Effects of 2600 MHz Radiofrequency Radiation in Brain Tissue of Male Wistar Rats and Neuroprotective Effects of Melatonin

2021 ◽  
Vol 42 (2) ◽  
pp. 159-172
Author(s):  
Kevser Delen ◽  
Bahriye Sırav ◽  
Sinem Oruç ◽  
Cemile M. Seymen ◽  
Dilek Kuzay ◽  
...  
2020 ◽  
pp. 1-13
Author(s):  
Sonali Pardhiya ◽  
Usha Singh Gaharwar ◽  
Rohit Gautam ◽  
Eepsita Priyadarshini ◽  
Jay Prakash Nirala ◽  
...  

2021 ◽  
pp. 100174
Author(s):  
John Afees Olanrewaju ◽  
Okoro Iheanyichukwu ◽  
Owolabi Joshua Oladele ◽  
Olatunji Sunday Yinka ◽  
Adelodun Stephen Taiye ◽  
...  

Author(s):  
Neveen A. Salem ◽  
Amani M. Alsaedi ◽  
Bedor G. Alasmari ◽  
Razan Z. Almarghalani ◽  
Shahad M. Algobe ◽  
...  

Pregabalin (Lyrica) is an analog of the gamma-aminobutyric acid neurotransmitter,   approved for the treatment of epilepsy, generalized anxiety disorder, neuropathic pain, and fibromyalgia. The possibility for abuse and/or dependence on pregabalin has risen recently. Pregabalin is controlled in many countries including Saudi Arabia. However, unofficial use of this substance is also on the increase. The purpose of this study is to assess the potential neurotoxic effects associated with overdose prolonged pregabalin supplementation. Forty male Wistar rats were divided into Group (1) normal control received distilled water, Group (2) received pregabalin (150mg/kg), Group (3) received pregabalin (300 mg/kg), and Group (4) received pregabalin (600 mg/kg). pregabalin consumption in different doses resulted in significant dysregulation in neurotransmitter release, upsurge oxidative stress markers via enhancing lipid peroxidation and depleting antioxidant markers. Also, pregabalin doses evoked brain tissue inflammation through elevating TNF-α, IL-1β, and MCP-1, Moreover promoted brain tissue apoptosis by activating caspase -3 and suppressed Bcl2. Pregabalin effects on the aforementioned parameters were dose-dependent. These findings could highlight the potential neurotoxic effect of prolonged abuse of pregabalin supplementation through dysregulating brain neurochemical, inflammatory, oxidant/antioxidant, and apoptotic mediators.


Author(s):  
Ibrahim Ethem Torun ◽  
Yasemin Baranoglu Kılınc ◽  
Erkan Kilinc

ABSTRACT Background: Epilepsy has neuropsychiatric comorbidities such as depression, bipolar disorder, and anxiety. Drugs that target epilepsy may also be useful for its neuropsychiatric comorbidities. Objective: To investigate the effects of serotonergic modulation on pro-inflammatory cytokines and the seizures in pentylenetetrazole (PTZ)-induced seizure model in rats. Methods: Male Wistar rats were injected intraperitoneally with serotonin, selective serotonin reuptake inhibitor fluoxetine, 5-HT1B/D receptor agonist sumatriptan, or saline 30 min prior to PTZ treatment. Behavioral seizures were assessed by the Racine's scale. Concentrations of IL-1β, IL-6, and TNF-α in serum and brain tissue were determined by ELISA. Results: Serotonin and fluoxetine, but not sumatriptan, alleviated PTZ-induced seizures by prolonging onset times of myoclonic-jerk and generalized tonic-clonic seizures. The anti-seizure effect of fluoxetine was greater than that of serotonin. Likewise, serotonin and fluoxetine, but not sumatriptan, reduced PTZ-induced increases in the levels of IL-1β and IL-6 in both serum and brain tissue. None of the administered drugs including PTZ affected TNF-α concentrations. Conclusions: Our findings suggest that endogenous and exogenous serotonin exhibits anticonvulsant effects by suppressing the neuroinflammation. It seems that 5-HT1B/D receptors do not mediate anticonvulsant and anti-neuroinflammatory effects of serotonin.


2020 ◽  
Vol 15 (10) ◽  
pp. 1934578X2096619
Author(s):  
Ratchanee Rodsiri ◽  
Hattaya Benya-aphikul ◽  
Narudol Teerapattarakan ◽  
Oraphan Wanakhachornkrai ◽  
Weerawan Boonlert ◽  
...  

Oxyresveratrol, a polyphenolic compound, has been reported as having antioxidant and anti-inflammatory effects. This study determined the neuroprotective effects of oxyresveratrol, extracted from the heartwood of Artocarpus lakoocha Roxburgh (Moraceae), on parkinsonism induced by rotenone. Male Wistar rats were divided into control, rotenone (PD), and rotenone plus oxyresveratrol (OXY) groups. The OXY rats received oxyresveratrol (300 mg/kg orally) on days 1-20. Rotenone (3 mg/kg subcutaneously) was given to PD and OXY rats on days 15, 16, 18, and 20. Motor function was determined by the rotarod test. Brains were collected to analyze dopaminergic neurons, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase activities. OXY rats exhibited a longer latency to fall than PD rats in the rotarod test ( P < 0.01) on day 16. The number of dopaminergic neurons in PD rats was lower than that in controls ( P < 0.01), while that of OXY rats was not different from controls. OXY rats showed a reduction in MDA levels ( P < 0.01) and increased catalase activity ( P < 0.05), while SOD activity was unaltered. The results suggest that oxyresveratrol pretreatment ameliorates motor impairment induced by rotenone and preserves dopaminergic neurons. The neuroprotective mechanism of oxyresveratrol is involved with its antioxidant properties.


2019 ◽  
Vol 8 (2) ◽  
pp. 1635-1646
Author(s):  
T.A. Abayomi ◽  
O.S. Tokunbo ◽  
O David ◽  
O.O. Obembe ◽  
B.J. Dare

This study was designed to evaluate the therapeutic potentials and neuroprotective effects of methanol extract of Buchholzia coriacea (BC) seeds on sodium azide (NaN3) induced neurotoxicity of the prefrontal cortex in male Wistar rats. Neurotoxicity occurs as a result of exposure to neurotoxins in the environment, of which NaN3 is a potent neurotoxin. Thirty male Wistar rats were were randomly divided into 5 groups. Group A were administered with distilled water. Group B was administered with NaN3 for 28 days. Group C was administered with NaN3 for 28 days and thereafter B. coriacea for 21 days. Group D was administered with B. coriacea for 21 days and then NaN3 for 28 days. Group E was administered with only B. coriacea for 21 days. After treatment, neurobehavioral assessment was carried out after which the rats were sacrificed, and the prefrontal cortex excised. The prefrontal cortex was then processed for histological and biochemical analysis (SOD, MDA, GSH, and CAT). Pre-treatment and post-treatment with Buchholzia coriacea revitalized the cells of the Prefrontal cortex which were damaged by NaN3 exposure. Oxidative stress levels also decreased as a result of B. coriacea treatment, suggesting neuroprotective effects of Buchholzia Coriacea.Keywords: Buchholzia coriacea, Sodium Azide, Neurodegeration, Prefrontal cortex


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