A comparative study of PMMA/PEG polymer nanocomposites doped with different oxides nanoparticles for potential optoelectronic applications.

PMMA/PEG and PMMA/PEG doped with SiO, TiO and AlO were fabricated using the solution-casting technique. The composites were characterized by X-ray diffraction and scanning electron microscopy (FE-SEM), which revealed that the amorphous nature of PMMA/PEG blend doped with AlO was hindered by the crystalline nature of those doped with SiO and TiO. The absorption of PMMA/PEG blend doped with AlO is higher, band gap energies were decreased from 4.

PI3K/AKT signaling activation by roflumilast ameliorates rotenone-induced Parkinson's disease in rats.

Parkinson's disease (PD) is the second most common progressive age-related neurodegenerative disorder. Paramount evidence shed light on the role of PI3K/AKT signaling activation in the treatment of neurodegenerative disorders. PI3K/AKT signaling can be activated via cAMP-dependent pathways achieved by phosphodiesterase 4 (PDE4) inhibition.

Capsaicin, The Vanilloid Receptor TRPV1 Agonist in Neuroprotection: Mechanisms Involved and Significance.

Hot peppers, also called chilli, chilli pepper, or paprika of the plant genus Capsicum (family Solanaceae), are one of the most used vegetables and spices worldwide. Capsaicin (8-methyl N-vanillyl-6-noneamide) is the main pungent principle of hot green and red peppers. By acting on the capsaicin receptor or transient receptor potential cation channel vanilloid subfamily member 1 (TRPV1), capsaicin selectively stimulates and in high doses defunctionalizes capsaicin-sensitive chemonociceptors with C and Aδ afferent fibers.

Protective effect of hot peppers against amyloid β peptide and brain injury in AlCl-induced Alzheimer's disease in rats.

Objectives: This study investigated the therapeutic effect of red hot pepper ( annuum) methanolic extract in induced Alzheimer's disease using AlCl in male rats.

Materials And Methods: Rats were injected with AlCl intraperitoneally (IP) daily for two months. Starting from the 2nd month of AlCl, rats received, in addition, IP treatments with extract (25 and 50 mg/kg) or saline.

Curcumin modulation of L-dopa and rasagiline-induced neuroprotection in rotenone model of Parkinson's disease.

Objectives: Parkinson's disease (PD) is one of the most incurable, chronic, and progressive neurodegenerative disorders Worldwide. Curcumin, a natural polyphenolic anti-oxidant compound, has a long history in traditional medicine. We investigate the effect of curcumin on brain oxidative stress, DNA fragmentation, and motor changes in rotenone-induced PD in mice.

Inhibition of aluminum chloride-induced amyloid Aβ peptide accumulation and brain neurodegeneration by flower decoction.

Objectives: To investigate the potential therapeutic effect of flower decoction on aluminum chloride (AlCl)-induced neurotoxicity.

Materials And Methods: Rats received daily intraperitoneal injections of AlCl at 10 mg/kg for two months and were treated with decoction at 50 or 100 mg/kg or saline during the 2 month of the study. The control group received saline.

Protective effect of cannabinoids on gastric mucosal lesions induced by water immersion restrain stress in rats.

Objectives: This study aimed to determine the impact of cannabinoid agonists and antagonists on the mucosal lesion progress in the stomach induced by water-immersion restraint stress (WIRS).

Materials And Methods: Rats subjected to WIRS for 4 hr were treated with Dimethyl sulfoxide (DMSO), CBR1 agonist (NADA, 1 mg/kg), CBR1 antagonist (Rimonabant, 1 mg/kg), CBR2 agonist (GW405833 1 mg/kg) or CBR2 antagonist (AM630, 1 mg/kg SC) 30 min before WIRS. Microscopic lesions, oxidative stress, inflammatory cytokines biomarkers, and (Myeloperoxidase) MPO in gastric tissues were determined.

Bee venom attenuates neurodegeneration and motor impairment and modulates the response to L-dopa or rasagiline in a mice model of Parkinson's disease.

Objectives: This study aimed to investigate the effect of bee venom, a form of alternative therapy, on rotenone-induced Parkinson's disease (PD) in mice. Moreover, the possible modulation by bee venom of the effect of L-dopa/carbidopa or rasagiline was examined.

Materials And Methods: Rotenone (1.

The effect of low dose amphetamine in rotenone-induced toxicity in a mice model of Parkinson's disease.

Objectives: The effects of low dose amphetamine on oxidative stress and rotenone-induced neurotoxicity and liver injury were examined in a mice model of Parkinson's disease.

Materials And Methods: Male mice were treated with rotenone (1.5 mg/kg, every other day for two weeks, subcutaneously).

The role of K channel blockade and activation in the protection against neurodegeneration in the rotenone model of Parkinson's disease.

Aims: Several studies suggested that ATP-sensitive potassium channels (K) are potential therapeutic targets for protection against various neurodegenerative disorders, yet, there is an ongoing controversy regarding their role in Parkinson's disease (PD). Thus, the aim of the current study is to investigate the protective effect of K blockade and activation in the mice rotenone model of PD.

Main Methods: PD has been induced by 9 subcutaneous injections of rotenone (1.

Correction to: Capsaicin Exerts Anti-convulsant and Neuroprotective Effects in Pentylenetetrazole-Induced Seizures.

The original version of this article unfortunately contains an error in the Y axis units in Fig. 1b, c (the symbol µ is not clear: µmol/g.tissue).

Capsaicin Exerts Anti-convulsant and Neuroprotective Effects in Pentylenetetrazole-Induced Seizures.

The transient receptor potential vanilloid-1 (TRPV1) receptor has been implicated in the development of epileptic seizures. We examined the effect of the TRPV1 agonist capsaicin on epileptic seizures, neuronal injury and oxidative stress in a model of status epilepticus induced in the rat by intraperitoneal (i.p.

Does nicotine impact tramadol abuse? Insights from neurochemical and neurobehavioral changes in mice.

Nicotine and tramadol concomitant drug dependence pose increasing social, economic as well as public threats. Accordingly, the present study investigated neurochemical, neurobehavioral and neuropathological changes in the brain subsequent to the interaction of nicotine and tramadol. To this end, tramadol (20 mg/kg, i.

Grape Seed Extract Alone or Combined with Atropine in Treatment of Malathion Induced Neuro- and Genotoxicity.

The aim of this study was to investigate the effect of treatment with grape seed extract (GSE) on the neurotoxic and genotoxic effects of acute malathion exposure. Rats received malathion (150 mg/kg by i.p.

Protection by Neostigmine and Atropine Against Brain and Liver Injury Induced by Acute Malathion Exposure.

We examined the effect of treatment with neostigmine alone or with atropine on brain oxidative stress and on brain and liver tissue damage following acute malathion toxicity. Rats were intraperitoneally treated with malathion 150 mg/kg along with neostigmine (200 or 400 μg/kg) or neostigmine (200 μg/kg) + atropine (1 mg/kg) and euthanized 4 h later. Results indicated that compared with the saline group, malathion resulted in (i) higher brain malondialdehyde (MDA) and nitric oxide (46.

Nitric oxide synthase inhibitors protect against brain and liver damage caused by acute malathion intoxication.

Objective: To investigate the effect of N-nitro-l-arginine methyl ester (l-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, on oxidative stress and tissue damage in brain and liver and on DNA damage of peripheral blood lymphocytes in malathion intoxicated rats.

Methods: Malathion (150 mg/kg) was given intraperitoneally (i.p.

Bougainvillea spectabilis flowers extract protects against the rotenone-induced toxicity.

Objective: To investigate the effect of two extracts of Bougainvillea spectabilis (B. spectabilis) flowers with yellow and pink/purple on brain oxidative stress and neuronal damage caused in rats by systemic rotenone injection.

Methods: Rotenone 1.

Determination of delta-9-tetrahydrocannabinol content of cannabis seizures in Egypt.

Objective: To determine the delta-9-tetrahydrocannabinol (THC) content of cannabis seizures in Egypt.

Methods: Unheated and heated extracts of cannabis seizures were prepared from the dried flowering tops and leaves (marijuana) or from the resin (hashish) and subjected to analysis using high performance liquid chromatography (HPLC).

Results: The heated resin extract had the peak of THC in a relative ratio of 31.

Cannabis exacerbates depressive symptoms in rat model induced by reserpine.

Cannabis sativa is one of the most widely recreational drugs and its use is more prevalent among depressed patients. Some studies reported that Cannabis has antidepressant effects while others showed increased depressive symptoms in Cannabis users. Therefore, the present study aims to investigate the effect of Cannabis extract on the depressive-like rats.

Novel neuroprotective and hepatoprotective effects of citric acid in acute malathion intoxication.

Objective: To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure.

Methods: Rats were received intraperitoneal (i.p.

Acetylcholinesterase, butyrylcholinesterase and paraoxonase 1 activities in rats treated with cannabis, tramadol or both.

Objective: To investigate the effect of Cannabis sativa resin and/or tramadol, two commonly drugs of abuse on acetylcholinesterase and butyrylcholinesterase activities as a possible cholinergic biomarkers of neurotoxicity induced by these agents.

Methods: Rats were treated with cannabis resin (5, 10 or 20 mg/kg) (equivalent to the active constituent Δ-tetrahydrocannabinol), tramadol (5, 10 and 20 mg/kg) or tramadol (10 mg/kg) combined with cannabis resin (5, 10 and 20 mg/kg) subcutaneously daily for 6 weeks. Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities were measured in brain and serum.

Gastric acid inhibitory and gastric protective effects of Cannabis and cannabinoids.

Cannabis sativa has long been known for its psychotropic effect. Only recently with the discovery of the cannabinoid receptors, their endogenous legends and the enzymes responsible for their synthesis and degradation, the role of this 'endocannabinoid system' in different pathophysiologic processes is beginning to be delineated. There is evidence that CB1 receptor stimulation with synthetic cannabinoids or Cannabis sativa extracts rich in Δ(9)-tetrahydrocannabinol inhibit gastric acid secretion in humans and experimental animals.

The paths to neurodegeneration in genetic Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder, which results from the loss of specific population of neurons, namely the pigmented dopamine secreting neurons of the substnatia nigra pars compatica (SNPc) of midbrain. The exact cause leading to nigrostriatal cell death is not yet known. In recent years, accumulating evidence from the identified molecular events in familial forms of PD contributed much to unraveling the mechanisms by which dopaminergic neurons die in PD and which hopefully would lead to the development of therapeutic interventions.