Publications by authors named "Azam Abareshi"

12 Publications

  • Page 1 of 1

Angiotensin-Converting Enzyme Inhibitor Captopril: Does it Improve Renal Function in Lipopolysaccharide-induced Inflammation Model in Rats.

Saudi J Kidney Dis Transpl 2020 Jul-Aug;31(4):727-738

Neurogenic Inflammation Research Center; Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Renin-angiotensin system as an important regulator of renal function has also a major role in inflammation. In the present study, the effects of captopril on renal dysfunction, renal cytokine levels, and renal tissue oxidative damage were investigated in lipopolysaccharide (LPS)-induced inflammation model in rats. Treatment of five groups of the rats was carried out as follows: (1) saline as a control, (2) LPS 1 mg/kg, and (3-5) 10, 50, or 100 mg/kg captopril 30 min, respectively, before LPS. The treatments were given for 12 days. Finally, the animals were deeply anesthetized, the blood samples were obtained, and the renal tissues were removed and kept for biochemical measurements. Administration of LPS increased serum blood urea nitrogen and creatinine (P < 0.001). Pretreatment with all doses of captopril decreased these parameters (P < 0.001). LPS also increased interleukin-6 (IL-6), malondialdehyde, and nitric oxide metabolites in the renal tissues (P<0.05 - P < 0.001), which was prevented by captopril (P < 0.05 - P < 0.001). The total thiol concentration and superoxide dismutase and catalase activities in the kidney of the LPS group were lower than the control (P < 0.001), while they were enhanced when the animals were cotreated by captopril (P <0.01 - P < 0.001). The results of the present study showed that captopril improved renal function and attenuated tissue oxidative stress in LPS-induced inflammation model in rats.
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http://dx.doi.org/10.4103/1319-2442.292306DOI Listing
July 2021

The effects of captopril on lipopolysaccharide-induced sickness behaviors in rats.

Vet Res Forum 2019 15;10(3):199-205. Epub 2019 Sep 15.

Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Neuro-immune mediators play an important role in the development of sickness behaviors. In the present study, the effect of captopril on sickness behaviors caused by lipopolysaccharide (LPS) was studied in the rats. The animals were randomized into the following groups: control, sham, 10 mg kg captopril - LPS (Capto 10-LPS), 50 mg kg captopril - LPS (Capto 50-LPS), and 100 mg kg captopril - LPS (Capto 100-LPS). Behavioral tests including open-field (OF), elevated plus maze (EPM) and forced swimming (FS) test were performed, and the serum level of interleukin-6 (IL-6) was assessed. In OF, the number of crossings in the central zone in Capto 10-LPS, Capto 50-LPS, and Capto 100-LPS groups was higher than that of the sham group. In EPM, the open arm entry numbers in the sham group were lower compared to the control group. Furthermore, pretreatment by captopril increased the entries to the open arms. In FS test, the immobility time of the sham group was longer than that of the control group. In Capto 10-LPS, Capto 50-LPS, and Capto 100-LPS groups, immobility was shorter compared to the sham group. In addition, the IL-6 level was higher in the sham group compared to the control group, and treatment with 50 and 100 mg kg of captopril restored the IL-6 level in comparison with the sham group. Results confirmed that pretreatment with captopril ameliorated LPS-caused sickness behaviors and attenuated IL-6 as an inflammatory marker in the rats.
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http://dx.doi.org/10.30466/vrf.2018.90760.2198DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6828174PMC
September 2019

HTLV-1 infection-induced motor dysfunction, memory impairment, depression, and brain tissues oxidative damage in female BALB/c mice.

Life Sci 2018 Nov 21;212:9-19. Epub 2018 Sep 21.

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Neurogenesis-inflammation Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Aims: The HTLV-1 infection is associated with a neuro-inflammatory disease. In the present study, the behavioral consequences and brain oxidative damages were evaluated in HTLV-1-infected BALB/c mice.

Material And Methods: 20 female BALB/c mice were divided into two groups comprising control and HTLV-1-infected. The HTLV-1-infected group was inoculated with a 10 MT-2 HTLV-1-infected cell line. Two months later, the behavioral tests were conducted. Finally, oxidative stress was assessed in the cortex and hippocampus tissues.

Key Findings: In the HTLV-1-infected group, running time and latency to fall, travel distance and time spent in the peripheral zone, total crossing number and total traveled distance in open field test, the latency of entrance into the dark compartment in the passive avoidance test, the new object exploration percentage, and discrimination ratio were significantly lower than in the control group. The immobility time, time spent in the dark compartment in passive avoidance test, and total exploration time significantly increased in the HTLV-1-infected group compared to the control group. In the cortical tissue of the HTLV-1 group, the malondialdehyde levels were elevated while the total thiol levels decreased in comparison to the control group. The activity of superoxide dismutase in the cortical and hippocampal tissues, and catalase activity in cortical tissue significantly decreased in the HTLV-1 group in comparison to the control group.

Significance: The HTLV-1 infection seems to induce depression-like behavior, motor dysfunction, disruption in working and fear memory and also oxidative stress in the cortex and hippocampus.
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http://dx.doi.org/10.1016/j.lfs.2018.09.031DOI Listing
November 2018

prevented liver and renal tissue damage in lipopolysaccharide-treated rats.

Saudi J Kidney Dis Transpl 2018 May-Jun;29(3):554-566

Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Liver and renal dysfunction accompanying with the tissues' oxidative damage has been reported to occur during Inflammation. Nigella sativa has been well known for its antioxidant and anti-inflammatory effects. The aim of this study was to investigate preventive effects of N. sativa on liver and renal tissue damage in lipopolysaccharide (LPS) -treated rats. The rats were divided into five groups: (1) control; (2) LPS (1 mg/kg, IP, for 10 days), (3-5) N. sativa hydroethanolic extract (100, 200, or 400 mg/kg) before LPS. Compared to LPS group, treatment by the extract decreased alondialdehyde, nitric oxide (NO) metabolites, and interleukin-6 while increased thiol content and superoxide dismutase and catalase activities in both renal and liver tissues. N. sativa extract also decreased serum aspartate aminotransferase, alanine aminotrans-ferase, and alkaline phosphatase concentration, while it increased serum protein and albumin compared with LPS group. In LPS group, serum blood urea nitrogen and creatinine were higher than control group. The extract reversed the negative effects of LPS. The results demonstrated that the N. sativa prevented liver and renal tissue damage in LPS-treated rats. It is suggested that the effects are due to its antioxidant and anti-inflammatory effects.
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http://dx.doi.org/10.4103/1319-2442.235184DOI Listing
October 2019

The effect of captopril on lipopolysaccharide-induced lung inflammation.

Exp Lung Res 2018 May - Jun;44(4-5):191-200. Epub 2018 May 30.

a Neurogenic Inflammation Research Centre, Mashhad University of Medical Sciences , Mashhad , Iran.

Purpose: As an angiotensin converting enzyme (ACE) inhibitor, the effects of captopril on inflammation has been previously examined. Captopril has been shown to have anti-inflammatory and antioxidant effects. Imbalance in the oxidant/antioxidant system is one of the major causes of inflammation. In the present study, the effects of captopril on total and differential white blood cells (WBC), oxidative stress andlung histopathological changes produced by lipopolysaccharide (LPS) were investigated in rat.

Materials And Method: The rats were divided into: control (saline-treated), LPS (1 mg/kg), 12.5, 25 or 50 mg/kg captopril-treated before LPS administration (LPS+Cap12.5, LPS+Cap25 and LPS+Cap50) and Cap-treated, 50 mg/kg before saline administration (as positive control group)groups. The levels of total and percentage of differential WBC in blood, and the oxidative stress index in the serum were evaluated. Lung histopathological changes were also examined.

Results: In the LPS group, total WBC count, percentage of neutrophils, basophils, eosinophils, and monocytes in the blood, oxidative stress indices in serum, lung pathological changes were significantly higher than the control group (p < 0.05 to p < 0.001). Pathological changes of lung, serum oxidative stress indices of LPS+Cap50 group, total WBC counts of LPS+Cap25 and LPS+Cap50 groups, as well as percentage of neutrophils, monocytes, and basophils in LPS+Cap50 group and percentage of eosinophils in LPS+Cap50 and LPS+Cap25 groups, were significantly decreased compared to the LPS group (p < 0.05 to p < 0.001).

Conclusion: The results of this study showed that captopril dose-dependently reduced total and differential WBC counts, while it improved serum oxidant/antioxidant biomarkers and histopathological changes in LPS-treated rats. These results indicate a therapeutic potential for captopril on systemic inflammation and oxidative stress against LPS-induced lung injuries.
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http://dx.doi.org/10.1080/01902148.2018.1473530DOI Listing
February 2019

Protective effects of on synaptic plasticity impairment induced by lipopolysaccharide.

Vet Res Forum 2018 15;9(1):27-33. Epub 2018 Mar 15.

Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

In the present study the protective effect of () on synaptic plasticity impairment induced by lipopolysaccharide (LPS) in rats was investigated. Fifty-eight rats were grouped and treated as follows: 1) control (saline), 2) LPS, 3) LPS, and 4) In a Morris water maze test, the escape latency and traveled path to find the platform as well as time spent and the traveled distance in target quadrant (Q) were measured. Long term potentiation (LTP) from CA area of hippocampus followed by high frequency stimulation to Schafer collateral was studied and slope, slope 10-90% and amplitude of field excitatory field potential (fEPSP) were calculated. The escape latency and traveled path in LPS group were significantly higher than those in the control group while, in LPS group these parameters were significantly lower than those in LPS group. The rats in LPS group spent less time and traveled shorter distance in Q than the rats in the control group while, in LPS group the rats spent more time and traveled longer distance than the rats in LPS group. LPS significantly decreased slope, slope 10-90% and amplitude of fEPSP while, in LPS group these parameters increased compared to LPS group. The results indicated that the hydro-alcohol extract of protected against synaptic plasticity and spatial learning and memory impairment induced by LPS in rats.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5913558PMC
March 2018

Memory enhancing effect of Nigella Sativa hydro-alcoholic extract on lipopolysaccharide-induced memory impairment in rats.

Drug Chem Toxicol 2019 May 28;42(3):270-279. Epub 2018 Mar 28.

g Department of Physiology, School of Medicine , Jiroft University of Medical Sciences , Jiroft , Iran.

In this study, the effects of Nigella Sativa (NS) hydro-alcoholic extract on lipopolysaccharide (LPS)-induced learning and memory impairments, hippocampal cytokine levels, and brain tissues oxidative damage were investigated in rats. The rats were grouped and treated: (1) control (saline), (2) LPS (1 mg/kg i.p.), and (3-5) 100, 200, or 400 mg/kg NS hydro-alcoholic extract 30 min before LPS injection. The treatment was started since 6 days before the behavioral experiments and continued during the behavioral tests (LPS injection 2 h before each behavioral experiment). Finally, the brains were removed for biochemical assessments. In Morris water maze (MWM) test, LPS increased the escape latency and traveled path compared to control group, whereas all doses of NS hydro-alcoholic extract decreased them compared to LPS group. In passive avoidance (PA) test, the latency to enter the dark compartment in LPS group was shorter than control group while in all treated groups it was longer than LPS group. LPS increased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), and nitric oxide (NO) metabolites, and decreased thiol content, superoxide dismutase (SOD), and catalase (CAT) in the hippocampal tissues compared to control group while NS hydro-alcoholic extract decreased MDA and NO metabolites and increased thiol content, SOD, and CAT compared to LPS group. Findings of the current study indicated that the hydro-alcoholic extract of NS improved the LPS-induced learning and memory impairments induced by LPS in rats by improving hippocampal cytokine levels and brain tissues oxidative damage.
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http://dx.doi.org/10.1080/01480545.2018.1447578DOI Listing
May 2019

Effect of Angiotensin-converting Enzyme Inhibitor on Cardiac Fibrosis and Oxidative Stress Status in Lipopolysaccharide-induced Inflammation Model in Rats.

Int J Prev Med 2017 6;8:69. Epub 2017 Sep 6.

Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Background: Renin-angiotensin (Ang)-aldosterone system not only plays a key role in the regulation of circulatory homeostasis, but also it acts as a powerful pro-inflammatory mediator. The aim of this study was to evaluate the effect of captopril (Cap), a known Ang-converting enzyme inhibitor, on inflammation-induced cardiac fibrosis, and heart oxidative stress status in lipopolysaccharide (LPS)-induced inflammation in male rats.

Methods: Fifty male rats were randomly divided into five groups control, LPS (1 mg/kg/day), LPS + Cap 10 mg/kg, LPS + Cap 50 mg/kg and LPS + Cap 100 mg/kg. After 2 weeks, blood samples were taken, and hearts were harvested for evaluation of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide metabolite in serum and tissue hemogenate, histopathology (hematoxylin and eosin and Masson's trichrome) and oxidative stress status.

Results: Serum IL-6 and TNF-α concentration were higher in LPS group compared to control and Cap reduced them, significantly. Heart TNF-α and IL-6 contents in LPS group were significantly higher than control ( < 0.05). The administration of Cap significantly decreased inflammatory markers level to control ( < 0.05). The higher levels of malondialdehyde and lower antioxidative markers (total thiol, superoxide dismutase, and catalase) in the heart were observed in LPS group and treatment by Cap improved them, dose-dependently. Histopathological study revealed cardiac fibrosis and more collagen content in LPS group which significantly improved by Cap treatment.

Conclusions: Treatment by Cap reduced cardiac fibrosis possibly through improving oxidative stress status, and it can be considered to increase cardiac compliance in this condition.
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http://dx.doi.org/10.4103/ijpvm.IJPVM_322_16DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609356PMC
September 2017

The effect of on inflammation-induced myocardial fibrosis in male rats.

Res Pharm Sci 2017 Feb;12(1):74-81

Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, I.R. Iran.

(NS) () used as a protective and therapeutic traditional medicine. This study evaluates the effect of NS on inflammation-induced myocardial fibrosis, serum and tissue inflammatory markers, and oxidative stress status in male rats. Fifty male Wistar rats were divided into five groups: (1) control; (2) lipopolysaccharide (LPS), 1 mg/kg/day; (3) LPS + NS (hydroalcoholic extract), 100 mg/kg/day; (4) LPS + NS, 200 mg/kg/day; (5) LPS + NS, 400 mg/kg/day (n = 10 in each group). The duration of LPS administration was two weeks. At the end of the experiment, blood samples were taken and ventricles were homogenized and stained for histological evaluation. Serum nitrite levels were lower in LPS group than the control group (22.98 ± 1.03 vs 28.5 ± 0.93 μmol/L), in which they were significantly increased by NS treatment ( < 0.05). Higher levels of heart interlukine-6 (IL-6) and tumor necrosis factor-α (TNF-α) were observed in LPS group compared to the controls (IL-6: 6805 ± 656 vs 4733 ± 691 pg/mL; TNF-α: 6504 ± 501 vs 5309 ± 452 pg/mL), in which they were reduced by NS 400 mg/kg compared to LPS groups ( < 0.05). A significant increment of malondialdehyde and reduction in heart total thiol, superoxide dismutase and catalase concentrations were observed in LPS group (p < 0.05) which significantly restored with treatment by three doses of NS. Histopathological studies showed higher inflammatory cell infiltrates, cardiac fibrosis, and collagen deposition in LPS group, which were reduced by the administration of NS. Treatment by NS reduced myocardial fibrosis in inflammation-induced fibrosis, possibly through improving oxidative/anti-oxidative balance.
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http://dx.doi.org/10.4103/1735-5362.199050DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5333483PMC
February 2017

Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril.

Adv Med 2016 18;2016:7676512. Epub 2016 Oct 18.

Neurocognitive Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Renin-angiotensin system has a role in inflammation and also is involved in many brain functions such as learning, memory, and emotion. Neuroimmune factors have been proposed as the contributors to the pathogenesis of memory impairments. In the present study, the effect of captopril on spatial memory and synaptic plasticity impairments induced by lipopolysaccharide (LPS) was investigated. The rats were divided and treated into control (saline), LPS (1 mg/kg), LPS-captopril (LPS-Capto; 50 mg/kg captopril before LPS), and captopril groups (50 mg/kg) before saline. Morris water maze was done. Long-term potentiation (LTP) from CA1 area of hippocampus was assessed by 100 Hz stimulation in the ipsilateral Schaffer collateral pathway. In the LPS group, the spent time and traveled path to reach the platform were longer than those in the control, while, in the LPS-Capto group, they were shorter than those in the LPS group. Moreover, the slope and amplitude of field excitatory postsynaptic potential (fEPSP) decreased in the LPS group, as compared to the control group, whereas, in the LPS-Capto group, they increased compared to the LPS group. The results of the present study showed that captopril improved the LPS-induced memory and LTP impairments induced by LPS in rats. Further investigations are required in order to better understand the exact responsible mechanism(s).
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http://dx.doi.org/10.1155/2016/7676512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5088279PMC
October 2016

The effects of captopril on lipopolysaccharide induced learning and memory impairments and the brain cytokine levels and oxidative damage in rats.

Life Sci 2016 Dec 26;167:46-56. Epub 2016 Oct 26.

Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.

Aim: Renin-angiotensin system has a role in inflammation and also involves in learning and memory. In the present study, the effects of captopril on lipopolysaccharide (LPS) induced learning and memory impairments, hippocampal cytokine levels and brain tissues oxidative damage was investigated.

Materials And Methods: The rats were divided and treated : [1] saline (Control), [2] LPS (1mg/kg), [3-5] 10, 50 or 100mg/kg captopril 30min before LPS. The treatment was started since six days before the behavioral experiments and continued during the behavioral tests (LPS injection two h before each behavioral experiment).

Results: Administration of LPS prolonged the escape latency and traveled path to find the platform in Morris water maze (MWM) test (P<0.01-P<0.001) while, shortened the latency to enter the dark compartment in passive avoidance (PA) test (P<0.001). Pretreatment by all doses of captopril improved performances of the rats in MWM (P<0.05-P<0.001) and also prolonged the latency to enter the dark in PA test (P<0.001). LPS also increased IL-6, TNF-α, malondialdehyde (MDA) and nitric oxide(NO) metabolites in the hippocampal tissues (P<0.05-P<0.001) which were prevented by captopril (P<0.05-P<0.001). The thiol, superoxide dismutase(SOD) and catalase(CAT) in the hippocampus of LPS group were lower than the control (P<0.001) while, they were enhanced when the aniamls were pretraeted by captopril (P<0.01-P<0.001).

Conclusion: The results of present study showed that captopril improved the LPS-induced learning and memory impairments in rats which were accompanied with attenuating hippocampal cytokine levels and improving the brain tissues oxidative damage criteria.
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http://dx.doi.org/10.1016/j.lfs.2016.10.026DOI Listing
December 2016

The effects of Nigella sativa on sickness behavior induced by lipopolysaccharide in male Wistar rats.

Avicenna J Phytomed 2016 Jan-Feb;6(1):104-16

Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Objective: Neuroimmune factors contribute on the pathogenesis of sickness behaviors. Nigella sativa (NS) has anti-inflammatory, anti-anxiety and anti-depressive effects. In the present study, the effect of NS hydro-alcoholic extract on sickness behavior induced by lipopolysaccharide (LPS) was investigated.

Materials And Methods: The rats were divided into five groups (n=10 in each): (1) control (saline), (2) LPS (1 mg/kg, administered two hours before behavioral tests), (3-5) LPS-Nigella sativa 100 , 200 and 400 mg/kg (LPS-NS 100, LPS-NS 200 and LPS-NS 400, respectively). Open- field (OF), elevated plus maze (EPM) and forced swimming test (FST) were performed.

Results: In OF, LPS reduced the peripheral crossing, peripheral distance, total crossing and total distance compared to control (p<0.01- p<0.001). The central crossing, central distance and central time in LPS-NS 100, LPS-NS200 and LPS-NS 400 groups were higher than LPS (p<0.01- p<0.001). In EPM, LPS decreased the open arm entries, open arm time and closed arm entries while increased the closed time compared to control (p<0.001). Pretreatment by NS extract reversed the effects of LPS (p<0.05- p<0.001). In FST, LPS increased the immobility time while, decreased the climbing and active times compared to control (p<0.05- p<0.001). In LPS-NS 100, LPS-NS 200 and LPS-NS 400 groups the immobility time was less while, the active and climbing times were more than those of LPS (p<0.05- p<0.001).

Conclusion: The results of the present study showed that the hydro-alcoholic extract of NS reduced the LPS-induced sickness behaviors in rats. Further investigations are required for better understanding the responsible compound (s) and the underlying mechanism(s).
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884223PMC
June 2016