Publications by authors named "Rohollah Hosseini"

14 Publications

  • Page 1 of 1

Biochemical and molecular evidence on the role of vaspin in early detection of the insulin resistance in a rat model of high-fat diet and use of diazinon.

Toxicology 2019 01 22;411:1-14. Epub 2018 Oct 22.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Vaspin, as a newly discovered adipocytokine, can modulate obesity with insulin-sensitizing effects. This study mainly focused on the plasma level of vaspin in insulin resistant rats, which received high-fat diet (HFD) and diazinon (DZN) (70 mg/kg). Upon 30-day experiment, related oxidative stress and inflammatory markers of plasma, the toxic effects of DZN and HFD on the histological structure of the liver, as well as the expression levels of potential genes associated with insulin resistance, phosphatase and tensin homolog (PTEN) and Forkhead box protein O1 (FoxO1) were evaluated. Metabolic parameters implicated to the glucose and insulin statues such as homeostatic model assessment of insulin resistance (HOMA-IR), oral glucose tolerance test (OGTT) and fasting blood glucose (FBG) were determined. DZN significantly inhibited almost 50% of the plasma cholinesterase (ChE) activity. A remarkable increase of MDA level was observed in groups that received DZN and DZN + HFD. Animals treated with DZN or DZN + HFD showed significant changes in reactive oxygen species (ROS) level. The level of plasma tumor Necrosis Factor alpha (TNF-α) was noticeably elevated in the exposed groups. The highest elevation in vaspin level was observed in HFD group followed by DZN treated animals. In all treated groups, insulin level significantly increased and also, the area under the curve (AUC0-180) values of plasma glucose heightened considerably. The histopathological micrographs of HFD + DZN treated group indicated a severe fatty change. The plasma concentration of DZN was significantly higher in the DZN-treated group in comparison to the DZN + HFD group. FoxO1 and PTEN mRNA levels were significantly overexpressed in the DZN and HFD exposed groups. In HFD treated group, PTEN expression significantly increased compared with the DZN and DZN + HFD groups. Consequently, in contrast to oxidative stress and inflammatory biomarkers, vaspin level would be a more reliable diagnostic factor when it comes to the insulin resistance.
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http://dx.doi.org/10.1016/j.tox.2018.10.014DOI Listing
January 2019

The role of minocycline in alleviating aluminum phosphide-induced cardiac hemodynamic and renal toxicity.

Environ Toxicol Pharmacol 2018 Dec 2;64:26-40. Epub 2018 Oct 2.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Poisoning with aluminum phosphide (AlP) has been attributed to the high rate of mortality among many Asian countries. It affects several organs, mainly heart and kidney. Numerous literature demonstrated the valuable effect of minocycline in mitigating pathological symptoms of heart and kidney disease. The aim of the present study was to evaluate the probable protective effect of minocycline on cardiac hemodynamic parameters abnormalities and renal toxicity induced by AlP-poisoning in the rat model. AlP was administered by gavage at 12 mg/kg body weight followed by injection of minocycline for two interval times of 12 and 24 h, at 40, 80, 120 mg/kg body weight. Electrocardiographic (ECG) parameters were monitored, 30 min after AlP gavage for 6 h using an electronic cardiovascular monitoring device. Kidney tissue and serum were collected for the study of histology, mitochondrial complexes I, II, IV, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity, ADP/ATP ratio, mitochondrial cytochrome c release, apoptosis, lactate, BUN, and Cr levels. The results demonstrated that AlP induces ECG abnormalities, and failure of heart rate and blood pressure, which improved significantly by minocycline. Minocycline treatment significantly improved complexes I, IV, MPO and LDH activities, and also reduced the ADP/ATP ratio, lactate level, release of cytochrome c, and apoptosis in the kidney following AlP-poisoning. Also, the histological results showed an improvement of kidney injury in minocycline treated groups. In conclusion, the findings of this study showed that minocycline could improve cardiac hemodynamic abnormalities and kidney injury following AlP-poisoning, suggesting minocycline might be a possible candidate for the treatment of AlP-poisoning.
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http://dx.doi.org/10.1016/j.etap.2018.09.008DOI Listing
December 2018

The protective role of melatonin in chemotherapy-induced nephrotoxicity: a systematic review of non-clinical studies.

Expert Opin Drug Metab Toxicol 2018 09;14(9):937-950

a Department of Toxicology and Pharmacology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.

BSTRACT Introduction: The aim of this study was to investigate the potential role of melatonin in the prevention of chemotherapy-induced nephrotoxicity at the preclinical level. Areas to be covered: To illuminate the possible role of melatonin in preventing chemotherapy-related nephrotoxicity, Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed. A comprehensive search strategy was developed to include PubMed, Web of Science, Scopus, and Embase electronic databases from their inception to May 2018. Based on a set of prespecified inclusion and exclusion criteria, 21 non-clinical articles were ultimately included in the study. Expert opinion: Our findings clearly demonstrate that melatonin has a protective role in the prevention of chemotherapy-induced nephrotoxicity which may be caused by different chemotherapy agents such as cyclophosphamide, cisplatin, doxorubicin, methotrexate, oxaliplatin, etoposide, and daunorubicin. On the basis of current review of non-clinical studies, this protective effect of melatonin is attributed to different mechanisms such as reduction of oxidative stress, apoptosis, and inflammation. The findings presented in this review are based on non-clinical studies and thus conducting appropriate clinical trials to evaluate the real effectiveness of the concurrent use of chemotherapy agents with melatonin in the cancer patients is necessary.
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http://dx.doi.org/10.1080/17425255.2018.1513492DOI Listing
September 2018

Molecular and biochemical evidence on the role of zearalenone in rat polycystic ovary.

Toxicon 2018 Nov 26;154:7-14. Epub 2018 Jul 26.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Globally, food and animal feed contamination with mycotoxins is one of the most important challenges affecting human health. Zearalenone is a non-steroidal mycotoxin with estrogen-like activity that has been reported to induce reproductive dysfunctions including polycystic ovary in women. The aim of this study was to assess the possible impact of prolonged low dose zearalenone (0.1 mg/kg b.w.) exposure to increase the risk of developing polycystic ovary in rats. We found that zearalenone increases the plasma insulin, glucose, testosterone, progesterone and luteinizing hormone levels, while the plasma estradiol level was reduced. Zearalenone also incited tumor necrosis factor-α and the secreted frizzled-related protein-4 expressions. Histological examination showed atresia of follicles in the treated group. It is concluded that zearalenone intoxication intensely manipulates the plasma hormonal factors and the level of gene expressions related to the polycystic ovary in rats, thus increases the risk of its progression.
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http://dx.doi.org/10.1016/j.toxicon.2018.07.022DOI Listing
November 2018

Potentiating role of copper on spatial memory deficit induced by beta amyloid and evaluation of mitochondrial function markers in the hippocampus of rats.

Metallomics 2017 07;9(7):969-980

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, P.O. Box 14155-6451, Tehran, Iran.

Mounting evidence suggests that copper, a crucial element in normal brain function, plays an important role in the etiology of Alzheimer's disease, which is known as a neurodegenerative mitochondrial disorder. However, the precise mechanisms of its effects on cognitive and mitochondrial functions through the CNS have not been thoroughly recognized yet. In this study, we aimed to investigate the long-term (3-week) effects of copper sulfate (50, 100 and 200 mg kg day) exposure on learning and memory as well as on mitochondrial function in the hippocampus of rats in the presence and absence of beta amyloid (1 μg μl per side) intrahippocampally (IH). After three weeks of copper exposure through drinking water, acquisition and retention of spatial memory were measured by the Morris water maze (MWM) test. Various parameters of mitochondrial function were also evaluated. Our data show that copper damaged the spatial learning and memory and also exacerbated the memory deficit induced by Aβ injection in rats in a dose-dependent manner. Mitochondria isolated from the hippocampus of rats treated with copper showed significant increases in ROS formation, mitochondrial swelling, lipid peroxidation, glutathione oxidation, outer membrane damage, and collapse of MMP, decreased cytochrome c oxidase activity, and finally increased ADP/ATP ratios. Our results indicate that copper overloading in the hippocampus of rats causes mitochondrial dysfunction and subsequent oxidative stress leading to cognitive impairment. This study also reveals that copper can potentiate Aβ deleterious effects on spatial memory and brain mitochondrial function.
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http://dx.doi.org/10.1039/c7mt00075hDOI Listing
July 2017

Electrophysiological and molecular mechanisms of protection by iron sucrose against phosphine-induced cardiotoxicity: a time course study.

Toxicol Mech Methods 2015 23;25(4):249-57. Epub 2015 Apr 23.

a Department of Toxicology and Pharmacology, Faculty of Pharmacy and Pharmaceutical Sciences Research Center , Tehran University of Medical Sciences , Tehran , Iran and.

The present study was designed for determining the exact mechanism of cytotoxic action of aluminum phosphide (AlP) in the presence of iron sucrose as the proposed antidote. Rats received AlP (12 mg/kg) and iron sucrose (5-30 mg/kg) in various sets and were connected to cardiovascular monitoring device. After identification of optimum doses of AlP and iron sucrose, rats taken in 18 groups received AlP (6 mg/kg) and iron sucrose (10 mg/kg), treated at six different time points, and then their hearts were surgically removed and used for evaluating a series of mitochondrial parameters, including cell lipid peroxidation, antioxidant power, mitochondrial complex activity, ADP/ATP ratio and process of apoptosis. ECG changes of AlP poisoning, including QRS, QT, P-R, ST, BP and HR were ameliorated by iron sucrose (10 mg/kg) treatment. AlP initiated its toxicity in the heart mitochondria through reducing mitochondrial complexes (II, IV and V), which was followed by increasing lipid peroxidation and the ADP/ATP ratio and declining mitochondrial membrane integrity that ultimately resulted in cell death. AlP in acute exposure (6 mg/kg) resulted in an increase in hydroxyl radicals and lipid peroxidation in a time-dependent fashion, suggesting an interaction of delivering electrons of phosphine with mitochondrial respiratory chain and oxidative stress. Iron sucrose, as an electron receiver, can compete with mitochondrial respiratory chain complexes and divert electrons to another pathway. The present findings supported the idea that iron sucrose could normalize the activity of mitochondrial electron transfer chain and cellular ATP level as vital factors for cell escaping from AlP poisoning.
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http://dx.doi.org/10.3109/15376516.2015.1015086DOI Listing
May 2016

Quantification of verbascoside in medicinal species of Phlomis and their genetic relationships.

Daru 2014 Mar 20;22(1):32. Epub 2014 Mar 20.

Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Background: The genus Phlomis (Lamiaceae) is introduced by its valuable medicinal species, of which 17 species are growing wildly and ten of them are exclusively endemic of Iran. The main phytochemical characteristic of this genus is presence of iridoid glycosides including ipolamide, auroside, lamiide and also phenylethanoids such as verbascoside (acetoside) found in Lamiales order.Due to the broad range of biological and pharmacological activities of verbascoside and lack of any report on quantification of this compound within Iranian species of Phlomis, we conducted a research to achieve two main goals, finding a genetic biodiversity by RAPD (Randomly Amplified Polymorphic DNA), as well as detecting and quantifying verbascoside in nine species of Phlomis growing wildly in Iran.

Results: The results showed that various samples of P.olivieri possess different genetic distances from each other. Also, various species of P.olivieri display close relationships to P.anisodonta and P. persica. Phytoanalysis of Phlomis species by means of TLC scanner using verbascoside as a phytochemical marker showed that the highest concentration of verbascoside was found in P. anisodonta, however, P. bruguieri and P. olivieri (from Mazandaran) were in the second and third places. Interestingly, the lowest concentration of verbascoside was detected in P. olivieri (from Azerbayjan), exhibiting the effect of various growing areas and conditions on the measured levels of this compound.

Conclusions: verbascoside can be found in various species of Iranian Phlomis, of which P. anisodonta, P. bruguieri and P. olivieri might be the best choices. In addition, although the concentration of verbascoside in these plants may be affected by the growing areas and conditions, there are a good agreement between genetic relations and verbascoside levels.
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http://dx.doi.org/10.1186/2008-2231-22-32DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998186PMC
March 2014

In vitro antimicrobial comparison of chlorhexidine, persica mouthwash and miswak extract.

J Contemp Dent Pract 2012 Mar 1;13(2):147-52. Epub 2012 Mar 1.

Department of Periodontics, Dental Material Reseach Center, Mashhad University of Medical Sciences, Iran.

Aim: Herbal mouthwashes, such as persica (Salvadora persica, mint and yarrow extracts) and miswak extract have been shown to decrease gingival inflammation and plaque accumulation. The aim of this study was to compare the antimicrobial activities of persica and miswak extract with the conventional mouthwash chlorhexidine against Streptococcus salivarius, Streptococcus sanguis, Lactobacillus vulgaris and Candida albicans.

Materials And Methods: In this in vitro study, blood-agar culture (Merk, Germany) was used to grow the streptococcus strains, saburd-dextrose culture (Merk, Germany) was used to grow C. albicans and MRS-agar was used to grow L. vulgaris. Various concentrations of these substances (0.1, 0.05 and 0.025% of miswak extract, 0.1, 0.05, 0.025 and 0.0125% of persica, 0.2, 0.1, 0.05 and 0.025% of chlorhexidine) were added to paper disks, separately, inserted into culture plates and transferred into the incubator. The inhibition zone around each disk was measured after 24 hours and the data was analyzed by the Kruskal-Wallis test.

Results: Chlorhexidine possessed antibacterial activity at all concentrations tested. It was more effective than persica and miswak at all concentrations on S. salivarius (p = 0.022 for 0.1%, 0.009 for 0.05 and 0.025%). It had greater effect than the other two tested material on S.sanguis only at concentration 0.01%. Chlorhexidine was the most effective against S.salivarius; persica was the most effective against Lactobacillus (p = 0.005) and the least effective against S. salivarius; and miswak extract was the most effective against S. salivarius and S. sanguis at concentrations 0.1 and 0.05% (p = 0.005) and ineffective against L. vulgaris. None of these mouthwashes were effective against C. albicans.

Conclusion: This study revealed that chlorhexidine remains the gold standard as an antimicrobial agent, although herbal based mouthwashes do have marginal antimicrobial activities. It is necessary to conduct more clinical and microbiological studies focusing on periodontal pathogens and anaerobic microorganisms.

Clinical Significance: Mechanical plaque control is the main way for periodontal disease prevention and mouthrinses are used to improve its efficacy. Based on the results of this study, chlorhexidine has the most antibacterial effect and although persica mouthwash and miswak are routinely used in some Asian countries their antibacterial efficacies are suspected.
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http://dx.doi.org/10.5005/jp-journals-10024-1111DOI Listing
March 2012

Nicotine attenuates spatial learning deficits induced by sodium metavanadate.

Neurotoxicology 2012 Jan 19;33(1):44-52. Epub 2011 Nov 19.

Department of Pharmacology and Toxicology, Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Learning can be severely impaired as a consequence of exposure to environmental pollutants. Vanadium (V), a metalloid which is widely distributed in the environment, has been shown to exert toxic effects on a variety of biological systems including the nervous system. However, studies exploring the impact of vanadium on learning are limited. Herein, we investigated the effects of oral administration of sodium metavanadate (SMV) (15, 20 and 25mg/kg/day for 2weeks) on spatial learning using Morris water maze (MWM). Our results showed that pre-training administration of sodium metavanadate impaired learning in Morris water maze. Analyzing the role of cholinergic system in SMV-induced learning deficit, we found that bilateral intra-hippocampal infusion of nicotine (1μg/side) during training could significantly diminish the SMV-induced learning impairment. We next examined the expression of choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) as cholinergic markers in CA1 region of hippocampus as well as in medial septal area (MSA). Our molecular analyses showed that vanadium administration decreased ChAT and VAChT protein expression, an effect that was attenuated by nicotine. Altogether, our results confirmed the toxic effects of SMV on spatial acquisition, while also pointing to the neuroprotective effects of nicotine on SMV-induced impairments in learning capabilities. These findings might open a new avenue for the prevention of vanadium adverse effects on spatial learning and memory through activation of cholinergic signaling pathway.
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http://dx.doi.org/10.1016/j.neuro.2011.11.004DOI Listing
January 2012

Cholestasis induced nephrotoxicity: the role of endogenous opioids.

Life Sci 2010 Mar 12;86(13-14):488-92. Epub 2010 Feb 12.

Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran.

Aims: Elevated levels of endogenous opioids play a pivotal role in several deleterious consequences of cholestasis. Renal dysfunction occurs in cholestasis but its exact mechanism is still unknown. In this study, we investigated the role of endogenous opioids in cholestasis induced nephrotoxicity.

Main Methods: Thirty-five rats were divided into five groups. In groups 1 and 2 BDL rats received either daily subcutaneous 20mg/kg of naltrexone or its vehicle, for 7days after BDL. In groups 3 and 4, BDL or Sham rats received no injections. In group 5, normal rats received subcutaneous injections of 20mg/kg/day of naltrexone for 7days. At the 7th day, 24h urine was collected to measure urinary N-acetyl-beta-D-glucosaminidase (NAG) as an early marker of renal tubular injury. Kidney samples were then collected for light and electron microscopic studies.

Key Findings: BDL significantly increased NAG activity compared to sham groups. Naltrexone significantly reversed NAG activity to normal levels in BDL animals. Naltrexone treatment in BDL animals also significantly reversed ALT and AST to their normal levels. In light and electron microscopic studies, there were significant structural alterations in BDL samples, which were mostly prevented in naltrexone treated BDL animals.

Significance: Significant changes in urinary NAG activity and renal morphology of cholestatic rats were reversed by naltrexone treatment. These results suggest a possible role for endogenous opioids in inducing cholestatic nephrotoxicity.
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http://dx.doi.org/10.1016/j.lfs.2010.02.005DOI Listing
March 2010

Determination of urinary enzymes as a marker of early renal damage in diabetic patients.

J Clin Lab Anal 2007 ;21(6):413-7

Alborz Hospital, Social Security Organization, Karaj, Iran.

Diagnosis of diabetic nephropathy in the early stages is very important since there are no clinical signs or symptoms. Urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion has been recommended as a tubular dysfunction marker that elevates before other markers, such as microalbuminuria and a decrease in creatinine clearance. In this study, we compared excretion of urinary enzymes with other markers that are used routinely in diabetic nephropathy assessment. Urinary NAG, lactate dehydrogenase (LDH), alkaline phosphatase (AP) activities, urea, creatinine, and albumin, with levels of serum glucose and creatinine and whole blood glycosylated hemoglobin (HbA1c) were measured in 32 diabetes mellitus patients and 25 healthy subjects (controls). Notably, urinary NAG, AP, LDH excretion, and microalbuminuria in the diabetic patients group were significantly increased compared to those in the control groups (P<0.001, P<0.05, P<0.01, and P<0.01, respectively). Meanwhile, our results showed that the urinary NAG excretion had the highest sensitivity and specificity (100% and 87.5%, respectively) compared to other markers. We showed that measuring urinary NAG excretion could be useful for the assessment of renal failure in diabetes mellitus patients and confirmed the use of NAG as a routine screening test.
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http://dx.doi.org/10.1002/jcla.20212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6649252PMC
March 2008

Synthesis and analgesic activity of 2-phenoxybenzoic acid and N-phenylanthranilic acid hydrazides.

Biol Pharm Bull 2006 Jun;29(6):1180-5

Department of Medicinal Chemistry, Faculty of Pharmacy, Islamic Azad University, Tehran, Iran.

A series of 2-phenoxybenzoic acid and N-phenylanthranilic acid hydrazides were synthesized and evaluated for their analgesic activities. Several compounds were significantly more potent than mefenamic acid and diclofenac sodium in abdominal constriction and formalin tests.
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http://dx.doi.org/10.1248/bpb.29.1180DOI Listing
June 2006

Evaluation of oxidative stress and genotoxicity in organophosphorus insecticide formulators.

Hum Exp Toxicol 2005 Sep;24(9):439-45

Laboratory of Toxicology, Department of Toxicology and Pharmacology, Faculty of Pharmacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran.

The aim of this study was to evaluate genotoxicity and oxidative stress in workers who formulate organophosphorus (OP) pesticides. In this survey, blood leukocytes and erythrocytes of a group of 21 pesticide formulating workers and an equal number of control subjects were examined for genotoxicity and oxidative stress parameters. The mean comet tail length and mean comet length were used to measure DNA damage. Lipid peroxidation level, catalase, superoxide dismutase (SOD) and glutathione peroxidase activities in erythrocytes were analysed as biomarkers of oxidative stress. In addition, the acetylcholinesterase activity was measured as a biomarker of toxicity. The average duration of employment of workers in the factory was 97 months. Results indicated that chronic exposure (multiple-dose, greater than or equal to 6 months duration) to OP pesticides was associated with increased activities of catalase, SOD and glutathione peroxidase in erythrocytes. The level of lipid peroxidation and acetylcholinesterase activity did not show any significant differences between the two groups. The results also indicated that chronic exposure to OP pesticides was associated with increased DNA damage. It is concluded that human chronic exposure to OP pesticides may result in stimulated antioxidant enzymes and increased DNA damage in the absence of depressed acetylcholinesterase levels. Routine genotoxicity monitoring concomitant to acetylcholinesterase activity in workers occupationally exposed to OP insecticides is suggested.
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http://dx.doi.org/10.1191/0960327105ht549oaDOI Listing
September 2005

Synthesis and morphine enhancement activity of N-[5-(2-phenoxyphenyl)-1, 3, 4-oxadiazole-2-yl]-N'-phenylurea derivatives.

Arch Pharm (Weinheim) 2004 Apr;337(4):193-200

Department of Medicinal Chemistry and Pharmaceutical Sciences Research Center, Faculty ofPharmacy, Tehran University of Medical Sciences, Tehran, Iran.

The synthesis of N-[5-(2-phenoxyphenyl)-1, 3, 4-oxadiazole-2-yl]-N'-phenylurea derivatives is reported. The structures of these compounds are supported by their IR, (1)H-NMR and mass spectra. Conformational analysis and superimposition of energy minima conformers of these compounds on L-365, 260, a known 3-ureido-1, 4-benzodiazepine CCK-B antagonist, showed that the aromatic rings fell in the same contour. Morphine analgesia enhancement evaluation of the synthesized compounds in comparison with a control group showed that compounds 8a, 8c, 8h-8j, 8l, 8o have significant effects.
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http://dx.doi.org/10.1002/ardp.200300822DOI Listing
April 2004