Effects of PPAR-γ agonist, pioglitazone on brain tissues oxidative damage and learning and memory impairment in juvenile hypothyroid rats

Baghcheghi, Yousef; Salmani, Hossein; Beheshti, Farimah; Shafei, Mohammad Naser; Sadeghnia, Hamid Reza; Soukhtanloo, Mohammad; Bideskan, Alireza Ebrahimzadeh; Hosseini, Mahmoud

doi:10.1080/00207454.2019.1632843

Cited by 25 publications

(11 citation statements)

References 79 publications

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“…In animal models of diabetes (Kariharan et al, 2015) and Alzheimer's disease (Prakash and Kumar, 2014), PPAR-γ agonists have significantly improved memory impairment and increased hippocampal BDNF levels. Moreover, in our previous study, we have shown that pioglitazone, a PPAR-γ agonist, effectively reversed the learning and memory impairment induced by hypothyroidism in rats (Baghcheghi et al, 2019).…”

Section: Introductionmentioning

confidence: 85%

Brain‑derived neurotrophic factor and nitric oxide contribute to protective effects of rosiglitazone on learning and memory in hypothyroid rats

Baghcheghi

Beheshti

Salmani

et al. 2022

Acta Neurobiol. Exp.

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The effects of the well-known peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone (Rosi) on brain-derived neurotrophic factor (BDNF), nitric oxide (NO), and learning and memory were investigated in hypothyroid rats.Hypothyroidism was induced in immature Wistar rats by administration of propylthiouracil in drinking water. Rats were divided into four groups: control, hypothyroid, and hypothyroid treated with Rosi at doses of 2 mg/kg or 4 mg/kg. Memory was then assessed by the Morris water maze (MWM) and passive avoidance (PA) tests. Following anesthetization, brain samples were collected for biochemical measurements. Hypothyroidism increased the escape latency and traveled path in the learning trials of the MWM and decreased the time spent and the distance traveled in the target quadrant on the probe day. Hypothyroidism also impaired the avoidance behavior of rats in the PA test. Rosi improved the performance of rats in both MWM and PA tasks.Hypothyroidism also decreased hippocampal BDNF levels, increased NO metabolites, and induced oxidative damage in the brain.Treatment of hypothyroid rats with both doses of Rosi increased BDNF levels and decreased NO metabolites and malondialdehyde concentrations. In addition, thiol content and superoxide dismutase and catalase activities were increased in the brain regions of hypothyroid rats receiving Rosi. The administration of 4 mg/kg Rosi also significantly increased serum thyroxin levels. The results of the present study showed that BDNF and NO play a role in the protective effects of Rosi against learning and memory impairment in hypothyroid rats.

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Section: Introductionmentioning

confidence: 85%

Brain‑derived neurotrophic factor and nitric oxide contribute to protective effects of rosiglitazone on learning and memory in hypothyroid rats

Baghcheghi

Beheshti

Salmani

et al. 2022

Acta Neurobiol. Exp.

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“…On the other hand, an increased expression of neuronal NOS (nNOS) and elevated NO levels were detected in the hippocampus of hypothyroid rats [48]. This in turn may induce brain tissue oxidative damage and cognitive dysfunction of experimental animals [49].…”

Section: Discussionmentioning

confidence: 99%

The Neuroprotective Effect of α-Lipoic Acid and/or Metformin against the Behavioral and Neurochemical Changes Induced by Hypothyroidism in Rat

et al. 2022

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Objective: The present study evaluates the neuroprotective effect of alpha lipoic acid (ALA) and/or metformin (MET) on the behavioral and neurochemical changes induced by hypothyroidism. Methods: Rats were divided into control, rat model of hypothyroidism induced by propylthiouracil (PTU), and rat model of hypothyroidism treated with ALA, MET, or their combination. Results: Behaviorally, hypothyroid rats revealed impaired memory and reduced motor activity as indicated from the novel object recognition test (NORT) and open field test (OFT), respectively. Hypothyroidism induced a significant increase in lipid peroxidation (MDA) and a significant decrease in reduced glutathione (GSH) and nitric oxide (NO) in the cortex and hippocampus. These were associated with a significant increase in tumor necrosis factor-α (TNF-α) and a significant decrease in brain derived neurotrophic factor (BDNF). Hypothyroidism decreased significantly the levels of serotonin (5-HT), norepinephrine (NE), and dopamine (DA) and reduced the activities of acetylcholinesterase (AchE) and Na+,K+-ATPase in the cortex and hippocampus. Treatment of hypothyroid rats with ALA and/or MET showed an improvement in memory function and motor activity. Moreover, ALA and/or MET prevented the increase in MDA and TNF-α, and the decline in GSH, NO, BDNF, 5-HT, NE and DA. It also restored AchE and Na+,K+-ATPase activities in the studied brain regions. Conclusion: ALA and/or MET has a potential neuroprotective effect against the adverse behavioral and neurochemical changes induced by hypothyroidism in rats.

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“…Recent studies have provided further insight on the role of PPARγ in an oxidative context in brain cells. Pioglitazone has been shown to inhibit, significantly for all, albeit moderately for some, the decrease in total thiol, SOD and catalase levels and the increase in malondialdehyde (MDA, a marker of PUFA peroxidation) levels in hippocampal and cortical extracts, in a rat model of hypothyroidism, a phenotype known to cause neurological damage [48]. Pioglitazone has also been shown to induce expression of TFAM and PGC-1α along with increased mitochondrial biogenesis and to restore mitochondrial membrane potential after challenge with rotenone, an inhibitor of the mitochondrial transport chain complex 1, in rat oligodendrocyte cultures [49].…”

Section: Energy Supply Oxidative Stress and Mitochondriamentioning

confidence: 99%

PPAR Gamma and Viral Infections of the Brain

Layrolle

Payoux

Chavanas

2021

IJMS

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Peroxisome Proliferator-Activated Receptor gamma (PPARγ) is a master regulator of metabolism, adipogenesis, inflammation and cell cycle, and it has been extensively studied in the brain in relation to inflammation or neurodegeneration. Little is known however about its role in viral infections of the brain parenchyma, although they represent the most frequent cause of encephalitis and are a major threat for the developing brain. Specific to viral infections is the ability to subvert signaling pathways of the host cell to ensure virus replication and spreading, as deleterious as the consequences may be for the host. In this respect, the pleiotropic role of PPARγ makes it a critical target of infection. This review aims to provide an update on the role of PPARγ in viral infections of the brain. Recent studies have highlighted the involvement of PPARγ in brain or neural cells infected by immunodeficiency virus 1, Zika virus, or human cytomegalovirus. They have provided a better understanding on PPARγ functions in the infected brain, and revealed that it can be a double-edged sword with respect to inflammation, viral replication, or neuronogenesis. They unraveled new roles of PPARγ in health and disease and could possibly help designing new therapeutic strategies.

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Effects of PPAR-γ agonist, pioglitazone on brain tissues oxidative damage and learning and memory impairment in juvenile hypothyroid rats

Cited by 25 publications

References 79 publications

Brain‑derived neurotrophic factor and nitric oxide contribute to protective effects of rosiglitazone on learning and memory in hypothyroid rats

Brain‑derived neurotrophic factor and nitric oxide contribute to protective effects of rosiglitazone on learning and memory in hypothyroid rats

The Neuroprotective Effect of α-Lipoic Acid and/or Metformin against the Behavioral and Neurochemical Changes Induced by Hypothyroidism in Rat

PPAR Gamma and Viral Infections of the Brain

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