Consumption of Ashtanga Ghrita (clarified cow butter added with herb extracts) improves cognitive dysfunction induced by scopolamine in rats via regulation of acetylcholinesterase activity and oxidative stress

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Vineet Sharma ◽  
Zeba Firdaus ◽  
Himanshu Rai ◽  
Prasanta Kumar Nayak ◽  
Tryambak Deo Singh ◽  
...  

Abstract Objectives Ashtanga Ghrita (AG), an Indian traditional formulation, has been used to promote neuropharmacological activities. AG is made up of clarified cow butter (ghee) and eight different herbs. Methods To test whether scopolamine (SCP)-induced dementia and brain oxidative stress can be counteracted by AG, rats were separated into five groups (n=6/group): group one control, group two SCP (1 mg/kg b.w., i.p.) treated and group three to five were co-treated with different doses of AG (1.25, 2.5 and 5 g/kg b.w., orally) and SCP. After the treatment regimen, behavioral (Y-maze test) and brain biochemical changes were measured in all groups. Results Microbial load and heavy metals were found within permissible limits. Results from attenuated total reflection Fourier-transform infrared spectroscopy demonstrated the complexation/interaction of herbal phytoconstituents with the functional groups of Ghrita. Preliminary phytochemical analysis of AG exhibited the occurrence of flavonoids, phenolics, glycosides, steroids, triterpenes, tannins, and amino acids. Findings of the experimental study exhibited that AG significantly protected the rats from SCP-induced behavioral dysfunction and brain biochemical alterations. Conclusions This study demonstrates that AG protects the brain from SCP-induced dementia by promoting brain antioxidant activity and thus could be a promising drug for the treatment of neurodegenerative disease.

2021 ◽  
Vol 11 ◽  
Author(s):  
Omar M.E. Abdel-Salam ◽  
Eman R. Youness ◽  
Nadia A. Mohammed ◽  
Amr M.M. Ibrahim

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.


Author(s):  
Jafar Ahmadpouri ◽  
Saeid Valipour Chahardahcharic ◽  
Mahbubeh Setorki

Background: The oxidant-antioxidants balance in the living organism is constantly challenged by internal and external pressures. Maidenhair or Adiantum capillus-veneris (Acv) is rich in bioactive compounds with antioxidant effects.  Objectives: The present study aimed at investigating the effect of Acv hydroalcoholic extract on the oxidative stress rate of blood and brain of mice in the depression model caused by acute immobilization stress. Methods: In this study, 40 male Balb/C mice were randomly divided into five groups, including 1 (control, 2, 3, and 4) intervention (receiving doses of 100, 200, and 400 Acv extracts) and diazepam group. Acute stress was induced by motion limitation (2 hours) and electrochemical shock (0.5 mA, 2 min), and then the mice were treated intraperitoneally with the extract or drug for 21 days. First, the rate of depression was assessed by forced swimming. Then, the Total Antioxidant Capacity (TAC), serum Malondialdehyde (MDA), and the MDA level of the brain were determined. Results: The prescription of different doses of Acv extract and diazepam significantly reduced the duration of immobilization in the forced swimming test compared with the control group (P<0.05). Besides, Acv extract at different doses of  200 and 400 significantly increased serum FRAP (TAC) and significantly increased TAC of the brain compared with the control group. Administration of Acv extract at different doses of 200 and 400  and diazepam significantly decreased serum MDA but significantly decreased MDA of the brain of mice compared with the control group (P<0.05). Conclusion: Acv extract can reduce the symptoms of depression and protect against acute stress-related oxidative stressors


2020 ◽  
Vol 14 (2) ◽  
pp. 100-116
Author(s):  
Kavoos Tahmasebi ◽  
Mahvash Jafari ◽  
Farideh Izadi ◽  
Alireza Asgari ◽  
Hoosein Bahadoran ◽  
...  

Background: Exposure to diazinon (DZN) as an organophosphorus insecticide is associated with reducing the antioxidant capacity of cells. N-acetyl cysteine (NAC) is widely used in clinics to treat several diseases related to oxidative stress. Objective: The current study was aimed to evaluate the prophylactic and therapeutic roles of NAC on biochemical and oxidative changes induced by acute poisoning of DZN in various tissues of male Wistar rats. Methods: Thirty rats were divided into five groups: control group received corn oil as DZN solvent; DZN group received 100 mg/kg of DZN; NAC group received 160 mg/kg of NAC; NAC-DZN and DZN-NAC groups received 160 mg/kg of NAC before and after 100 mg/kg of DZN injection, respectively. Plasma and various tissues were prepared and evaluated for the measurement of the biochemical parameters and oxidative stress biomarkers. Results: Both prophylactic and therapeutic treatments by NAC ameliorated the increased lipid peroxidation and decreased glutathione level and superoxide dismutase, catalase and glutathione S-transferase activities in tissues (P<0.05). Moreover, treatment with the NAC caused a significant reduction in DZN-induced high levels of plasma biochemical parameters. Furthermore, acetylcholinesterase activity was positively correlated with both LDH (P=0.000) activity and GSH (P=0.001) level and negatively correlated with MDA (P=0.009) level in the brain. Conclusion: Results suggest that NAC could effectively ameliorate the DZN-induced oxidative stress and cholinergic hyperactivity in various tissues especially in the brain, through free radicals scavenging and GSH synthesis. Prophylactic approach exerted a stronger protective effect compared to a therapeutic treatment.


2021 ◽  
Vol 10 ◽  
pp. e2218
Author(s):  
Bahareh Eghbal ◽  
Ava Soltani Hekmat ◽  
Seyed Amin Kouhpayeh ◽  
Ali Ghanbariasad ◽  
Kazem Javanmardi ◽  
...  

Background: Electroconvulsive Therapy (ECT) as a well-established and effective therapeutic approach for the treatment of various psychiatric disorders is an excellent option to treat the major depressive disorder (MDD). The goal of this experimental study was to determine the possible sides effects of electroconvulsive shock (ECS) and duloxetine, a serotonin-norepinephrine Reuptake Inhibitors (SNRIs), and evaluate the safety of this therapeutic approach on behavioral factors, cardiovascular function, and brain oxidative stress markers on mice. Materials and Methods: Animals were divided into different groups receiving either ECS or different doses (10, 20, 40, 80, or 120 mg) of duloxetine alone or together. We evaluated the behavioral factors associated with administration of ECS with or without duloxetine. In addition, we monitored the ECGs (electrocardiogram) of animals prior to and after the experiment and also evaluated the oxidative stress markers including TAC, MDA, and GSH mice’s brains. Results: We did not detect any significant differences in terms of heart rate, RR interval, PR interval, QT, or corrected QT (QTc) between groups that received different doses of duloxetine in combination with ECS compare to the control group. Our findings suggest that while administration of ECS solely increased the oxidative stress markers and decreased the antioxidant capacity of the brain, a combination of duloxetine and ECS at certain doses alleviates the oxidative stress condition and increases the antioxidant capacity of the brain. Conclusion: Overall, this study suggests that the combination of ECS and duloxetine is safe and considerable for further studies on human subjects.


2007 ◽  
Vol 98 (3) ◽  
pp. 1820-1826 ◽  
Author(s):  
Eloi F. Rosa ◽  
Shirley Takahashi ◽  
Jeannine Aboulafia ◽  
Viviane L. A. Nouailhetas ◽  
Maria G. M. Oliveira

It has been shown that exercise is helpful against brain disorders. However, this may not be true for intense exercise (IE). Because it is easy to misadjust exercise intensity with physical condition, it is essential to know the effects of IE on cognitive process because it may have important consequences on people skills and work skills. We investigated the effects of IE on male C57Bl/6 mice, 3-mo-old, undergoing 10 days of intense and exhaustive running program on cognition and its possible relationship with brain oxidative stress. Cognition was evaluated by three different cognitive tests: passive avoidance task, contextual fear conditioning, and tone fear conditioning, performed 24 h after the last exercise session. Brain oxidative stress was evaluated by lipid peroxidation and protein oxidation. There was a remarkable memory reduction of exercised animals in comparison with the control group, associated with increase in the brain oxidative stress, with no alterations in shock sensitivity, locomotion and anxiety parameters. Concurrent vitamin C and E supplementation fully prevented the memory decrement induced by IE and partially recovered both the increased the brain lipid peroxidation and the protein oxidation. In conclusion, IE-induces a high index of brain oxidative stress and impairs memory in murine model that was prevented by vitamin C and E supplementation.


Author(s):  
Mohammad Fiasal Zaher ◽  
Mohamed Abdelfattah Bendary ◽  
Gamal Saeed Abd El-Aziz ◽  
Ahmad Shaker Ali

Aim: To evaluate the neuroprotective potential of thymoquinine (TQ) on the oxidative stress status of the brain in aluminum chloride (AlCl3)-induced AD in rats. Study Design:  Animal research study. Place and Duration of Study: King Fahd Medical Research Center (KFMRC), King Abdulaziz University, Saudi Arabia, April 2018-June 2019. Methodology: Thirty adult male Sprague Dawley albino rats were randomly divided into 3 groups. Group 1 (Control). Group 2 (AD): supplemented orally with AlCl3 (17 mg/kg/day) for 4 weeks. Group 3 (TQ/AD): supplemented concomitantly with oral TQ (10 mg/kg/day) and AlCl3 (17 mg/kg/day) for 4 weeks. At the end of the experiment, spatial working memory was assessed using the Y-maze spontaneous alternation test. Then, serum levels of malondialdehyde (MDA) and glutathione peroxidase enzyme (GPX) were assessed. Then, the rats were sacrificed, and the brain was isolated, and a light microscopic examination of the hippocampus was performed. Finally, the brain homogenate content of Aβ, tau protein and acetylcholine were biochemically determined. Results: The AD group showed a significant decreased in the spontaneous alteration performance (SAP %) in Y-maze. Also, in the AD group, serum MDA, Aβ and tau protein were significantly increased with a significant decrease of serum GPX and acetylcholine. Examination of H&E-stained sections of the hippocampus of the AD group revealed decreased thickness and disorganization of the pyramidal cell layer of CA1 and CA3 where many pyramidal cells lost their triangular shape and appeared shrunken. The molecular and polymorphic layers showed increased glial cells and congested blood capillaries. The dentate gyrus showed marked disorganization with some cell loss. Co-administration of TQ with AlCl3 in TQ/AD group, improved SAP % and significantly decreased serum MDA, Aβ, tau protein. It also increased serum GPX and acetylcholine levels. Also, TQ partially attenuated the histopathological changes in the hippocampus. Conclusion: TQ could mitigate the oxidative stress markers, neurodegenerative indices and histopathological alteration encountered in AD that all reflected on improving the cognitive behavior. This may implement TQ as an adjuvant medical strategy in ameliorating AD.


2019 ◽  
Vol 25 (3) ◽  
pp. 221-226
Author(s):  
Fereshteh Asgharzadeh ◽  
Mahmoud Hosseini ◽  
Rahimeh Bargi ◽  
Mohammad Soukhtanloo ◽  
Farimah Beheshti ◽  
...  

Background: Frequent seizure is followed by overproduction of free radicals and brain oxidative stress. Renin angiotensin system (RAS) has some effects on central nervous system. We designed this research to challenge the effect of captopril as an angiotensin converting enzyme (ACE) inhibitor against brain oxidative stress in pentylenetetrazole (PTZ) -induced seizures in mice. Methods: The groups were including (1) Control (saline); (2) PTZ (100 mg/kg, i.p.), (3-5) PTZ- captopril (Capto) that received three doses of Capto 10, 50 and 100 mg/kg 30 min before PTZ injection. Latency time in the onset minimal clonic seizures (MCS) and generalized tonic-clonic seizures (GTCS) were recorded. The level of malondialdehyde (MDA) and total thiol, as well as superoxide dismutase (SOD) and catalase (CAT) activity in the hippocampus and cortex were measured. Results: All doses of captopril postponed the onset of MCS and GTCS. Accumulation of MDA in the brain tissues of PTZ group was higher than control group, while total thiol content and CAT activity were lower. Pretreatment with captopril (100 mg/kg) diminished MDA concentration compared with PTZ group. Captopril (50 and 100 mg/kg) also increased the level of total thiol groups versus PTZ group. Captopril injection (50 and 100 mg/kg) elevated the activity of SOD and CAT in the brain tissues. In addition captopril administration diminished mortality rate caused by PTZ. Conclusion: Findings demonstrated that convulsions caused by PTZ were followed by oxidative stress status in the brain tissues. Pretreatment with captopril attenuated the effect of PTZ on brain tissue oxidative damage.<br />


2020 ◽  
Vol 21 (6) ◽  
pp. 480-487
Author(s):  
Med A. Smach ◽  
Jawhar Hafsa ◽  
Bassem Charfeddine ◽  
Hedi Dridi ◽  
Khalifa Limem ◽  
...  

Background: Arthrophytum scoparium (Pomel) Iljin (Amaranthaceae family) has been widely used in traditional Tunisian medicine to treat many disorders such as migraine, headache, and neurological disorders. This study investigates the effect of Arthrophytum scoparium Aqueous Extract (ASAE) on cognitive impairments and oxidative injury induced by galactose (10%) in a mouse model. Materials and Methods: The mice were divided randomly into 4 experimental groups, including the control group (saline water 9 ‰), Galactose group, Scop group (300 mg/kg/d), and Scop+Gal group (300 mg/kg/d). Mice received the corresponding solutions by intraperitoneal injection (i.p.) for 7 days before the Y-maze active tests. Galactose 10% was given to all groups except control and Scop groups, 30 min before the trial. Levels of Acetylcholinesterase Activity (AChE), Ascorbic Acid (AA), Gluthatione (GSH) and Malondialdehyde (MDA) in mice brains were examined. Results: Chronic administration of galactose significantly impaired cognitive performance in Y maze, caused marked oxidative damages and a significant increase in the acetylcholinesterase activity as compared to other groups. On the contrary, ASAE (300 mg/kg) treatment suppressed galactoseinduced oxidative damage by ameliorating the increased levels of GSH and AA. Moreover, ASAE treatment reduced brain AChE activities in the galactose-induced model. Conclusion: These findings suggest that ASAE exerts potent anti-amnesic effects via the modulation of cholinergic and antioxidant activities. The observed pharmacological activities should be further evaluated by detailed experimental studies and validated by clinical trials.


2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.


Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.


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