Effect of progesterone on phosphamidon-induced impairment of memory and oxidative stress in rats

2011 ◽  
Vol 30 (10) ◽  
pp. 1626-1634 ◽  
Author(s):  
Amit K Sharma ◽  
Swapan K Bhattacharya ◽  
Naresh Khanna ◽  
Ashok K Tripathi ◽  
Tarun Arora ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Organophosphorus Pesticides ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Control Group ◽  
Protein Thiols ◽  
Acute And Chronic Exposure ◽  
The Brain ◽  
And Oxidative Stress

Progesterone (a neurosteroid) is an important modulator of the nervous system functioning. Organophosphorus pesticides like phosphamidon have been shown to adversely affect memory and induce oxidative stress on both acute and chronic exposure. The present study was therefore designed to investigate the effects of progesterone (PROG) on phosphamidon-induced modulation of cognitive function and oxidative stress in rats. Cognitive function was assessed using step-down latency (SDL) on a passive avoidance apparatus and transfer latency (TL) on an elevated plus maze. Oxidative stress was assessed by examining the levels of thiobarbituric acid reactive species (TBARS) and non-protein thiols (NP-SH) in isolated homogenized whole brain samples. The results showed a significant reduction in SDL and prolongation of TL in the phosphamidon (1.74 mg/kg/d; p.o.) treated group at weeks 6 and 8 as compared to the control group. Two weeks treatment with PROG (15 mg/kg/d; i.p.) antagonized the effect of phosphamidon on SDL as well as TL. Phosphamidon alone produced a significant increase in the brain TBARS levels and decrease in the brain NP-SH levels. Treatment with PROG (15 mg/kg/d; i.p.) attenuated the effect of phosphamidon on oxidative stress. Together, the results showed that progesterone attenuated the cognitive dysfunction and increased oxidative stress induced by phosphamidon in the brain.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

scholarly journals Manganese Inhibits Indomethacin-Induced Hepatorenal Oxidative Stress in Wistar Rats

2020 ◽  
pp. 79-90
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Density Lipoprotein ◽  
Treated Group ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Cellular Processes ◽  
Concomitant Reduction ◽  
Liver And Kidney ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

Aim: Manganese (Mn) is an essential trace element in many cellular processes. However, there is dearth of literature on its influence on indomethacin-induced hepatorenal damage. Therefore, this study was conducted to investigate the effect of manganese on indomethacin-induced hepatorenal damage in rats. Methods: Rats were divided into four groups of eight rats consisting of control group, indomethacin (IND) alone (20 mg/kg), Mn alone (10 mg/kg) and co-treated group that were treated orally for 14 consecutive days. Twenty four hours after treatment, under pentobarbital anesthesia, blood was collected and liver was excised to prepare homogenate and histology staining. Liver and kidney function tests aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glutamine dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), glucose-6-phosphate dehydrogenase (G6PD), bilirubin (BIL), urea, creatinine, cholesterol (CHOL), triglycerides (TG), low and high density lipoprotein (LDL and HDL), electrolytes and oxidative stress superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO) biomarkers were assessed. Results: The results showed that indomethacin caused hepatorenal damage in rats manifested with increase in serum hepatic and renal function biomarkers. But co-administration of IND with Mn significantly (p < 0.05) decreased the level of hepatorenal biomarkers. Additionally, co-administration of IND with Mn improved the antioxidant status with concomitant reduction of LPO and restored the integrity of the liver and kidney histologically. Conclusion: The results of this study emphasize that co-administration of IND with Mn to rats alleviated IND-induced hepatorenal toxicities and oxidative stress in rats.

scholarly journals Protective effect of vitamin E on oxidative stress and sperm apoptosis in diabetic Mice

2019 ◽  
Vol 17 (2) ◽  
pp. 127 ◽  
Author(s):  
Khadijeh Mirzaei Khorramabadi ◽  
Ali Reza Talebi ◽  
Abolghasem Abbasi Sarcheshmeh ◽  
Aghdas Mirjalili
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Protective Effect ◽  
Sperm Morphology ◽  
Sperm Count ◽  
Treated Group ◽  
Control Group ◽  
Diabetic Mice ◽  
And Oxidative Stress ◽  
Sperm Movement

Background: Generation of free radicals and oxidative stress are a major contributorto diabetes. These factors lead to the development of diabetic testicles disorders.Objective: In this study, the protective effect of vitamin E on functional disordersassociated with diabetes induced oxidative stress in male reproductive systems hasbeen investigated.Materials and Methods: Thirty-three adult male Mice were divided into control,diabetic, and untreated diabetic groups. Streptozotocin was used to induce diabetes.In the treated group, vitamin E was given to the Mice intraperitoneally for 30 days.Then, animals were anesthetized and sacrificed. Animal testicles were isolated andhomogenized in phosphate buffer and used for measuring sperm count, motility andsurvival of sperm, MDA concentration and antioxidant capacity (TAC). Apoptosis wasalso performed with the TUNEL test.Results: The results of reduction (12.03±98.11) TAC, MDA concentration (–28.5±2.58),sperm motility (unstable sperma= 86.4±7.48), sperm count (171.51), Sperm morphology(natural morphology= 49.69±31.93) and abnormal morphology (9.77±49.7)with increased oxidative damage. These changes were statistically significant incomparison with the control group for all variables other than MDA (p= 0.05). Treatmentof vitamin E diabetic Mice improved the ability of antioxidants to prevent oxidativedamage in the testicles, restore the sperm movement, and increase the number ofnormal sperm as well as TAC. The level of apoptosis in the treated group has decreasedcompared to the untreated group.Conclusion: Vitamin E protects the reproductive system against diabetes mellitus.Therefore, it was concluded that vitamin E may be a suitable agent for protecting thesperm and testicular parameters against undesirable effects of diabetes.

scholarly journals Chlorogenic acid prevents alcohol-induced brain damage in neonatal rat

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Zikang Guo ◽  
Jiang Li
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Chlorogenic Acid ◽  
Inflammatory Mediators ◽  
Caspase 3 ◽  
Negative Control Group ◽  
Treated Group ◽  
Negative Control ◽  
Neonatal Rat ◽  
Control Group

AbstractThe present investigation evaluates the neuroprotective effect of chlorogenic acid (CA) in alcohol-induced brain damage in neonatal rats. Ethanol (12 % v/v, 5 g/kg) was administered orally in the wistar rat pups on postnatal days (PD) 7-9. Chlorogenic acid (100 and 200 mg/kg, p.o.) was administered continuously from PD 6 to 28. Cognitive function was estimated by Morris water maze (MWM) test. However, activity of acetylcholinesterase, inflammatory mediators, parameters of oxidative stress and activity of caspase-3 enzyme was estimated in the tissue homogenate of cerebral cortex and hippocampus of ethanol-exposed pups. It has been observed that treatment with CA attenuates the altered cognitive function in ethanol-exposed pups. There was a significant decrease in the activity of acetylcholinesterase in the CA treated group compared to the negative control group. However, treatment with CA significantly ameliorates the increased oxidative stress and concentration of inflammatory mediators in the brain tissues of ethanol-exposed pups. Activity of caspase-3 enzyme was also found significantly decreased in the CA treated group compared to the negative control group. The present study concludes that CA attenuates the neuronal damage induced in alcohol exposed neonatal rat by decreasing the apoptosis of neuronal cells.

Comparison of fluoxetine and 1-methyl-L-tryptophan in treatment of depression-like illness in Bacillus Calmette-Guerin-induced inflammatory model of depression in mice

2016 ◽  
Vol 27 (6) ◽  
Author(s):  
Proteesh Rana ◽  
Amit K. Sharma ◽  
Smita Jain ◽  
Pravin Deshmukh ◽  
S.K. Bhattacharya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Forced Swim Test ◽  
Tail Suspension Test ◽  
Thiobarbituric Acid ◽  
Interferon Γ ◽  
Saline Group ◽  
Kynurenine Pathway ◽  
Bacillus Calmette Guerin ◽  
Protein Thiols ◽  
The Brain

AbstractBackground:The inflammatory response system has been implicated in the pathophysiology of major depression. The pro-inflammatory cytokines like interferon-γ induce the enzyme indoleamine-2,3-dioxygenase (IDO) of the kynurenine pathway of tryptophan metabolism. The induction of IDO reduces the availability of tryptophan for serotonin synthesis. Furthermore, the metabolites of kynurenine pathway have neurotoxic property, which along with decreased serotonin may account for depression-like illness.Methods:The aim of this study was to compare the effects of treatment with fluoxetine and 1-methyl-L-tryptophan (1-MT) on Bacillus Calmette-Guerin (BCG)-induced inflammatory model of depression in mice. Behavioral tests included locomotor activity, forced swim test (FST) and tail suspension test (TST). Oxidative stress was assessed by examining the levels of thiobarbituric acid reactive species (TBARS) and non-protein thiols (NP-SH) in homogenized whole brain samples. Comet assays were performed to assess neurotoxicity.Results:The results of this study demonstrate that BCG treatment resulted in an increase in duration of immobility in FST and TST as compared to the saline group. Further, it produced a significant increase in the brain TBARS levels and decrease in the brain NP-SH levels. The hippocampal tissue from BCG group had significantly more comet cells than the saline group. 1-MT and fluoxetine were able to reverse the BCG-induced depression-like behavior and the derangement in oxidative stress parameters. Fluoxetine and 1-MT also reversed the BCG-induced neurotoxicity in such mice.Conclusions:1-Methyl-L-tryptophan exhibits antidepressant-like effect comparable to that of fluoxetine in treating BCG-induced depression-like behavior in mice.

scholarly journals Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Feng Liang ◽  
Xin Fu ◽  
Yunpengfei Li ◽  
Fanglei Han
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Protein Expression ◽  
Protective Effect ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Neuronal Injury ◽  
Cyclin B1 ◽  
The Brain ◽  
And Oxidative Stress

Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.

scholarly journals Melatonin protects the liver and erythrocytes against oxidative stress in cirrhotic rats

2010 ◽  
Vol 47 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Darlan Pase da Rosa ◽  
Silvia Bona ◽  
Douglas Simonetto ◽  
Claudio Zettler ◽  
Cláudio Augusto Marroni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Carbon Tetrachloride ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Hepatic Tissue ◽  
Control Group ◽  
Significant Impairment ◽  
Peroxidase Enzymes ◽  
Cirrhotic Group

CONTEXT: Cirrhosis is a progressive chronic hepatopathy which constitutes an irreversible stage of liver dysfunction. OBJECTIVES: To evaluate the oxidative stress in the blood of cirrhotic rats treated with the antioxidant melatonin. METHODS: Cirrhosis was induced through inhalation of carbon tetrachloride. Liver integrity was evaluated by measuring serum enzymes, oxidative damage measured by lipoperoxidation, and antioxidant enzyme activity in erythrocytes. Lipoperoxidation, total nitrates, collagen, and histology by picrosirius staining were evaluated in the livers of these animals (n = 15), which were divided in three groups: control, carbon tetrachloride, and carbon tetrachloride + melatonin. Melatonin (20 mg/kg) was administered intraperitoneal from week 10 of carbon tetrachloride inhalation. In order to shorten the cirrhosis induction time, phenobarbital (0.3 g/L) was added to the animals' drinking water. RESULTS: A significant impairment in the liver integrity of melatonin-treated animals as compared to cirrhotic animals was observed. In rat erythrocytes and liver, lipoperoxidation was significantly increased in the cirrhotic rats as compared to controls, as measured through thiobarbituric acid reactive substances, and significantly decreased in melatonin-treated animals as compared to cirrhotic ones. In blood, a decrease in superoxide dismutase and glutathione peroxidase enzymes was detected in the cirrhotic group as compared to the control group, with increased superoxide dismutase activity when melatonin was administered. A reduction in the levels of total nitrates was detected in the hepatic tissue of the animals in the carbon tetrachloride group as compared to the control group and an increase of these levels in the carbon tetrachloride + melatonin group. As for hepatic collagen, we found a significant increase in the carbon tetrachloride group as compared to the controls and a regression of these values in the treated group. In histology, the rats in the carbon tetrachloride group showed fibrosis and formation of fibrotic nodules, characterizing liver cirrhosis; there was reduction of nodules and fibrosis in the melatonin treated group. CONCLUSION: The data allow us to suggest that the observed oxidative stress is related to the damages caused by carbon tetrachloride and that the use of melatonin can minimize these damages

scholarly journals TBHQ Alleviated Endoplasmic Reticulum Stress-Apoptosis and Oxidative Stress by PERK-Nrf2 Crosstalk in Methamphetamine-Induced Chronic Pulmonary Toxicity

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Yun Wang ◽  
Yu-Han Gu ◽  
Ming Liu ◽  
Yang Bai ◽  
Li-Ye Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Pulmonary Toxicity ◽  
Inflammatory Responses ◽  
Pulmonary Arteries ◽  
Treated Group ◽  
Control Group ◽  
Antioxidative Stress ◽  
And Oxidative Stress

Methamphetamine (MA) leads to cardiac and pulmonary toxicity expressed as increases in inflammatory responses and oxidative stress. However, some interactions may exist between oxidative stress and endoplasmic reticulum stress (ERS). The current study is designed to investigate if both oxidative stress and ERS are involved in MA-induced chronic pulmonary toxicity and if antioxidant tertiary butylhydroquinone (TBHQ) alleviated ERS-apoptosis and oxidative stress by PERK-Nrf2 crosstalk. In this study, the rats were randomly divided into control group, MA-treated group (MA), and MA plus TBHQ-treated group (MA + TBHQ). Chronic exposure to MA resulted in slower growth of weight and pulmonary toxicity of the rats by increasing the pulmonary arterial pressure, promoting the hypertrophy of right ventricle and the remodeling of pulmonary arteries. MA inhibited the Nrf2-mediated antioxidative stress by downregulation of Nrf2, GCS, and HO-1 and upregulation of SOD2. MA increased GRP78 to induce ERS. Overexpression and phosphorylation of PERK rapidly phosphorylated eIF2α, increased ATF4, CHOP, bax, caspase 3, and caspase 12, and decreased bcl-2. These changes can be reversed by antioxidant TBHQ through upregulating expression of Nrf2. The above results indicated that TBHQ can alleviate MA-induced oxidative stress which can accelerate ERS to initiate PERK-dependent apoptosis and that PERK/Nrf2 is likely to be the key crosstalk between oxidative stress and ERS in MA-induced chronic pulmonary toxicity.

scholarly journals Attenuation of Apoptosis and Oxidative Stress by Endurance Training in the Cerebellum of Diabetic Rats

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Asma Taheri ◽  
Abdolhamid Habibi ◽  
Saeid Shakerian ◽  
Mohammad Reza Tabandeh ◽  
Masoud Nikbakht
Keyword(s):  
Oxidative Stress ◽  
Endurance Training ◽  
Exercise Group ◽  
Diabetic Rats ◽  
Moderate Intensity ◽  
Control Group ◽  
Diabetic Patients ◽  
The Brain ◽  
And Oxidative Stress ◽  
Training Protocol

Objectives: Identifying the effective exercise protocol that attenuates the functional and molecular disturbances in different regions of the brain, in particular the cerebellum, can help the proper management of neuropathies in diabetic patients. Methods: Twenty rats were randomly divided into four groups: (1) Normal control group (CON), (2) normal exercise group (TH), (3) diabetes control group (DC), and (4) diabetes exercise group (TD). Diabetes was induced by i.p injection of a single dose of streptozotocin (50 mg/kg). The endurance training protocol was performed on a treadmill for five days a week for six weeks with moderate intensity. The activities of antioxidant enzymes and the expression or release of apoptotic factors were analyzed based on data from rat cerebellum tissue at the end of the experiments. Results: Six weeks of endurance training improved the oxidative defense system by increasing the activities of SOD (from 3.70 ± 0.64 to 6.55 ± 0.56), GPx (from 3.42 ± 0.73 to 4.84 ± 0.62), and catalase (from 1.36 ± 0.23 to 3.59 ± 0.37) and reducing the MDA concentration (from 6.81 ± 1.34 to 4.33 ± 1.03) in the cerebellum of diabetic rats. Increased expression or cytosolic release of apoptotic effectors such as bax, caspase 3, and cytochrome c in the cerebellum of diabetic rats were attenuated following exercise training. Conclusions: Our research results showed that six weeks of endurance training may be helpful for the attenuation of neuropathies in diabetic patients by the attenuation of apoptosis and oxidative stress in the cerebellum.

Pycnogenol Protects against Pentylenetetrazole-Induced Oxidative Stress and Seizures in Mice

2019 ◽  
Vol 14 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Radha Goel ◽  
Prasoon Saxena
Keyword(s):  
Oxidative Stress ◽  
Neuronal Degeneration ◽  
Thiobarbituric Acid ◽  
Biochemical Parameter ◽  
Control Group ◽  
Histopathological Study ◽  
Standard Drug ◽  
Pine Tree ◽  
Cognitive Behaviour ◽  
The Brain

Background:Epilepsy is one of the most common and severe brain disorders in the world, characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition. Oxidative stress is a biochemical state in which reactive oxygen species are generated and associated with various diseases including epilepsy. Pycnogenol, a polyphenol obtained from the pine tree and has antioxidant & anti-inflammatory activity. So, the aim of the study was to evaluate the effect of Pycnogenol on pentylenetetrazole (PTZ)-induced seizures in mice.Methods:The mice of swiss strain each weighing 18-30g were used. Pycnogenol (50&100mg/kg) was suspended in carboxymethyl cellulose in saline and administered orally. Diazepam (1mg/kg, i.p) was used as a standard drug. The anticonvulsant effects of the drugs were measured using PTZ and cognitive behaviour was also assessed. The biochemical estimation was done by measuring Thiobarbituric acid, Superoxide dismutase, Catalase, and reduced glutathione followed by the histopathological study.Result:Pycnogenol 50 & 100mg/kg showed a significant increase in latency to PTZ-induced seizures, decrease in duration and frequency of convulsions compared to control animals; however, the effects were dose-dependent and were more significant at a higher dose. No impairment in cognitive functions like memory and muscle relaxant was observed following pycnogenol 50 & 100 mg/kg. The effect of Pycnogenol on biochemical parameter was found to be significant. It significantly (p<0.01) decreases the level of TBARS and increases the levels of SOD, catalase, and GSH in the brain tissue. The histopathological evaluation showed less neuronal degeneration in the brain due to PTZ-induced seizures in comparison to control group.Conclusion:Thus pycnogenol has a protective approach towards convulsion and can be included as an adjuvant therapy with antiepileptic drugs.

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