A Rapid Spectrophotometric Method for the Determination of Nitrite in Water.

Ashwagandha (Withania somnifera) root extract attenuates hepatic and cognitive deficits in thioacetamide-induced rat model of hepatic encephalopathy via induction of Nrf2/HO-1 and mitigation of NF-κB/MAPK signaling pathways

Aluminum (Al) is a ubiquitous element with known toxicity for both humans and animals. Herein, we aimed to investigate the potential role of melatonin (MEL) in hepatotoxicity and nephrotoxicity following aluminum chloride (AlCl3) treatment in rats. Adult male rats were treated with AlCl3 (34 mg/kg bwt) for eight weeks. Exposure to AlCl3 enhanced the serum activities of the liver transaminases (alanine aminotransferase and aspartate aminotransferase) and increased the level of bilirubin, in addition to the serum kidney function markers urea and creatinine. AlCl3 intoxication boosted oxidative stress, as evidenced by increases in the levels of lipid peroxidation (LPO) and nitric oxide (NO) along with simultaneous decreases in the levels of glutathione (GSH), various antioxidant enzymes, and Nrf2 mRNA expression. MEL (5 mg/kg bwt) treatment repressed LPO and NO levels, whereas it augmented GSH content. The activities of the antioxidant enzymes GPx, SOD, CAT, and GR were also restored concomitantly when MEL was administered before AlCl3. MEL also suppressed the apoptotic effect of AlCl3 by enhancing Bcl-2 protein expression in the liver and kidney and decreasing the expression levels of proinflammatory cytokines. Histopathological findings in the liver and kidney tissues confirmed the beneficial effect of MEL against AlCl3 toxicity. These findings indicate that MEL prevents AlCl3 toxicity by enhancing the antioxidant defense system.

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The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats.

Alzheimer’s disease (AD) is the most common type of dementia leading to progressive memory loss and cognitive impairment. Considering that pharmacological treatment options for AD are few and not satisfactory, increasing attention is being paid to dietary components that may affect the development of the disease. Such a dietary component may be caffeine contained in coffee, tea or energy drinks. Although epidemiological data suggest that caffeine intake may counteract the development of cognitive impairment, results of those studies are not conclusive. The aim of the present study is to review the existing experimental studies on the efficacy of caffeine against AD and AD-related cognitive impairment, focusing on the proposed protective mechanisms of action. In conclusion, the reports of studies on experimental AD models generally supported the notion that caffeine may exert some beneficial effects in AD. However, further studies are necessary to elucidate the role of caffeine in the effects of its sources on cognition and possibly AD risk.

Potential of Caffeine in Alzheimer's Disease-A Review of Experimental Studies.

determine if the effectiveness of minocycline in reducing b-amyloid-induced abnormal tau processing and neuronal death is mediated by glia. Secondly to investigate the role of glia in Ab-mediated degenerative pathways. Methods: We have investigated the effect of minocycline treatment on Ab-induced tau processing and neuronal death in primary neuronal, mixed and glial cultures. Mixed cortical cultures were prepared from E18 rat embryos, and neuronal cultures were derived following the suppression of glial proliferation with cytosine arabinoside. Analysis of mixed cultures by immunocytochemistry determined that these cultures contain 4.3 6 0.4% astrocytes and negligible numbers of microglia (<0.0001%). Glial cultures, containing astrocytes, microglia and small numbers of oligodendrocytes were prepared from P2 rat pups. Cultures were pre-treated with 20mM minocycline for 24h prior to treatment with 10mM soluble oligomeric Ab. Neuronal cell death, caspase activation, pathological changes in tau proteins and the secretion of inflammatory mediators were assessed by a variety of methods. Results: We show that the presence of astrocytes accelerates the onset of neuronal death in response to Ab, and that the neuroprotective influence of minocycline is only observed when astrocytes are present. Furthermore, we observe that astrocytes are required for Ab-induced tau phosphorylation, and that astrocytes mediate caspase-3-mediated cleavage of tau in response to Ab. In glial cultures, we find increased secretion of several inflammatory factors upon Ab treatment, including IL-1a, IL6 and IL10. Pre-treatment of glial cultures with minocycline suppresses the secretion of these pro-inflammatory mediators. The influence of specific inflammatory factors on Ab-induced neurotoxicity is currently under investigation. Conclusions: These results suggest that glia, and more specifically astrocytes, play a major role in Ab-induced abnormal tau processing and neuronal death. These findings also confirm that glia are a primary target of minocycline. It is possible that suppression of specific neuroinflammatory responses, either alone or in combination with other treatments, may represent an effective therapeutic strategy for the treatment of Alzheimer’s disease.

Involvement of phosphoinositide 3-kinase gamma in the neuro-inflammatory response and cognitive impairments induced by beta-amyloid 1-40 peptide in mice

Objective: The present study aims to investigate the neuroprotective effect of caffeine against aluminum chloride (AlCl3)-induced neurotoxicity in rats.Methods: Twenty-one male albino rats were div...

Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity

Objective: To evaluate the neuroprotective effect of ashwagandha extract against aluminum chloride-induced neurotoxicity in rats. Methods: Rats were divided into control, aluminum-intoxicated rats treated daily with aluminum trichloride (AlCl3) (100 mg/kg, orally) for 30 d and aluminum-intoxicated animals protected by receiving daily ashwagandha extract (200 mg/kg, orally) one hour before AlCl3 administration for 30 d. Levels of lipid peroxidation, nitric oxide, reduced glutathione and tumor necrosis factor-α were measured in the cortex, hippocampus and striatum. In addition, the activities of Na+, K+, ATPase and acetylcholinesterase were determined in the three studied brain regions. Results: Aluminum increased the levels of lipid peroxidation and nitric oxide in the cortex, hippocampus and striatum and decreased the reduced glutathione level in the hippocampus and striatum. In rats protected with ashwagandha extract, non significant changes were observed in lipid peroxidation, nitric oxide and reduced glutathione. In addition, ashwagandha extracts prevented the increased activity of acetylcholinesterase and Na+, K+, ATPase induced by AlCl3 in the cortex, hippocampus and striatum. The present findings also showed that the significant increase in tumor necrosis factor-α induced by AlCl3 in the cortex and hippocampus was prevented by ashwagandha extract. Conclusions: The present results suggest that ashwagandha extract possesses antioxidant and anti-inflammatory effects against aluminum neurotoxicity. In addition, ashwagandha extract could prevent the decline in cholinergic activity by maintaining normal acetylcholinesterase activity. The later effect could recommend the use of ashwagandha as a memory enhancer.

Protective effect of ashwagandha (Withania somnifera) against neurotoxicity induced by aluminum chloride in rats

Background Learning disorder (LD) is manifested by significant difficulties in the acquisition and use of reasoning, reading, writing, or mathematical abilities, despite average intelligence and proper education. Its etiological factors were suggested to be related to neurodevelopmental alterations. Measurement of the levels of brain-derived neurotrophic factor (BDNF) and coenzyme Q10 (CoQ10) was targeted in children with LD in comparison with typically developing (TD) ones. Materials and methods This study included 82 Egyptian Arabic-speaking children matched for age and sex and socioeconomic status, comprising 42 with specific LD (group I) and 40 TD children (group II). All participants were subjected to clinical and full neurological examination after reporting a full medical history. Furthermore, LD group was subjected to Stanford–Binet intelligence scale, dyslexia assessment test, and phonological awareness test, which evaluates cognitive and learning aptitudes. The levels of BDNF and CoQ10 were determined in serum by enzyme-linked immunosorbent assay. Results All children with LD obtained a score of 1 or more as at-risk quotient by the dyslexia assessment test, which indicated a specific reading disorder. The BDNF and CoQ10 levels in the LD group were significantly less than those in the TD group. No correlations were found between the measured markers and each other or between them and the measured factors of the used tests. Conclusion The detected low levels of BDNF and CoQ10 in children with specific LD with impairment in reading would be suspected to be related to etiological or exaggerating factors for the deficits in such children.

Brain-derived neurotrophic factor and coenzyme Q10 levels in blood of children with learning disorder

The current objective is to evaluate the effect of frankincense oil on the convulsions and the associated neurochemical alterations produced in pilocarpine-induced status epilepticus rat model. Rats were divided randomly into: control, status epilepticus rat model and rat model of status epilepticus pretreated with frankincense oil daily for 5 days before pilocarpine treatment. On the fifth day, after pilocarpine injection, rats were observed to evaluate the severity of seizures for 2 h. The oxidative stress parameters malondialdehyde, reduced glutathione and nitric oxide, the proinflammatory cytokines interleukin-6 and interleukin-1β and acetylcholinesterase were determined in the cortex, hippocampus and striatum. Dopamine, norepinephrine and serotonin were measured in the cortex and striatum. The status epilepticus model exhibited repetitive seizures in the form of generalized tonic- clonic convulsions after 30 min. of pilocarpine injection. This was associated with a significant increase in the levels of malondialdehyde and nitric oxide and a significant decrease in reduced glutathione in the three regions. A significant increase was also observed in interleukin-1β, interleukin-6 and acetylcholinesterase. In the cortex and striatum, a significant decrease was recorded in monoamine levels. Pretreatment of rat model of status epilepticus with frankincense oil decreased the severity of seizures that appeared in the form of tremors and facial automatisms and prevented the increase in malondialdehyde, nitric oxide, interleukin-1β, interleukin-6 and acetylcholinesterase and the decrease in reduced glutathione induced by pilocarpine in the studied brain regions. Frankincense oil failed to restore the decreased level of cortical serotonin and dopamine. In the striatum, frankincense oil improved the levels of serotonin and norepinephrine but failed to restore the decreased dopamine levels. It is clear from the present results that frankincense oil reduced the severity of seizures induced by pilocarpine. This could be mediated by its potent antioxidant and anti-inflammatory effects.

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Effect of frankincense oil on the neurochemical changes induced in rat model of status epilepticus

BACKGROUND: The risk of obesity among autism spectrum disorder (ASD) children is high which could be related to a disorder in their metabolism. Brain derived neurotrophic factor (BDNF) is involved in metabolic control, language behavior, and intellectual development. Serotonin has a role in satiety and energy expenditure.


AIM: Therefore, the aim of this study was to measure the serum levels of BDNF and serotonin in obese compared to non-obese ASD children. The influence of obesity on ASD severity, intellectual, and language development was also investigated.


METHODS: The study included 60 autistic children (Group I: 30 ASD children with obesity and Group II: 30 ASD children without obesity). The serum BDNF and serotonin levels were estimated by ELISA and by high-performance liquid chromatography.


RESULTS: All participants manifested delayed language development. Almost all of them had intellectual disability. The difference between groups regarding ASD severity, language, and intellectual development was non-significant. However, BDNF level in obese group was less than that in the other group while serotonin was higher in the obese group with significant statistical difference. 

CONCLUSION: The difference between the groups regarding the levels of BDNF and serotonin, which are involved in the brain development, could be related to obesity. The influence of obesity on ASD severity, intellectual, and language development of ASD children was not distinctive in the participants. The influence of such markers on ASD severity and cognitive performance needs further investigations.

Mohamed E Elhadidy

Papers

Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity

Protective effect of ashwagandha (Withania somnifera) against neurotoxicity induced by aluminum chloride in rats

Brain-derived neurotrophic factor and coenzyme Q10 levels in blood of children with learning disorder

Effect of frankincense oil on the neurochemical changes induced in rat model of status epilepticus

Brain Derived Neurotrophic Factor and Serotonin Levels in Autistic Children: Do They Differ in Obesity?