Publications by authors named "Elham Abbasloo"

9 Publications

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Chronic treatment with apelin, losartan and their combination reduces myocardial infarct size and improves cardiac mechanical function.

Clin Exp Pharmacol Physiol 2020 03 17;47(3):393-402. Epub 2019 Dec 17.

Physiology Research Center, Semnan University of Medical Sciences, Semnan, Iran.

The renin-angiotensin system (RAS) has a deleterious and apelin/APJ system has protective effect on the ischaemic heart. The collaboration between these systems in the pathophysiology of myocardial infarction is not clear. We determined the effect of chronic pretreatment with apelin, losartan and their combination on ischaemia-reperfusion (IR) injury in the isolated perfused rat heart and on the expression of apelin-13 receptor (APJ) and angiotensin type 1 receptor (AT1R) in the myocardium. During 5 days before the induction of IR, saline (vehicle), apelin-13 (Apl), F13A (apelin antagonist), losartan (Los, AT1R antagonist) and the combination of Apl and Los were administered intraperitoneally in rats. Ischaemia was induced by left anterior descending (LAD) artery occlusion for 30 minutes followed by reperfusion for 55 minutes in the Langendorff isolated heart perfusion system. Pretreatment with Apl, Los and the combination of Apl + Los significantly reduced infarct size by about 30, 33 and 48 percent respectively; and significantly improved the left ventricular function indices such as left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP) and rate pressure product (RPP). IR increased AT1R protein level but it did not change APJ significantly. AT1R expression was reduced in groups treated with Apl, Los and Apl + Los. Findings showed that chronic pretreatment with apelin along with AT1R antagonist had more protective effects against IR injury. Combination therapy may diminish the risk of IR-induced heart damage, by reducing AT1R expression, in the heart of patients with coronary artery disease that are at the risk of MI and reperfusion injury.
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http://dx.doi.org/10.1111/1440-1681.13195DOI Listing
March 2020

Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model.

Iran J Immunol 2018 Mar;15(1):14-27

Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.

Background: IGF-1 and certain other cytokines have been shown to exert inflammatory/anti-inflammatory roles in chronic joint diseases.

Objective: To assess the effect of IGF-1, IL-27 and IL-35, their interaction and their receptor expression in a rheumatoid arthritis model.

Methods: Freund's adjuvant-induced chronic joint inflammation was operated on 160 male rats. Animals were divided into histopathology and receptor expression groups, each composed of 10 subgroups including; control, vehicle, IGF-1, IL-27, IL-35, their antagonists, IGF-1+IL-27 antagonist and IGF-1+IL-35 antagonist. After two weeks, vehicle or agonist/antagonists were injected into the joint space every other day until day 28 where joint histopathology was performed. The expression of IGF-1, IL-27 and IL-35 receptors were assessed by western blot analysis.

Results: IGF-1 did not show pro- or anti- inflammatory functions; endogenous IL-27 and IL-35, on the other hand, exerted inflammatory effects. IL-27 and IL-35 antagonists exerted the highest anti-inflammatory effects. The total inflammation scores were 0.55 ± 0.06, 4.63 ± 0.40, 3.63 ± 0.60, 2.50 ± 0.38 and 1.63 ± 0.40 regarding control, vehicle, IGF-1 Ant., IL-27 Ant. and IL-35 Ant., respectively. IGF-1 receptor expression was reduced in chronic joint inflammation and all three antagonists augmented the IGF-1 receptor expression. IL-27 and IL-35 receptors were up-regulated by chronic joint inflammation.

Conclusion: Overall, the results demonstrated the pro-inflammatory role of endogenous IL-27 and IL-35 along with the over expression of their receptors in chronic joint inflammation. IL-27 and IL-35 antagonists exerted the most anti-inflammatory effects and increased IGF-1 receptor expression. These two antagonists may be potential agents for new treatment strategies in chronic joint inflammatory diseases.
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http://dx.doi.org/IJIv15i1A2DOI Listing
March 2018

The Effects of Methanolic Extract of Melissa officinalis on Experimental Gastric Ulcers in Rats.

Iran Red Crescent Med J 2016 Jul 15;18(7):e24271. Epub 2016 May 15.

Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, IR Iran.

Background: Melissa officinalis (MO) has potent antioxidant activity. Recent research has demonstrated the anti-ulcer properties of some medicinal plants through their antioxidant properties.

Objectives: The aim of this study was to evaluate the effects of methanolic extracts of MO on experimental gastric ulcers in rats.

Materials And Methods: Male Wistar rats (200 - 250 g) were starved for 24 hours prior to the induction of gastric ulceration by either indomethacin (48 mg/kg/oral) or water immersion restraint (WIR) stress. Experimental rats received either ranitidine (25 mg/kg) or MO extract (150, 300 and 450mg/kg) orally 2 hours prior to WIR stress or indomethacin treatment, for the evaluation of their gastroprotective effects. The control group received the same volume of saline. Gastric lesions were scored according to the surface of lesions on the ulcer index. Superoxide dismutase (SOD) and glutathione peroxidase (GPX) were determined as measures of antioxidant defense, and malondialdehyde (MDA) was determined to measure tissue oxidation.

Results: MO extract (150 and 300 mg/kg) significantly decreased the ulcer index in both the indomethacin (1.3 ± 0.09 and 1.5 ± 0.19, respectively) and WIR stress groups (1.5 ± 0.17 and 1.5 ± 0.22, respectively), as compared to the control rats (2.5 ± 0.28) (P < 0.01). MO extract (450 mg/kg) significantly reduced ulcer index readings in WIR stress rats (1.8 ± 0.31 vs. 2.4 ± 0.15 in the WIR group), however, MO extract at a dose of 450 mg/kg did not prevent indomethacin-induced gastric ulceration (2.4 ± 0.26). There was no significant difference in the ulcer index for MO extract- (150 and 300 mg/kg) and ranitidine-treated rats (P > 0.05). Also, MO extract (150 and 300 mg/kg) significantly reduced MDA serum levels (0.69 ± 0.6 µmol/L and 0.85 ± 0.24 µmol/L, respectively, vs. 4.5 ± 1.9 µmol/L in the saline group) and significantly increased antioxidants' SOD activities (296.3 ± 146.4 U/mL and 561.4 ± 120 U/mL, respectively, vs. 190.2 ± 63.8U/mL in the control group) and GPX levels (8273 ± 3049 U/mL and 14574 ± 5012 U/mL, respectively), compared to the control (3236 ± 1699 U/mL).

Conclusions: Our results showed that MO extract may have a gastroprotective effect against experimental gastric ulcers in rats. The exact mechanism has not yet been determined, but it may be due to enhancing enzymatic antioxidant defenses and inhibiting lipid peroxidation.
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http://dx.doi.org/10.5812/ircmj.24271DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5020425PMC
July 2016

Induction of antinociceptive tolerance to the chronic intrathecal administration of apelin-13 in rat.

Neuropeptides 2016 Dec 6;60:7-12. Epub 2016 Aug 6.

Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran.

Pain represents a major contributing factor to the individual's quality of life. Although pain killers as opioids, endogenous or exogenous peptides can decrease pain perception, the chronic use of them leads to antinociceptive tolerance. It has been demonstrated that neuropeptide apelin has potent antinoceptive effect. However, the possibility of the induction of its antinociceptive tolerance has not yet been clarified. The tail-flick test was used to assess the nociceptive threshold. All experiments were carried out on male Wistar rats which received intrathecal apelin for 7days. To determine the role of apelin and opioid receptors on the development of apelin analgesic tolerance, their receptor antagonists (F-13 A and naloxone, respectively) were injected simultaneously with apelin. The lumbar spinal cord was assayed to determine apelin receptor levels by the western blotting method. Plasma corticosterone levels were assayed using ELISA. Results showed that apelin (3μg/rat) induced strong thermal antinociception. In addition, chronic apelin produced tolerance to its antinociceptive effect and down regulated spinal apelin receptor. F-13 A and naloxone could inhibit apelin tolerance development. The corticosterone levels did not change following drug administration. Taken together, the data indicated that apelin like other analgesic drugs leads to the induction of side effects such as analgesic tolerance which is mediated partly via the apelin and opioid receptors activation.
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http://dx.doi.org/10.1016/j.npep.2016.08.001DOI Listing
December 2016

The anti-inflammatory properties of Satureja khuzistanica Jamzad essential oil attenuate the effects of traumatic brain injuries in rats.

Sci Rep 2016 08 18;6:31866. Epub 2016 Aug 18.

Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.

Traumatic brain injury (TBI) is a major health concern affecting the general public as well as military personnel. However, there is no FDA-approved therapy for the treatment of TBIs. In this work, we investigated the neurotherapeutic effects of the well-known natural Iranian medicine Satureja Khuzistanica Jamzad (SKJ) essential oil (SKEO) on the outcomes of diffused experimental TBI, with particular attention paid to its anti-inflammatory and anti-apoptotic effects. Male Wistar rats were treated with doses of 50, 100 and 200 (mg/kg, i.p) SKEO after induction of diffused TBIs. The results showed that injecting SKEO (200 mg/kg) 30 minutes after TBI significantly reduced brain oedema and damage to the blood-brain barrier (BBB) and limited the post-TBI increase in intracranial pressure. The veterinary coma scale (VCS) scores significantly improved in the treatment group. Also, inflammatory marker assays showed reduced levels of TNF-α, IL-1β, and IL-6 and increased IL-10 in the treated groups. Moreover, the immunohistochemical results indicated that SKEO not only reduced neuronal death and BBB permeability but also affected astrocytic activation. Overall, our data indicate potential clinical neurological applications for SKEO.
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http://dx.doi.org/10.1038/srep31866DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989136PMC
August 2016

The effect of interleukins 27 and 35 and their role on mediating the action of insulin Like Growth Factor -1 on the inflammation and blood flow of chronically inflamed rat knee joint.

Cytokine 2016 May 17;81:117-26. Epub 2016 Mar 17.

Gastroenterology and Hepathology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran.

Introduction: Previous studies have shown that some cytokines mediate the effect of IGF-1 on inflammation and also association between IGF-1 and vascular endothelial dysfunction. Due to the discrepancies in the inflammatory and anti-inflammatory roles of IL-27 and IL-35, the effects of these cytokines and their IGF-1-mediating role were investigated regarding chronic joint inflammation and synovial blood flow.

Method: Male rats were divided into two main groups of histopathology (n=80) and blood flow (n=72). These were further divided into ten subgroups of control, vehicle, IGF-1, IL-27, IL-35, their antagonists, IGF-1+IL-27 antagonist, and IGF-1+IL-35 antagonist. Inflammation was induced by intra-articular injection of complete Freund adjuvant. Two weeks later (in order to induce chronic inflammation), vehicle or drugs were injected into the joint space every other day until day 28, on which inflammatory indices were assessed histopathologically. In the second subgroups, vehicle or drugs were administered by super-fusion on day 28 and their effects on the joint blood flow (JBF, laser Doppler perfusion method) and the systemic blood pressure were assessed.

Results: Endogenous IL-27 and IL-35 had inflammatory roles and IGF-1 had no effect. IL-27 and IL-35 antagonists had the highest anti-inflammatory and anti-angiogenesis effects and these effects were inhibited by IGF-1. Total inflammation score was 4.5 ± 0.42, 3.50 ± 0.5, 2.25 ± 0.45 and 1.50 ± 0.42 for vehicle, IGF-1 antagonist, IL-27 antagonist and IL-35 antagonist respectively. A significant increase was induced in JBF by IGF-1 antagonist and combination of IGF-1+IL-35 antagonist.

Conclusion: IL-27 and IL-35 antagonists may be suitable goals for the treatment of chronic joint inflammation while their anti-inflammatory effects are not exerted via the changes in JBF.
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http://dx.doi.org/10.1016/j.cyto.2016.03.010DOI Listing
May 2016

The brain cytokine levels are modulated by estrogen following traumatic brain injury: Which estrogen receptor serves as modulator?

Int Immunopharmacol 2015 Sep 22;28(1):279-87. Epub 2015 Jun 22.

Dept. of Biochemistry, Medical School of Afzalipour, Kerman University of Medical Sciences, Kerman, Iran.

The present study was designed to explore whether administration of estrogen affects brain cytokine levels in TBI. We also sought determine which one of type of classical estrogen receptors (ERs) is involved. Ovariectomized female rats were divided in to eight groups. Estrogen or vehicle was administered following TBI (E2 and oil groups). Antagonist of ER(ICI 182, 780) or vehicle was also administered following TBI (ICI and DMSO groups). The ICI or vehicle was administered either before induction of TBI and administration of estrogen (ICI+E2 and DMSO+E2 groups). TBI was induced by Marmarou's method. In addition to brain water content, the levels of brain proinflammatory and anti-inflammatory cytokines were measured 24 hours post- TBI. Present results demonstrated that, estrogen reduced TBI- induced brain edema. The antiedema effect of estrogen was attenuated by ICI. The brain measures of IL-1β, IL-6 and TNF-α in TBI were also reduced by estrogen. The anti-inflammatory effect of estrogen was attenuated by ICI. The inhibition level of estrogen by ICI was 53.2%, 12.09% and 48.45% for IL-1β, IL-6 and TNF-α, respectively. Estrogen also elevated IL-10 in TBI. ICI inversely controlled the effect of estrogen on IL-10, by 33.84%. This effect was not observed once ICI was used alone. The estrogen administration following TBI probably results in proinflammatory cytokines reduction, and inversely enhancement of anti-inflammatory cytokines. In our study, the neuroprotective effect of estrogen is proposed to be mediated by both ERα and ERα, and accordingly the inhibition of neuroprotective effect of estrogen by ICI.
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http://dx.doi.org/10.1016/j.intimp.2015.05.046DOI Listing
September 2015

The Effects of Estrogen Receptors' Antagonist on Brain Edema, Intracranial Pressure and Neurological Outcomes after Traumatic Brain Injury in Rat.

Iran Biomed J 2015 30;19(3):165-71. Epub 2015 May 30.

Physiology Research Center, Institute of Neuropharmacology and Physiology Department, Kerman University of Medical Sciences, Kerman, Iran.

Background: In previous studies, the neuroprotective effect of 17β-estradiol in diffuse traumatic brain injury has been shown. This study used ICI 182,780, a non-selective estrogen receptor antagonist, to test the hypothesis that the neuroprotective effect of 17β-estradiol in traumatic brain injury is mediated by the estrogen receptors.

Methods: The ovariectomized rats were divided into eight groups. Brain injury was induced by Marmarou's method. Estrogen was injected 30 minutes after traumatic brain injury, and ICI 182,780 was injected before traumatic brain injury and also before estrogen treatment. In one group only ICI 182,780 was injected. The brain water content and Evans blue dye content were measured 24 and 5 hours after traumatic brain injury, respectively. The neurologic outcomes and intracranial pressure were assessed before, 4, and 24 hours after traumatic brain injury.

Results: Brain water content and Evans blue content were less in estrogen-treated group comparison to vehicle group. ICI 182,780 eliminated the effects of estrogen on brain edema and brain blood barrier permeability. Intracranial pressure was increased significantly after trauma, and estrogen decreased intracranial pressure at 4 and 24 hours after traumatic brain injury in comparison to vehicle. This inhibitory effect was also eliminated by treatment with ICI182,780. ICI 182,780 also inhibited the estrogen induced increase in neurologic outcomes following traumatic brain injury. However, the use of ICI 182,780 alone had no neuroprotective effect after traumatic brain injury.

Conclusion: The results suggest that classical estrogen receptors have probably a role in the neuroprotective function of estrogen following traumatic brain injury.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571012PMC
http://dx.doi.org/10.7508/ibj.2015.03.006DOI Listing
March 2016