scholarly journals Neuroprotective Effects of Low Dose Anandamide in Pentylenetetrazole-Induced Kindling in Rats

2019 ◽  
Vol 12 (1) ◽  
pp. 25-40 ◽  
Author(s):  
Omar M. E. Abdel-Salam ◽  
Amany A. Sleem ◽  
Marawan Abd El-Baset Mohamed Sayed ◽  
Eman R. Youness ◽  
Nermeen Shaffie
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Neutrophil Elastase ◽  
Cannabinoid Receptor ◽  
Treated Group ◽  
Paraoxonase 1 ◽  
Neuroprotective Effects ◽  
Chemical Kindling ◽  
Brain Oxidative Stress ◽  
Endogenous Cannabinoid

Anandamide (N-arachidonoylethanolamine) is an endogenous cannabinoid receptor CB1 ligand that exhibits neuroprotective effects in the brain. In this study, the effect of exogenously given anandamide on pentylenetetrazole (PTZ)-induced chemical kindling oxidative stress and brain damage in rats was studied. Rats were intraperitoneally (i.p.) injected with 35 mg/kg PTZ once every 48 hours for 12 times to induce seizures. Anandamide was i.p. given. 30 min prior to PTZ injection at 100 or 200 mg/kg. Injections of PTZ induced significant increase in brain lipid peroxidation (malondialdehyde: MDA), and nitric oxide associated with marked decrease in brain reduced glutathione (GSH). There were also significant decrements in acetylcholinesterase (AChE) concentration, butyrylcholinesterase (BChE) and paraoxonase-1 (PON-1) activities in brain tissue of PTZ injected rats. Meanwhile, there was no significant effect for PTZ on the concentration of brain neutrophil elastase. Anandamide administered at 100 and 200 mg/kg significantly decreased MDA and increased GSH contents and at 200 mg/kg significantly decreased nitric oxide in brain of PTZ-treated rats. The drug also caused significant increments in AChE concentration and PON-1 activity but had no significant effect on BChE or neutrophil elastase in rats treated with PTZ. Anandamide given at the dose of 200mg/kg significantly decreased the mean seizure scores over the study period by 22.3% and the frequency of myoclonic jerks and rearing (stage 3) by 56.7% compared with the vehicle-treated group. Anandamide given at 100 and 200 mg/kg completely inhibited the development of generalized tonic-clonic seizures (stage 5). It is concluded that in the PTZ-induced seizures, the cannabinoid receptor CB1 agonist anandamide decreases brain oxidative stress, neuronal injury, and exerts an antiepileptic activity.

Effect of Propofol and Fentanyl on Brain Oxidative Stress after Systemic Lipopolysaccharide Injection in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Omar M.E. Abdel-Salam ◽  
Eman R. Youness ◽  
Nadia A. Mohammed ◽  
Amr M.M. Ibrahim
Keyword(s):  
Oxidative Stress ◽  
Active Form ◽  
Saline Group ◽  
Paraoxonase 1 ◽  
Stress Markers ◽  
Anesthetic Agents ◽  
Systemic Endotoxemia ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Different Doses

Systemic inflammation causes brain oxidative stress, a prerequisite for neurodegeneration. In this study, we investigated the effect of the anesthetic agents propofol and fentanyl on brain oxidative stress during mild systemic endotoxemia induced by lipopolysaccharide (LPS) endotoxin. For this purpose, rats were administered LPS (400 μg/kg, intraperitoneally; i.p.), treated at the same time with different doses of propofol or fentanyl, i.p., and euthanized 4 h later. Other groups were treated with the saline, only propofol, or only fentanyl. Oxidative stress markers including malondialdehyde (MDA), nitric oxide (NO), and reduced glutathione (GSH) were determined. In addition, nuclear factor kappaB (NF-kB), paraoxonase-1 (PON-1), and butyrylcholinesterase (BChE) activities were measured in the brain tissue. Results showed that compared with the saline group, administration of LPS caused a marked and significant increase in brain MDA and NO combined with depletion of GSH and decreased PON-1 and BChE activities. Additionally, the active form of NF-kB was significantly increased in the brain of LPS only-treated rats. Treatment with propofol or fentanyl led to a marked and significant decrease in the levels of brain MDA and NO together with a significant increase in GSH and restoration of PON-1 and BChE activities. Furthermore, lower levels of active form of NF-kB were found following treatment with propofol or fentanyl compared with those in the LPS only group. Collectively, these results suggest that propofol and fentanyl exhibit an antioxidant action and attenuate the endotoxin-induced brain oxidative stress.

scholarly journals Sitagliptin-Dependent Differences in the Intensity of Oxidative Stress in Rat Livers Subjected to Ischemia and Reperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Małgorzata Trocha ◽  
Małgorzata Krzystek-Korpacka ◽  
Anna Merwid-Ląd ◽  
Beata Nowak ◽  
Małgorzata Pieśniewska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Tbars Level ◽  
Rat Livers

Purpose. Ischemia/reperfusion (IR) is the main cause of liver damage after transplantation. We evaluated the effect of sitagliptin (STG) on oxidative stress parameters in the rat liver under IR. Methods. Rats were treated with STG (5 mg/kg) (S and SIR) or saline solution (C and CIR). Livers from CIR and SIR were subjected to ischemia (60 min) and reperfusion (24 h). During reperfusion, aminotransferases (ALT and AST) were determined in blood samples. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), paraoxonase-1 (PON1), glutathione peroxidase (GPx), and the mRNA expression of SOD1 were determined in liver homogenates after reperfusion. Different regions of livers were also histologically evaluated. Results. The PON1 activity was higher, and the TBARS level was lower in SIR than in CIR. There was an inverse relationship between TBARS and PON1 levels in the whole cohort. The GPx activity was lower in ischemic than in nonischemic groups regardless of the STG treatment. In SIR, the SOD1 activity was higher compared to that in CIR. In S, the expression of SOD1 mRNA was the highest of all examined groups and positively correlated with the SOD1 activity in the whole animal cohort. During IR aminotransferases, the activity in the drug-treated group was lower in all examined points of time. In drug-treated groups, the percentage of steatosis was higher than that in nontreated groups regardless of IR. Conclusions. The protective effect of STG on the rat liver, especially its antioxidant properties, was revealed under IR conditions.

scholarly journals Virgin Coconut Oil Ameliorates Colchicine Induced Cognitive Dysfunction- A Preclinical Study

2020 ◽  
Vol 26 (1) ◽  
pp. 1-12
Author(s):  
Jeena John ◽  
Naveen Kumar Sapa ◽  
Rekha R Shenoy
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Frontal Cortex ◽  
Cognitive Dysfunction ◽  
Unsaturated Fatty Acids ◽  
Ketone Bodies ◽  
Coconut Oil ◽  
Treated Group ◽  
Virgin Coconut Oil ◽  
Neuroprotective Effects

Background : Virgin coconut oil (VCO) has been identified as a potential cognitive strengthener associated with Alzheimer’s disease (AD). It contains medium chain fatty acids (MCFA) which are absorbed and easily metabolized by the liver to form ketone bodies. Ketone bodies are converted to acetyl Co-A in the brain which then enters the citric acid cycle to provide ATP and also serves as precursors of acetylcholine in neurons. Sunflower oil (SO) contains poly unsaturated fatty acids which has both anti-inflammatory and neuroprotective actions. To compare the neuroprotective effects of VCO and SO on biochemical parameters involved in the cognitive dysfunction induced by colchicine through intracerebroventricular (i.c.v) route.To assess the role of polyphenols and MCFA present in VCO in preventing oxidative stress and its influence on in neuroprotection and memory enhancement. Methods: In the present study, we induced dementia through i.c.v injection of colchicine after giving the diet enriched VCO and SO in rats for 60 days. Rats were sacrificed on the 22nd day after the administration of colchicine. Behavioral parameters were assessed during the study period and biochemical estimations were performed using frontal cortex and hippocampus isolated from rat brain. Results: From the memory and learning tests by Morris water maze, VCO treated group performed better than SO treated rats. VCO reversed the antagonistic effects induced by colchicine by decreasing the acetylcholinesterase and malondialdehyde levels and increasing the levels of catalase and superoxide dismutase. SO only reduced malondialdehyde levels in cortex and hippocampus. Conclusion: The results demonstrated potential beneficiary effects of VCO in the cognitive dysfunction induced by colchicine by enhancing acetylcholine levels in the frontal cortex and hippocampus and also by reducing oxidative stress induced by physiological oxidants.

scholarly journals Apoptotic Inducement of Neuronal Cells by Aluminium Chloride and the Neuroprotective Effect of Eugenol in Wistar Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Samuel Bolaji Mesole ◽  
Okpanachi Omachonu Alfred ◽  
Uthman Ademola Yusuf ◽  
Lwiindi Lukubi ◽  
Dailesi Ndhlovu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Anaesthetic Agent ◽  
Neuroprotective Effect ◽  
Aluminium Chloride ◽  
Neuroprotective Effects ◽  
Stress Markers ◽  
Bax Protein

Aluminium is known to accelerate oxidative stress, amyloid beta (Aβ) deposition, and plaque formation in the brain of rats. Objective. The present study is aimed at studying the neuroprotective effects of eugenol following aluminium-induced neurotoxicity on caspase-3, apoptotic proteins (Bcl-2 and Bax), and oxidative stress markers in Wistar rats such as superoxide dismutase (SOD), glutathione peroxidase (GPx), nitric oxide (NO), and assay oxidative stress to mitochondrial DNA (mtDNA) by measuring the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG). Materials and methods. Twenty (20) adult Wistar rats were randomly divided into four (4) groups with five animals in each group. Route of administration was oral throughout the duration of this study and this study lasted for 21 days. Rats were sacrificed 24 hours after administration of the last dose (i.e., day 22) with 0.8 mg/kg ketamine as an anaesthetic agent. Results. Exposure to AlCl3 resulted in a significant (p<0.01) elevation in the levels of nitric oxide and 8-hydroxy-2-deoxyguanosine (8-OHdG), enhanced the activity of caspase-3, increased the level of proapoptotic protein Bax and reduced the levels of antiapoptotic protein Bcl-2, and significantly (p<0.01) reduced the levels of SOD and GPx. However, treatment with eugenol resulted in a significant reduction (p<0.01) in the levels of nitric oxide (NO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, inhibited the activity of caspase-3, increased levels of Bcl-2 and significantly (p<0.05) reduced levels of Bax protein, respectively, and also significantly (p<0.05) increased the levels of SOD and GPx. Our results would hereby suggest that eugenol would provide a therapeutic value against aluminium-induced oxidative stress as related to antioxidant and antiapoptotic activities.

scholarly journals Administration of Quercetin Ameliorates Lipopolysaccharide Induced Neuroinflammation and Oxidative Stress in Adult Zebrafish

2021 ◽  
Author(s):  
Sukhdev Singh ◽  
Kuleshwar Sahu ◽  
Lakshay Kapil ◽  
Charan Singh ◽  
Arti Singh
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Treated Group ◽  
Post Treatment ◽  
Test Time ◽  
Adult Zebrafish ◽  
Neuroprotective Effects ◽  
Behavioral Abnormalities ◽  
Bottom Zone ◽  
Quercetin Treatment

Abstract Background: Quercetin is a natural flavonoid which is known to have numerous pharmacological activities such as antioxidative, anti-inflammatory and neuroprotective effects against various neurological disorders. Lipopolysaccharide (LPS) is a potent endotoxin, reported to cause various neurological disorders such as Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Stroke (Brain Attack), Meningitis. Aim: The present study was designed to investigate the possibility thatquercetin ameliorates LPS induced oxidative stress and neuroinflammation in adult zebrafish. Materials and methods: Zebrafish (weighing 470-530 mg) were treated with single injection of LPS (1 mg/kg) intraperitoneally (i.p.) followed by post treatment for 7 days with quercetin (50 and 100 mg/kg; i.p.). After sacrificed, brain was harvested and subjected for biochemical, molecular and histological analyses. Results: Results revealed post treatment with quercetin was able to ameliorate the behavioral abnormalities as in novel diving test- time spent in top zone (TSTZ), and number of entries in top zone was significantly more as compared to time spent in bottom zone (TSBZ). In light-dark chamber test- time spent in light zone (TSLZ), and number of entries in light zone was significantly more as compared to time spent in dark compartment (TSDC). Additionally, results of histopathology (H & E stain) studies showed less disruption in neuronal cells as compared to LPS treated group. Moreover, results of molecular analysis implies that quercetin treatment significantly decrease TNF-α and IL-1β level as compared to LPS treated animals. Further, results of biochemical analysis reveal that quercetin reduce the level of LPO, nitrite, AChEs and increases anti-oxidant GSH. Conclusion: Quercetin treatment helps to prevent oxidative damage and neuroinflammation in LPS treated adult zebrafish.

Abstract 256: Renal Denervation Preconditions the Myocardium by Promoting Nitric Oxide Signaling and Attenuating Oxidative Stress in Spontaneously Hypertensive Rats

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
David J Polhemus ◽  
Juan Gao ◽  
Daniel R Kapusta ◽  
David J Lefer
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Hypertensive Rats ◽  
Carbonyl Content ◽  
Spontaneously Hypertensive ◽  
Myocardial Oxidative Stress

Background: Recent clinical studies suggest that renal denervation (RDN) not only decreases blood pressure (BP) and sympathetic nerve activity, but may also exert additional systemic cardioprotective actions. We investigated whether RDN preconditions the heart against subsequent myocardial ischemia/reperfusion (MI/R) injury in spontaneously hypertensive rats (SHR). Materials and Methods: SHR (20w old) received either bilateral radiofrequency (RF) RDN or sham RDN (Biosense Webster Stockert 70 RF generator). After 4w of BP recording, Plasma and left ventricle (LV) tissue were collected for measurement of nitric oxide (NO) metabolites, nitrite (NO2-, ion chromatography) and S-Nitrosothiol (RSNO). RT PCR was used to examine transcriptional changes. Colorimetric assays were used to quantify malondialdehyde (MDA) and carbonyl content. In additional studies, 4w after RDN (n = 8) or Sham (n = 9) treatment, SHR were subjected to 30m of left coronary artery ischemia followed by 24h reperfusion and myocardial infarct/area-at-risk (AAR) was determined. Results: 4w after treatment, mean BP was significantly decreased in RDN compared to Sham SHR (157±2 vs 142±2 mmHg, p < 0.05). Plasma NO2- levels were elevated 4w following RDN (p < 0.01). Cardiac NO2- levels increased from 2.6 to 3.2 nmol/mg (p < 0.05) and RSNO levels increased from 0.5 to 1.1 nmol/mg (p < 0.05) following RDN. Moreover, myocardial oxidative stress was markedly attenuated as measured by carbonyl content (p < 0.05) and MDA levels (p < 0.01). Greater transcription of antioxidants, SOD1 (p < 0.05) and GPX-1 (p < 0.05) were also observed in the RDN treated group. SHR receiving RDN therapy exhibited a trend in infarct size reduction (42% per AAR reduction, p = 0.09) compared to sham following MI/R. We observed 2-fold greater survival in the RDN treated group (88%, 7 of 8) compared to sham (44%, 4 of 9) following MI/R. Conclusions: RDN produced a sustained elevation in NO bioavailability and signaling in the heart and blood. Additionally, RDN attenuated myocardial oxidative stress and augmented the antioxidant defense system in SHR. Although further studies are warranted, preliminary results indicate that these mechanisms may promote myocardial preconditioning and improve survival in the setting of MI/R injury.

Potential Prognostic, Diagnostic and Therapeutic Markers for In-stent Reocclusion in Advanced Age Patients After Coronary Stenting

2018 ◽  
Vol 24 (28) ◽  
pp. 3359-3365 ◽  
Author(s):  
Xia Li ◽  
Fenglin Zhang ◽  
Hualan Zhou ◽  
Youdong Hu ◽  
Xiang Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Inflammatory Response ◽  
Coronary Stenting ◽  
Advanced Age ◽  
Paraoxonase 1 ◽  
Diagnostic Significance ◽  
Stent Restenosis ◽  
Response Status ◽  
Superoxide Dismutase 3

Background: Oxidative stress and inflammatory response played important roles in advanced atherosclerosis. We tried to confirm clinical diagnostic significance of the assessments of oxidative stress and inflammatory response status with in-stent reocclusion in 283 advanced age patients (80～90 years) after coronary stenting. Methods: : We analyzed levels of circulating superoxide dismutase 3 (SOD3), nitric oxide (NO), endothelial nitric oxide synthase (eNOS), malondialdehyde (MDA), acrolein（ACR）, and paraoxonase-1 （PON-1）in advanced age patients with in-stent restenosis and reocclusion after coronary stenting. <p> Results: Levels of SOD3, eNOS, NO and PON-1 were lowered (P<0.001) and levels of MDA and ACR were increased (P<0.001). Conclusion: The assessments of the biomarkers of oxidative stress and inflammatory response (levels of MDA and ACR) and anti-oxidant biomarkers (levels of eNOS, NO, SOD3 and PON-1) could be considered as potential prognostic and diagnostic indicators of in-stent reocclusion in advanced age patients after coronary stenting.

scholarly journals The 5-HT1A Agonist Buspirone Decreases Liver Oxidative Stress and Exerts Protective Effect Against CCl4– Toxicity

2017 ◽  
Vol 1 (1) ◽  
pp. 13-26
Author(s):  
Omar M.E. Abdel-Salam ◽  
Nermeen M. Shaffie ◽  
Nadia A. Mohammed ◽  
Eman R. Youness ◽  
Safaa M. Youssef Morsy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Caspase 3 ◽  
Histopathological Examination ◽  
Serum Markers ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Beneficial Effects ◽  
Anxiolytic Drug

We aimed to study the effect of buspirone, an anxiolytic drug and 5-HT1A agonist on liver injury induced by carbon tetrachloride (CCl4) in rats. Rats were orally treated with CCl4 (2.8 mL/kg in olive oil) along with buspirone at 10, 20 or 30 mg/kg once daily starting with CCl4 and for one week thereafter. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as well as alkaline phosphatase (ALP) activities were determined in the serum. Markers of oxidative stress: lipid peroxidation (malondialdehyde; MDA), reduced glutathione (GSH), nitric oxide (nitrite/nitrate) levels were measured in the liver. Moreover, paraoxonase 1 activity was determined in the liver and serum. The administration of CCl4 led to significant increases in serum ALT, AST, and ALP activities. Results showed that there were significantly increased hepatic MDA, nitrite and decreased GSH levels. PON1 activity decreased both in the liver and serum, respectively. The immunohistochemical investigations using anti-caspase-3 antibody revealed that CCl4 caused apoptosis to many hepatocytes. DNA studies showed that CCl4 caused hypoploidy in hepatocytes. Rats treated with 20-30 mg/kg buspirone showed significant decrease in serum ALT and AST by 19.5-34.3% and 24.2-31.4%, respectively. Serum ALP decreased by 21.7% after 30 mg/kg buspirone. In the liver, the higher dose of the drug resulted in decreased MDA (by 15.8%), decreased nitric oxide (17.4%) and increased GSH (by 20.1%). Significantly increased serum PON1 activity by 43.9-53.5% was observed after treatment with 20-30 mg/kg buspirone. On histopathologic examination of liver sections, there was mild protective effect for the drug at 30 mg/kg. Sections stained with anti- caspase- 3 confirmed the results obtained from histopathological examination. Moreover, buspirone given at 30 mg/kg resulted in an increase in % of cells containing normal values of DNA. These results indicate that buspirone decreases liver oxidative stress and exerts protective effect against CCl4- toxicity. The study thus indicates more beneficial effects of buspirone as an anxiolytic drug and that the drug could be used safely in patients with liver disease.

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