Publications by authors named "Kowsar Bavarsad"

10 Publications

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Human T-Cell Leukemia Virus Type 1 Changes Leukocyte Number and Oxidative Stress in the Lung and Blood of Female BALB/c Mice.

Adv Biomed Res 2021 30;10. Epub 2021 Jan 30.

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Background: Human T-cell leukemia virus type 1(HTLV-1) infection is likely to induce nonneoplastic inflammatory pulmonary diseases. Therefore, an experimental study was conducted to evaluate the leukocytes' number alteration and oxidative stress in the lung and blood of HTLV-1-infected BALB/c mice, which could be of benefit for the recognition of HTLV-1 mechanism in the induction of pulmonary disorders.

Materials And Methods: Twenty female BALB/c mice were divided into two groups of control and HTLV-1-infected animals. The HTLV-1-infected group was inoculated with 10 MT-2 HTLV-1-infected cells. Two months later, the infection was confirmed using real-time polymerase chain reaction, and then lung pathological changes, total and differential inflammatory cell counts in the blood and bronchoalveolar lavage fluid (BALF), along with oxidative stress biomarker levels in the BALF and lung tissue were evaluated.

Results: In the HTLV-1-infected group, the peribronchitis score ( < 0.01), the number of total leukocytes, neutrophils, lymphocytes, and monocytes ( < 0.05) in the blood and BALF were increased. The number of eosinophils in the blood of the HTLV-1-infected group was higher than in the control group ( < 0.01), whereas the number of basophils of BALF was increased in the HTLV-1-infected group ( < 0.001). The lung and BALF oxidative stress results showed that the MDA level was increased, while the total thiol level and superoxide dismutase activity were decreased in the HTLV-1-infected group ( < 0.01).

Conclusion: The HTLV-1 infection seems to induce pulmonary inflammatory reactions by recruiting leukocytes as well as inducing oxidative stress in the lung tissue.
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http://dx.doi.org/10.4103/abr.abr_117_20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8095261PMC
January 2021

Effects of levothyroxine on lung inflammation, oxidative stress and pathology in a rat model of Alzheimer's disease.

Respir Physiol Neurobiol 2020 06 5;277:103437. Epub 2020 Apr 5.

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

Background: In this study, the effect of levothyroxine (L-T4) on tracheal responsiveness, lung inflammation, oxidative stress and pathological features in a rat model of Alzheimer's disease (AD), was evaluated.

Methods: An animal model of AD was established by intracerebroventricular injection of streptozotocin (STZ) (3 mg/kg) in rats. The rats were then treated for 3 weeks with L-T4 (10 and 100 μg/kg).

Results: In AD animals, tracheal responsiveness to methacholine and ovalbumin (p < 0.05), white blood cell (WBC) count (p < 0.05 to p < 0.01), malondialdehyde (MDA) concentration (p < 0.05) and inflammation score (p < 0.01) were increased, but superoxide dismutase (SOD) activity and total thiol content (for both cases p < 0.05) were decreased compared to the controls. Tracheal responsiveness to methacholine and MDA concentration (p < 0.05) were decreased in AD animals treated with T4 compared to the AD group. Bronchial inflammation in terms of total and some differential WBC in the BALF and inflammatory score, was significantly worsened in AD animals treated with high dose of T4 (p < 0.05 to p < 0.001) compared to the controls.

Conclusion: Alzheimer's disease may cause lung inflammation and treatment with low dose of T4 improved MDA level and lung inflammation.
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http://dx.doi.org/10.1016/j.resp.2020.103437DOI Listing
June 2020

Voluntary exercise and estradiol reverse ovariectomy-induced spatial learning and memory deficits and reduction in hippocampal brain-derived neurotrophic factor in rats.

Pharmacol Biochem Behav 2019 12 5;187:172819. Epub 2019 Nov 5.

Laboratory of Learning and Memory, Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran; Department of Physiology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Electronic address:

Ample evidences have demonstrated the beneficial effects of physical exercise on cognitive functions such as learning and memory. It is well established that female sex hormones have an important role in regulating learning and memory. This study was designed to investigate the effects of voluntary exercise and estrogen replacement on learning and memory deficits and reduction in hippocampal brain derived neurotrophic factor (BDNF) levels induced by ovariectomy. Ovariectomized rats were given daily vehicle or 17 β-estradiol (20 μg/kg) and allowed to freely exercise in a running wheel over the course of 2 weeks. After this period, they were trained and tested on a water-maze spatial task for 5 consecutive days, followed by a probe test one day later. At the end of the behavioral tests, all animals were decapitated and their hippocampal levels of BDNF were measured. Ovariectomy impaired spatial learning and memory and reduced hippocampal BDNF levels. Exercise significantly improved performance during both training and the retention of the water-maze task and increased hippocampal BDNF. Exercise, 17 β-estradiol and their combination recovered the impairing effects of ovariectomy on learning and memory performance. The combined treatment did not produce stronger effect than either exercise or 17 β-estradiol alone. Our findings provide an important evidence about positive influences of regular exercise and estrogen treatment against cognitive and BDNF deficits induced in ovariectomized rats, an experimental model of menopause.
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http://dx.doi.org/10.1016/j.pbb.2019.172819DOI Listing
December 2019

The effects of thyroid hormones on memory impairment and Alzheimer's disease.

J Cell Physiol 2019 Jan 24. Epub 2019 Jan 24.

Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

Thyroid hormones (THs) have a wide and important range of effects within the central nervous system beginning from fetal life and continuing throughout the adult life. Thyroid disorders are one of the major causes of cognitive impairment including Alzheimer's disease (AD). Several studies in recent years have indicated an association between hypothyroidism or hyperthyroidism and AD. Despite available evidence for this association, it remains unclear whether thyroid dysfunction results from or contributes to the progression of AD. This review discusses the role of THs in learning and memory and summarizes the studies that have linked thyroid function and AD. Eventually, we elaborate how THs may be effective in treating AD by putting forward potential mechanisms.
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http://dx.doi.org/10.1002/jcp.28198DOI Listing
January 2019

Protective effects of curcumin against ischemia-reperfusion injury in the liver.

Pharmacol Res 2019 03 15;141:53-62. Epub 2018 Dec 15.

Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address:

Liver ischemia/reperfusion (I/R) injury is a major complication of hepatic surgery and transplantation. It is one of the leading causes of morbidity and mortality because of post-surgery hepatic dysfunction. Several studies have suggested different mechanisms are involved in the pathogenesis of I/R injury in the liver that includes oxidative stress, inflammation, mitochondria dysfunction, liver Kupffer cells (KCs) activation, vascular cell adhesion molecule overexpression, and facilitation of polymorphonuclear neutrophil injury. Curcumin is a natural product extracted from Curcuma longa that is known to suppress these pathways and as a result reduces liver ischemia-reperfusion injury. This paper gives an overview of the protective effects of curcumin against I/R injury in the liver and discusses the studies that have linked biological functions of curcumin with liver I/R injury improvement.
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http://dx.doi.org/10.1016/j.phrs.2018.12.014DOI Listing
March 2019

Protective Effects of Curcumin Against Ischemia-Reperfusion Injury in the Nervous System.

Mol Neurobiol 2019 Feb 9;56(2):1391-1404. Epub 2018 Jun 9.

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

Ischemia-reperfusion injury (I/R injury) is a common feature of ischemic stroke which occurs when blood supply is restored after a period of ischemia. Although stroke is an important cause of death in the world, effective therapeutic strategies aiming at improving neurological outcomes in this disease are lacking. Various studies have suggested the involvement of different mechanisms in the pathogenesis of I/R injury in the nervous system. These mechanisms include oxidative stress, platelet adhesion and aggregation, leukocyte infiltration, complement activation, blood-brain barrier (BBB) disruption, and mitochondria-mediated mechanisms. Curcumin, an active ingredient of turmeric, can affect all these pathways and exert neuroprotective activity culminating in the amelioration of I/R injury in the nervous system. In this review, we discuss the protective effects of curcumin against I/R injury in the nervous system and highlight the studies that have linked biological functions of curcumin and I/R injury improvement.
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http://dx.doi.org/10.1007/s12035-018-1169-7DOI Listing
February 2019

Effects of levothyroxine on learning and memory deficits in a rat model of Alzheimer's disease: the role of BDNF and oxidative stress.

Drug Chem Toxicol 2020 Jan 21;43(1):57-63. Epub 2018 Jun 21.

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

The effect of levothyroxine (L-T4) on the learning and memory impairment induced by streptozotocin (STZ) and brain tissue oxidative damage in rats was evaluated. An animal model of the Alzheimer's disease (AD) was established by intracerebroventricular injection of STZ (3 mg/kg) in male Wistar rats (250 ± 50 g). After that, the rats were treated for 3 weeks with L-T4 (10, 100 μg/kg) or normal saline. Passive avoidance (PA) learning and spatial memory were evaluated using shuttle box and Morris water maze (MWM), respectively. Finally, the rats were euthanized, their blood samples were collected for further thyroxine assessment and their brains were removed after decapitation in order to measure the oxidative stress parameters and brain-derived neurotrophic factor (BDNF). In the MWM, latency (s) increased in the AD rats compared with the normal control group while it decreased in the 10 μg/kg L-T4 injected AD rats compared with the AD group. In the PA, the latency for entering the dark compartment was lower in the AD group than in the normal control group and it decreased in the 10 μg/kg L-T4 injected AD rats. The low dose of L-T4 (10 μg/kg) reduced malondialdehyde concentration but increased thiols concentration, superoxide dismutase, catalase activities and BDNF level in hippocampal tissues of the AD rats. Injection of L-T4 (10 μg/kg) alleviated memory deficits and also improved factors of oxidative stress and BDNF level in the STZ-induced AD rats.
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http://dx.doi.org/10.1080/01480545.2018.1481085DOI Listing
January 2020

A comparison of the effects of seeds hydro-alcoholic extract and Vitamin C on biochemical, hemodynamic and functional parameters in cardiac tissue of rats with subclinical hyperthyroidism.

Avicenna J Phytomed 2018 Mar-Apr;8(2):161-169

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

Objective: The present study was performed to evaluate the effects of hydro-alcoholic extract of () seeds and Vitamin C on biochemical and hemodynamic parameters in cardiac tissue of rats with subclinical hyperthyroidism.

Materials And Methods: Forty eight male rats were divided into six groups of 8 and treated for 4 weeks. T4 group received daily injection of levothyroxine sodium (20 μg/kg) and control group was given daily injection of saline. T4-Po groups were given T4 plus 100, 200, and 400 mg/kg of seeds extract in drinking water daily. T4-Vit C group received T4 plus daily injection of Vitamin C (100 mg/kg). At the end of the experiment, body weight, serum free T4 level, left ventricular developed pressure (LVDP), malondialdehyde (MDA) and total thiol levels were measured.

Results: Free T4 levels were increased in all groups that were treated with T4. Weight gain was decreased in T4 and T4-Po100 groups compared to control group (p<0.001 and p<0.05). However, body weight was increased in T4-Po (200 and 400) and T4-Vit C groups compared to T4 group. LVDP was increased in T4 group compared to control group but, LVDP was decreased in T4-Po and T4-Vit C groups. Malondialdehyde was decreased in T4-Po groups and T4-Vit C group compared to T4 group. Total thiol groups were increased in T4-Po (200 and 400) and T4-Vit C groups compared to T4 group.

Conclusion: The results showed that extract has a protective effect on cardiac dysfunction due to subclinical hyperthyroidism induced by levothyroxine sodium in rats.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5885330PMC
April 2018

Gallic acid prevents memory deficits and oxidative stress induced by intracerebroventricular injection of streptozotocin in rats.

Pharmacol Biochem Behav 2013 Oct 11;111:90-6. Epub 2013 Sep 11.

Department of Pharmacology, School of Medicine, Physiology and Atherosclerosis Research Centers, Ahvaz Jundishapur Univ. of Med. Sciences (AJUMS), Ahvaz, Iran. Electronic address:

In the present study, we evaluated the effects of gallic acid (GA; 30 mg/kg, orally, once daily for 26 days starting from day 5 prior to streptozotocin injection) on cognitive impairment and cerebral oxidative stress induced by intracerebroventricular-streptozotocin (ICV-STZ; bilaterally, two doses of 3 mg/kg) injection as an animal model of sporadic Alzheimers type (SDAT) in rats. The results showed that ICV-STZ-injection reduced the passive avoidance and spatial memory performance associated with decreased non-enzymatic [total thiol concentration, -58.5%, -50.7%] and enzymatic [superoxide dismutase (SOD, -30.2%, -32.9%), catalase (CAT, -43.5%, -50.7%), glutathione peroxidase (GPx, -57.1%, -61.7%)] activities and increased the level of thio-barbituric acid reactive species (TBARS, +103.5%, +82.5%) in the hippocampus and cerebral cortex, respectively. In contrast, chronic administration of GA significantly prevented cognitive deficits and biochemical alterations in the ICV-STZ rats. These findings highlight the beneficial role of GA in the ICV-STZ rats via enhancement of cerebral antioxidant defense system. Thus, it may have a therapeutic value for the treatment of SDAT.
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http://dx.doi.org/10.1016/j.pbb.2013.09.002DOI Listing
October 2013

Voluntary exercise does not ameliorate spatial learning and memory deficits induced by chronic administration of nandrolone decanoate in rats.

Horm Behav 2013 Jan 12;63(1):158-65. Epub 2012 Oct 12.

Laboratory of Learning and Memory, Research Center and Department of Physiology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.

Chronic exposure to the anabolic androgenic steroids (AAS) nandrolone decanoate (ND) in supra-physiological doses is associated with learning and memory impairments. Given the well-known beneficial effects of voluntary exercise on cognitive functions, we examined whether voluntary exercise would improve the cognitive deficits induced by chronic administration of ND. We also investigated the effects of ND and voluntary exercise on hippocampal BDNF levels. The rats were randomly distributed into 4 experimental groups: the vehicle-sedentary group, the ND-sedentary group, the vehicle-exercise group, and the ND-exercise group. The vehicle-exercise and the ND-exercise groups were allowed to freely exercise in a running wheel for 15 days. The vehicle-sedentary and the ND-sedentary groups were kept sedentary for the same period. Vehicle or ND injections were started 14 days prior to the voluntary exercise and continued throughout the 15 days of voluntary exercise. After the 15-day period, the rats were trained and tested on a water maze spatial task using four trials per day for 5 consecutive days followed by a probe trial two days later. Exercise significantly improved performance during both the training and retention of the water maze task, and enhanced hippocampal BDNF. ND impaired spatial learning and memory, and this effect was not rescued by exercise. ND also potentiated the exercise-induced increase in hippocampal BDNF levels. These results seem to indicate that voluntary exercise is unable to improve the disruption of cognitive functions by chronic ND. Moreover, increased levels of BDNF may play a role in ND-induced impairments in learning and memory. The harmful effects of ND and other AAS on learning and memory should be taken into account when athletes decide to use AAS for performance or body image improvement.
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http://dx.doi.org/10.1016/j.yhbeh.2012.10.003DOI Listing
January 2013