scholarly journals Protective Effect of PPARγAgonists on Cerebellar Tissues Oxidative Damage in Hypothyroid Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yousef Baghcheghi ◽  
Farimah Beheshti ◽  
Hossein Salmani ◽  
Mohammad Soukhtanloo ◽  
Mahmoud Hosseini
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Drinking Water ◽  
Oxidative Damage ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Group I ◽  
Biochemical Measurements ◽  
Thiol Content

The aim of the current study was to investigate the effects of peroxisome proliferator-activated receptor gamma (PPARγ) agonists on cerebellar tissues oxidative damage in hypothyroid rats. The animals included seven groups: group I (control), the animals received drinking water; group II, the animals received 0.05% propylthiouracil (PTU) in drinking water; besides PTU, the animals in groups III, IV, V, VI, and VII, were injected with 20 mg/kg vitamin E (Vit E), 10 or 20 mg/kg pioglitazone, and 2 or 4 mg/kg rosiglitazone, respectively. The animals were deeply anesthetized and the cerebellar tissues were removed for biochemical measurements. PTU administration reduced thiol content, superoxide dismutase (SOD), and catalase (CAT) activities in the cerebellar tissues while increasing malondialdehyde (MDA) and nitric oxide (NO) metabolites. Vit E, pioglitazone, and rosiglitazone increased thiol, SOD, and CAT in the cerebellar tissues while reducing MDA and NO metabolites. The results of present study showed that, similar to Vit E, both rosiglitazone and pioglitazone as PPARγagonists exerted protective effects against cerebellar tissues oxidative damage in hypothyroid rats.

Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARγ and abrogation of oxidative stress and inflammation

2014 ◽  
Vol 92 (9) ◽  
pp. 717-724 ◽  
Author(s):  
Ayman M. Mahmoud
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Liver Lipid ◽  
Inos Mrna ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Protective Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Intraperitoneal Dose

The most important reason for the non-approval and withdrawal of drugs by the Food and Drug Administration is hepatotoxicity. Therefore, this study was undertaken to evaluate the protective effects of hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats. The rats received a single intraperitoneal dose of CYP of 200 mg/kg body mass, followed by treatment with hesperidin, orally, at doses of 25 and 50 mg/kg for 11 consecutive days. CYP induced hepatic damage, as evidenced by the significantly elevated levels of serum pro-inflammatory cytokines, serum transaminases, liver lipid peroxidation, and nitric oxide. As a consequence, there was reduced glutathione content, and the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were markedly reduced. In addition, CYP administration induced a considerable downregulation of peroxisome proliferator activated receptor gamma (PPARγ) and upregulation of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) mRNA expression. Hesperidin, in a dose-dependent manner, rejuvenated the altered markers to an almost normal state. In conclusion, hesperidin showed a potent protective effect against CYP-induced oxidative stress and inflammation leading to hepatotoxicity. The study suggests that hesperidin exerts its protective effect against CYP-induced hepatotoxicity through upregulation of hepatic PPARγ expression and abrogation of inflammation and oxidative stress.

scholarly journals The Effect of Short-chain Fatty Acid Supplementation on Acute Colonic Inflammation in Rats Fed With Western Diet: Role of the Peroxisome Proliferator-activated Receptor-gamma

2021 ◽  
Author(s):  
Mustafa Sevim ◽  
Çiğdem Çantalı-Öztürk ◽  
Ali Mergen ◽  
Eda Ceren Güllü ◽  
Elif Yaren Ayvaz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Lipid Profile ◽  
Short Chain Fatty Acids ◽  
Normal Diet ◽  
Short Chain ◽  
Albino Rats ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Colonic Inflammation ◽  
Peroxisome Proliferator Activated Receptor

Abstract Increased incidence of inflammatory bowel disease (IBD) is associated with the consumption of westernized diet (WD). In male Wistar albino rats induced with colitis by oral intake of dextran-sulfate sodium (DSS) for 10 days, we investigated how colitis-induced oxidative damage is affected by WD consumption started 3 weeks before DSS intake. Secondly, the putative protective effects of short-chain fatty acids (SCFAs) were evaluated in both WD-fed and normal diet (ND)-fed rats. WD consumption prior to colitis induction alleviated oxidative damage and suppressed inflammatory response of the colon via the modulation of peroxisome proliferator-activated receptor (PPAR)-γ activity, suggesting a preconditioning impact of the WD. Moreover, addition of SCFA to WD abolished the elevations in lipid profile, while SCFA added to either ND or WD during the 10-day development of colonic inflammation depressed the pro-inflammatory TNF-α and IL-6 expressions and upregulated IL-10, but the reduction in oxidative damage due to WD was not further changed. The results demonstrated that acute colonic inflammation is alleviated when it is preceded by the consumption of WD, and SCFAs improved WD-induced disruption in lipid profile, implicating that SCFAs would be advantageous in IBD patients comorbid with metabolic syndrome.

scholarly journals BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function

2021 ◽  
Vol 18 (5) ◽  
pp. 2367
Author(s):  
Ryuni Kim ◽  
Hyebeen Kim ◽  
Minju Im ◽  
Sun Kyu Park ◽  
Hae Jung Han ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Inflammatory Responses ◽  
Mammalian Target Of Rapamycin ◽  
Inhibitory Effect ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Dry Extract ◽  
Myotube Formation ◽  
Species Production

BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.

scholarly journals Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis

2021 ◽  
Vol 11 (3) ◽  
pp. 325
Author(s):  
Fatima M. Shakova ◽  
Yuliya I. Kirova ◽  
Denis N. Silachev ◽  
Galina A. Romanova ◽  
Sergey G. Morozov
Keyword(s):  
Rat Model ◽  
Nuclear Translocation ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Protein Markers ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pharmacological Agents ◽  
Ischemic Brain ◽  
Neuroprotective Therapy ◽  
Dependent Protein

The pharmacological induction and activation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), a key regulator of ischemic brain tolerance, is a promising direction in neuroprotective therapy. Pharmacological agents with known abilities to modulate cerebral PGC-1α are scarce. This study focused on the potential PGC-1α-modulating activity of Mexidol (2-ethyl-6-methyl-3-hydroxypyridine succinate) and Semax (ACTH(4–7) analog) in a rat model of photochemical-induced thrombosis (PT) in the prefrontal cortex. Mexidol (100 mg/kg) was administered intraperitoneally, and Semax (25 μg/kg) was administered intranasally, for 7 days each. The expression of PGC-1α and PGC-1α-dependent protein markers of mitochondriogenesis, angiogenesis, and synaptogenesis was measured in the penumbra via immunoblotting at Days 1, 3, 7, and 21 after PT. The nuclear content of PGC-1α was measured immunohistochemically. The suppression of PGC-1α expression was observed in the penumbra from 24 h to 21 days following PT and reflected decreases in both the number of neurons and PGC-1α expression in individual neurons. Administration of Mexidol or Semax was associated with preservation of the neuron number and neuronal expression of PGC-1α, stimulation of the nuclear translocation of PGC-1α, and increased contents of protein markers for PGC-1α activation. This study opens new prospects for the pharmacological modulation of PGC-1α in the ischemic brain.

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