.92 and 5.69), spreadability (51 and 55 mm), a shear thinning manner and in vitro release within 8 hours proper for topical use. Preclinical studies should be processed to determine the suitability of these gels for wound healing.
https://tips.sums.ac.ir/article_42224_03495b10253fd8500d1f543fbb8f95fb.pdf
2017-06-01
105
112
Fatemeh
Ahmadi
ahmadi_f@sums.ac.ir
1
AUTHOR
Sardar
Rezaee
2
AUTHOR
Shohreh
Alipour
3
LEAD_AUTHOR
ORIGINAL_ARTICLE
The Hepatoprotective Role of Thiol Reductants against Mitoxantrone-Induced Liver Injury
Mitoxantrone is anthracycline antibiotic highly effective against various human cancers. Hepatotoxicity is associated with mitoxantrone administration. On the other hand, there is no effective therapeutic option against chemotherapy-induced liver injury. The current investigation was designed to evaluate the effect of thiol reductants on mitoxantrone-induced liver injury in two experimental models. As an ex vivo model, isolated rat liver was exposed to increasing concentrations of mitoxantrone (100, 250, 750, and 1000 µM) alone or in combination with thiol-reductants (Dithiothreitol; DTT, and N-acetyl cysteine; NAC). In addition, rats (in vivo) received mitoxantrone (2.5 mg/kg, i.p, at days 1, 10, and 20), NAC (100 and 300 mg/kg/day, i.p, for 20 consecutive days) and DTT (15 and 30 mg/kg/day, i.p, for 20 consecutive days), then liver and serum pathological changes were monitored. Mitoxantrone-induced liver injury was evident in both ex vivo and in vivo experiments as assessed by pathological changes in biomarkers of liver injury, along with tissue histopathological changes. Furthermore, an increase in liver tissue markers of oxidative stress was detected in the mitoxantrone-treated group. It was found that thiol reductants significantly mitigated mitoxantrone hepatotoxicity. The data indicate that thiol reductants might serve as hepatoprotective agents against chemotherapy-induced liver injury.
https://tips.sums.ac.ir/article_42225_d625af0b2803f4e20967106a9e19c7d7.pdf
2017-06-01
113
122
Antineoplastic agents
Chemotherapy
Drug-Induced Liver Injury (DILI)
glutathione
Hepatotoxicity
Hossein
Niknahad
niknahadh@sums.ac.ir
1
Department of Pharmacology-Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
AUTHOR
Helia
Hosseini
2
AUTHOR
Fatemeh
Gozashtegan
3
AUTHOR
Farzaneh
Ebrahimi
4
AUTHOR
Negar
Azarpira
5
AUTHOR
Narges
Abdoli
6
AUTHOR
Reza
Heidari
rezaheidari@hotmail.com
7
LEAD_AUTHOR
Corsini A, Bortolini M. Drug-Induced Liver Injury: The Role of Drug Metabolism and Transport. J Clin Pharmacol. 2013;53;463-474.
1
Thatishetty AV, Agresti N, O'Brien CB. Chemotherapy-Induced Hepatotoxicity. Clinic Liver Dis. 2013;17;671-686.
2
Chun YS, Laurent A, Maru D, Vauthey J-N. Management of chemotherapy-associated hepatotoxicity in colorectal liver metastases. Lancet Oncol. 2009;10;278-286.
3
King PD, Perry MC. Hepatotoxicity of Chemotherapy. The Oncologist. 2001;6;162-176.
4
Morgan C, Tillett T, Braybrooke J, Ajithkumar T. Management of uncommon chemotherapy-induced emergencies. Lancet Oncol. 2011;12;806-814.
5
Robinson K, Lambiase L, Li J, Monteiro C, Schiff M. Case report: Fatal Cholestatic Liver Failure Associated with Gemcitabine Therapy. Dig Dis Sci.48;1804-1808.
6
Floyd J, Mirza I, Sachs B, Perry MC. Hepatotoxicity of Chemotherapy. Seminar Oncol. 2006;33;50-67.
7
Shah RR, Morganroth J, Shah DR. Hepatotoxicity of Tyrosine Kinase Inhibitors: Clinical and Regulatory Perspectives. Drug Safety. 2013;36;491-503.
8
Llesuy SF, Arnaiz SL. Hepatotoxicity of mitoxantrone and doxorubicin. Toxicology. 1990;63;187-198.
9
Kingwell E, Koch M, Leung B, Isserow S, Geddes J, Rieckmann P, Tremlett H. Cardiotoxicity and other adverse events associated with mitoxantrone treatment for MS. Neurology. 2010;74;1822-1826.
10
Alderton PM, Gross J, Green MD. Comparative Study of Doxorubicin, Mitoxantrone, and Epirubicin in Combination with ICRF-187 (ADR-529) in a Chronic Cardiotoxicity Animal Model. Cancer Res. 1992;52;194-201.
11
Tokarska-Schlattner M, Zaugg M, Zuppinger C, Wallimann T, Schlattner U. New insights into doxorubicin-induced cardiotoxicity: The critical role of cellular energetics. J Mol Cell Cardiol. 2006;41;389-405.
12
Bulucu F, Ocal R, Karadurmus N, Sahin M, Kenar L, Aydin A, Oktenli C, Koc B, Inal V, Yamanel L, Yaman H. Effects of N-Acetylcysteine, Deferoxamine and Selenium on Doxorubicin-Induced Hepatotoxicity. Biol Trace Element Res. 2009;132;184.
13
Injac R, Strukelj B. Recent Advances in Protection against Doxorubicin-induced Toxicity. Technol Cancer Res Treat. 2008;7;497-516.
14
Zhang S, Liu X, Bawa-Khalfe T, Lu L-S, Lyu YL, Liu LF, Yeh ETH. Identification of the molecular basis of doxorubicin-induced cardiotoxicity. Nature Med. 2012;18;1639-1642.
15
Suk KT, Kim DJ. Drug-induced liver injury: present and future. Clin Mol Hepatol. 2012;18;249-257.
16
Stephens C, Andrade RJ, Lucena MI. Mechanisms of drug-induced liver injury. Current Opin Allergy Clin Immunol. 2014;14;286-292.
17
Jones DP, Lemasters JJ, Han D, Boelsterli UA, Kaplowitz N. Mechanisms of pathogenesis in drug hepatotoxicity putting the stress on mitochondria. Mol Intervention. 2010;10;98.
18
Rossato LG, Costa VM, Dallegrave E, Arbo M, Dinis-Oliveira RJ, Santos-Silva A, Duarte JA, de Lourdes Bastos M, Palmeira C, Remião F. Cumulative mitoxantrone-induced haematological and hepatic adverse effects in a subchronic in vivo study. Basic Clin Pharmacol Toxicol. 2014;114;254-262.
19
Bessems M, Tolba R, Doorschodt BM, Leuvenink HGD, Ploeg RJ, Minor T, van Gulik TM, others. The isolated perfused rat liver: standardization of a time-honoured model. Lab Animal. 2006;40;236-246.
20
Ferrigno A, Richelmi P, Vairetti M. Troubleshooting and improving the mouse and rat isolated perfused liver preparation. J pharmacol Toxicol Method. 2012;67;107-114.
21
Heidari R, Rasti M, Shirazi Yeganeh B, Niknahad H, Saeedi A, Najibi A. Sulfasalazine-induced renal and hepatic injury in rats and the protective role of taurine. BioImpacts. 2016;6;3-8.
22
Heidari R, Taheri V, Rahimi HR, Shirazi Yeganeh B, Niknahad H, Najibi A. Sulfasalazine-induced renal injury in rats and the protective role of thiol-reductants. Renal Failure. 2016;38;137-141.
23
Heidari R, Jamshidzadeh A, Niknahad H, Safari F, Azizi H, Abdoli N, Ommati MM, Khodaei F, Saeedi A, Najibi A. The Hepatoprotection Provided by Taurine and Glycine against Antineoplastic Drugs Induced Liver Injury in an Ex Vivo Model of Normothermic Recirculating Isolated Perfused Rat Liver. Trend Pharm Sci. 2016;2;59-76.
24
Heidari R, Sadeghi N, Azarpira N, Niknahad H. Sulfasalazine-Induced Hepatic Injury in an Ex Vivo Model of Isolated Perfused Rat Liver and the Protective Role of Taurine. Pharm Sci. 2015;21.
25
Rossato LG, Costa VM, Dallegrave E, Arbo M, Silva R, Ferreira R, Amado F, Dinis-Oliveira RJ, Duarte JA, Bastos MdL, Palmeira C, Remião F. Mitochondrial Cumulative Damage Induced by Mitoxantrone: Late Onset Cardiac Energetic Impairment. Cardiovas Toxicol. 2014;14;30-40.
26
Heidari R, Jamshidzadeh A, Keshavarz N, Azarpira N. Mitigation of Methimazole-Induced Hepatic Injury by Taurine in Mice. Sci Pharm. 2014;83;143-158.
27
Heidari R, Jamshidzadeh A, Niknahad H, Mardani E, Ommati MM, Azarpira N, Khodaei F, Zarei A, Ayarzadeh M, Mousavi S, Abdoli N, Yeganeh BS, Saeedi A, Najibi A. Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia. Toxicolog Report. 2016;3;870-879.
28
Heidari R, Jafari F, Khodaei F, Shirazi Yeganeh B, Niknahad H. The Mechanism of Valproic Acid-Induced Fanconi Syndrome Involves Mitochondrial Dysfunction and Oxidative Stress in Rat Kidney. Nephrology. 2017;In-Press.
29
Heidari R, Babaei H, Eghbal MA. Cytoprotective Effects of Organosulfur Compounds against Methimazole-Induced Toxicity in Isolated Rat Hepatocytes. Adv Pharm Bull. 2013;3;135-142.
30
Sedlak J, Lindsay R. Estimation of Total, Protein-Bound, and Nonprotein Sulfhydryl Groups in Tissue with Ellmanâs Reagent Analyt Biochem. 1968;25;192-205.
31
Heidari R, Babaei H, Roshangar L, Eghbal MA. Effects of Enzyme Induction and/or Glutathione Depletion on Methimazole-Induced Hepatotoxicity in Mice and the Protective Role of N-Acetylcysteine. Adv Pharm Bull. 2014;4;21-28.
32
Niknahad H, Heidari R, Firuzi R, Abazari F, Ramezani M, Azarpira N, Hosseinzadeh M, Najibi A, Saeedi A. Concurrent Inflammation Augments Antimalarial Drugs-Induced Liver Injury in Rats. Adv Pharm Bull. 2016;6;617â625.
33
Heidari R, Niknahad H, Jamshidzadeh A, Azarpira N, Bazyari M, Najibi A. Carbonyl Traps as Potential Protective Agents against Methimazole-Induced Liver Injury. J Biochem Mol Toxicol. 2015;29;173-181.
34
Moezi L, Heidari R, Amirghofran Z, Nekooeian AA, Monabati A, Dehpour AR. Enhanced anti-ulcer effect of pioglitazone on gastric ulcers in cirrhotic rats: The role of nitric oxide and IL-1b. Pharmacol Rep. 2013;65;134-143.
35
Rodriguez-Frias EA, Lee WM. Cancer Chemotherapy I: Hepatocellular Injury. Clinic Liver Dis. 2007;11;641-662.
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ORIGINAL_ARTICLE
Molecular Docking and Thermodynamic Studies of the Interactions between Aspirinate Complexes of Transition metals and Cyclooxygenase-2 Enzyme: Quantum Chemical Calculations based on the ONIOM method
In the present research, molecular docking and thermodynamic properties of the transition metal complexes of aspirin were calculated against Cyclooxygenase-2 (COX-2) enzyme. Density functional theory with dispersion function (DFT-D) using LANL2DZ basis set calculation was carried out to study the structural and thermodynamic properties of the interaction between aspirinate complexes of transition metals and COX-2. The ONIOM2 (wB97X-D/LANL2DZ:UFF) method was applied to the interaction of transition metal complexes with COX-2 binding site. The Interaction enthalpies and the Gibbs free energies between aspirinate complexes of Cu(II), Zn(II), Fe(III), and In(III) as anti-inflammatory complexes and COX-2 enzyme in the gas phase were calculated. The structure as well as the thermodynamics of optimized metal complexes was debated from the biological point of view. In the gas phase, the interaction was relatively strong and transition metal complexes could be used as potential anti-inflammatory drugs.
https://tips.sums.ac.ir/article_42226_5114ab9b755ac402c4a5bb37cfee521a.pdf
2017-06-01
123
134
Maryam
Mortazavi
maryam_mortazavi5@yahoo.com
1
AUTHOR
Amirhossein
Sakhteman
asakhteman@razi.tums.ac.ir
2
AUTHOR
Anahita
Hessami
3
AUTHOR
Hossein
Sadeghpour
sadeghpurh@sums.ac.ir
4
Department of Medicinal Chemistry, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
LEAD_AUTHOR
ORIGINAL_ARTICLE
The effect of different positively charged silver nanoparticles against bacteria, fungi and mammalian cell line.
The bactericidal efficiency of various positively charged silver nanoparticles has been extensively evaluated in literature, but there is no report on efficacy of various positive charged silver nanoparticles. The goal of this study is to evaluate the role of different positive electrical charge at the surface of silver nanoparticles on antibacterial activity against a panel of microorganisms and their biofilm activities and their cytotoxicity. Four different silver nanoparticles were synthesized by different methods, providing four different electrical surface charges (two ionic liquids (imidazolium and pyridinium) with 12 and 18 alkyl chain length) namely C12Im, C12Py, C18Im and C18Py, respectively. The antibacterial activity of these nanoparticles was tested against gram-positive (i.e., Staphylococcus aureus, Bacillus subtilis), gram-negative (i.e., Escherichia coli and Salmonella typhi) bacteria and Candida albicans as fungi. Disc diffusion and micro-dilution tests were used to evaluate the bactericidal activity of the nanoparticles according to CLSI methods. Also primary cytotoxicity assay of nanosilvers was assessed by MTT test.According to the obtained results, C12Py showed the highest bactericidal activity against all microorganisms tested. C18Im had the least and the C12Im had intermediate antibacterial activity. The most resistant bacteria were Escherichia coli. Different positive surface charge of silver nanoparticles was a significant factor affecting their bactericidal activity. Although the nanoparticles capped with pyridinium and 12 alkyl chains showed the highest level of effectiveness against the organisms tested, the silver nanoparticles capped with imidazolium and 12 alkyl chains were also potent against most bacterial species. Cytotoxicity of the silver nanoparticles was negligible.
https://tips.sums.ac.ir/article_42227_ca9d1a47f44bafd6bf0bf07a97b326e6.pdf
2017-06-01
135
142
Ahmad
Gholami
gholami@sums.ac.ir
1
AUTHOR
Mohammad-Bagher
Ghoshoon
2
AUTHOR
Parisa
Ghafari
3
AUTHOR
Younes
Ghasemi
ghasemiy@sums.ac.ir
4
LEAD_AUTHOR