scholarly journals Effects of Physical Activity and Ginkgo Biloba on Cognitive Function and Oxidative Stress Modulation in Ischemic Rats

2016 ◽  
Vol 26 (03) ◽  
pp. 158-164 ◽  
Author(s):  
Hassan Bafandeh Gharamaleki ◽  
Ladan Vaghef
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Treadmill Running ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Neuroprotective Effects ◽  
Memory Impairments ◽  
And Oxidative Stress

AbstractEither exercise or Ginkgo biloba is reported to improve cognitive functioning. The aim of this study is to compare the protective effects of forced exercise and Ginkgo biloba on oxidative stress as well as memory impairments induced by transient cerebral ischemia. Adult male Wistar rats were treated with treadmill running or Ginkgo biloba extract for 2 weeks before cerebral ischemia. Memory was assessed using a Morris water maze (MWM) task. At the end of the behavioral testing, oxidative stress biomarkers were evaluated in the hippocampus tissue. As expected, the cerebral ischemia induced memory impairment in the MWM task, and oxidative stress in the hippocampus. These effects were significantly prevented by treadmill running. Indeed, it ameliorated oxidative stress and memory deficits induced by ischemia. In contrast, Ginkgo biloba was not as effective as exercise in preventing ischemia-induced memory impairments. The results confirmed the neuroprotective effects of treadmill running on hippocampus-dependent memory.

Benefit Agmatine Effects in Experimental Multiple Sclerosis. CNS Nitrosative and Oxidative Stress Suppression / Protektivni Efekti Agmatina U Eksperimentalnoj Multiploj Sklerozi. Supresija Nitrozativnog I Oksidativnog Stresa U CNS-U

2014 ◽  
Vol 31 (4) ◽  
pp. 233-243
Author(s):  
Ivana Stojanović ◽  
Srđan Ljubisavljević ◽  
Ivana Stevanović ◽  
Slavica Stojnev ◽  
Radmila Pavlović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Clinical Symptoms ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Autoimmune Encephalomyelitis ◽  
Sod Activity ◽  
Neuroprotective Effects ◽  
Sprague Dawley Rats ◽  
And Oxidative Stress

Summary The aim of this study was to investigate the exogenous agmatine influence on nitrosative and oxidative stress parameters in acute phase of multiple sclerosis (MS) experimental model, experimental autoimmune encephalomyelitis (EAE). EAE was induced by subcutaneous injection of myelin basic protein (50 μg per animal). Sprague-Dawley rats were divided into five groups: I group - (CG), treated by PBS (i.p.), II group - (EAE), III group - (CFA), treated with Complete Freund’s adjuvant (0.2 ml subcutaneously), IV group - (EAE+AGM), treated by agmatine (75 mg/kg bw i.p.) upon EAE induction and V group - (AGM), received only agmatine in the same dose. The animals were treated every day during experiment - from day 0 to 15, and clinically scored every day. They were sacrificed on day 16 from MBP application. NO2+NO3, S-nitrosothiols (RSNO), malondyaldehide (MDA) and reduced glutathione (GSH) concentrations and superoxide dismutase (SOD) activity were determined in rat whole encephalitic mass (WEM) and cerebellum homogenates. Agmatine exerted strong protective effects on EAE clinical symptoms (p<0.05). In EAE brain homogenates, NO2+NO3, RSNO and MDA concentrations were increased compared to CG values. Agmatine treatment diminished NO2+NO3, RSNO and MDA levels in EAE animals (p<0.05). In EAE rats, GSH level and SOD activity were decreased compared to CG values, but agmatine treatment increased both parameters compared to EAE untreated animals (p<0.05). Immunohistochemical staining supported the clinical and biochemical findings in all groups. The CNS changes in EAE are successfully supressed by agmatine application, which could be the the new aspect of the neuroprotective effects of agmatine.

scholarly journals Protective effects of ethanolic extract of Alhagi maurorum roots on renal failure induced by acetaminophen in mice

2021 ◽  
Vol 8 (1) ◽  
pp. 16-22
Author(s):  
Seham I AL-Nafea ◽  
Mohammed O Aljahdali
Keyword(s):  
Oxidative Stress ◽  
Ethanolic Extract ◽  
Ethanol Extract ◽  
Serum Levels ◽  
High Dose ◽  
Root Extract ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Protective Actions ◽  
And Oxidative Stress

The protective actions of ethanol Alhagi maurorum (AM) root ethanol extract on acetaminophen-induced oxidative stress and renal toxicity in mice was evaluated. Forty male SWR strain albino mice aged 8 weeks were grouped into five groups. G1 (n=5): as control. G2 (n=5): administered orally a single dose of acetaminophen (2000mg/kg). G3 (n=10) administrated orally 200 mg/kg of roots ethanol extract for one week then acetaminophen as G2 at 8th day and; G4 (n=10) administrated orally 400 mg/kg of roots ethanol extract for one week then acetaminophen as G2 at 8th day; G5 (n=10) administrated orally 600 mg/kg of roots ethanol extract for one week then acetaminophen as G2 at 8th day. At end of experiments, the mice were killed under anesthesia and blood samples were gathered to preform complete blood test (CBC), serum levels of urea and creatinine and oxidative stress biomarkers as superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) using available Elisa mice kits. Kidneys were removed and histologically examined. Acetaminophen intake significantly elevated WBCs, neutrophils, monocytes, urea and creatinine levels and significantly decreased RBCs, hemoglobin, hematocrit, GSH, SOD and CAT (P <0.05). Treatment with Alhagi maurorum roots extract especially high dose (600 mg/kg) resulted in decreased in WBCs, neutrophils, monocytes, urea and creatinine levels and significantly increased RBCs, hemoglobin, hematocrit, GSH, SOD and CATversusacetaminophen group. Alhagi maurorum root extract treatment similarly decreased renal histological alteration induced by acetaminophen. This study can be utilized as prove of reading that Alhagi maurorum ethanol root extract especially high dose might be administered to prevent renal destruction induced by acetaminophen due to its antioxidant activity

scholarly journals Mitochondrial effects of Ginkgo biloba extract

2012 ◽  
Vol 24 (S1) ◽  
pp. S18-S20 ◽  
Author(s):  
Anne Eckert
Keyword(s):  
Oxidative Stress ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Mitochondrial Enzymes ◽  
Protective Effects ◽  
Protective Capacity ◽  
Slowing Down ◽  
Median Lifespan ◽  
Regulatory Effects ◽  
Induced Defects

ABSTRACTOxidative stress and mitochondrial failure promote altered protein degradation, reduced neurotransmission, synapse loss and tau/hyperphosphorylation, which are early stages in the development of Alzheimer's disease (AD). A growing volume of data confirms that Ginkgo biloba extract (GBE) reduces oxidative stress and improves mitochondrial respiration and thus may be useful in preventing or slowing down the progression of AD. Treatment of Caenorhabditis elegans with GBE- extract reduces oxidative stress and extends median lifespan compared with controls. Levels of reactive oxygen species, including the superoxide anion radical, were reduced in brains from GBE-treated mice compared with controls. In older mice, GBE resulted in a protective effect by increasing production of adenosine triphosphate in neurons. A respiratory experiment indicated that GBE was able to rescue Aβ-induced defects in energy metabolism, with results suggesting long-term regulatory effects on mitochondria. GBE also had a selective effect on the activities of mitochondrial enzymes that assemble the electron transport system. The flavonoids, bilobalide and some of the ginkgolides (B and J) had a high protective capacity, indicating that a combination of several compounds within standardized Gingko biloba extracts contribute disproportionately for these protective effects.

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