scholarly journals Chronic Inhibition of FAAH Reduces Depressive-Like Behavior and Improves Dentate Gyrus Proliferation after Chronic Unpredictable Stress Exposure

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
A. R. Tejeda-Martínez ◽  
J. M. Viveros-Paredes ◽  
G. V. Hidalgo-Franco ◽  
E. Pardo-González ◽  
V. Chaparro-Huerta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dentate Gyrus ◽  
Depressive Disorders ◽  
Adrenal Glands ◽  
Enzyme Inhibitor ◽  
Acid Amide ◽  
Relative Weight ◽  
Antidepressant Effect ◽  
Chronic Unpredictable Stress ◽  
Neural Precursors

Symptoms of depressive disorders such as anhedonia and despair can be a product of an aberrant adaptation to stress conditions. Chronic unpredictable stress model (CUS) can generate an increase in the activity of the hypothalamic-pituitary-adrenal axis (HPA) and induce a reduction of neurotrophin signaling and the proliferation of neural progenitors in the adult dentate gyrus, together with increased oxidative stress. Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH). We aimed to evaluate the effects of FAAH inhibitor, URB597, on depressive-like behavior and neural proliferation of mice subjected to a model of CUS. URB597 was administered intraperitoneally at a dose of 0.2 mg/kg for 14 days after CUS. Depressive-like behaviors, anhedonia, and despair were evaluated in the splash and forced swimming tests, respectively. Alterations at the HPA axis level were analyzed using the relative weight of adrenal glands and serum corticosterone levels. Oxidative stress and brain-derived neurotrophic factor (BDNF) were also evaluated. Fluorescence immunohistochemistry tests were performed for the immunoreactivity of BrdU and Sox2 colabeling for comparison of neural precursors. The administration of URB597 was able to reverse the depressive-like behavior generated in mice after the model. Likewise, other physiological responses associated with CUS were reduced in the treated group, among them, increase in the relative weight of the adrenal glands, increased oxidative stress, and decreased BDNF and number of neural precursors. Most of these auspicious responses to enzyme inhibitor administration were blocked by employing a cannabinoid receptor antagonist. In conclusion, the chronic inhibition of FAAH generated an antidepressant effect, promoting neural progenitor proliferation and BDNF expression, while reducing adrenal gland weight and oxidative stress in mice under the CUS model.

scholarly journals Inhibition of Central Angiotensin Converting Enzyme Exerts Anxiolytic Effects by Decreasing Brain Oxidative Stress

2011 ◽  
Vol 30 (2) ◽  
pp. 109-114 ◽  
Author(s):  
Alin Ciobica ◽  
Lucian Hritcu ◽  
Veronica Nastasa ◽  
Manuela Padurariu ◽  
Walther Bild
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Elevated Plus Maze ◽  
Enzyme Inhibitor ◽  
Lipid Peroxidation Product ◽  
Converting Enzyme ◽  
Plus Maze ◽  
Antioxidant Defense Enzymes ◽  
Brain Oxidative Stress

Inhibition of Central Angiotensin Converting Enzyme Exerts Anxiolytic Effects by Decreasing Brain Oxidative StressThis study investigated the effects of angiotensin II and captopril intracerebroventricular administration on anxiety status and brain oxidative stress. Elevated plus maze was used in order to asses the anxiety-like behavior, while the biochemical analysis included the determination of some antioxidant defense enzymes like superoxide dismutase and glutathione peroxidase and also a lipid peroxidation product (malondialdehyde). Our results provide additional evidence of angiotensin II induced anxiety-like effects and increased prooxidant status. Moreover, the blockade of angiotensin II, by the administration of an angiotensin converting enzyme inhibitor (captopril) resulted in anxiolytic effects and decreased oxidative stress status. In addition, we found a significant correlation between the time spent by rats in the open arms of the elevated plus maze and oxidative stress markers. This could raise important therapeutic issues regarding the anxiolytic effects of some angiotensin converting enzyme inhibitors used primarily for hypertension, such as captopril. Also, it seems that oxidative stress could play an important part in these actions.

scholarly journals Oxidative Stress and Nucleic Acid Oxidation in Patients with Chronic Kidney Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Chih-Chien Sung ◽  
Yu-Chuan Hsu ◽  
Chun-Chi Chen ◽  
Yuh-Feng Lin ◽  
Chia-Chao Wu
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Nucleic Acid ◽  
Kidney Disease ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Enzyme Inhibitor ◽  
Alpha Tocopherol ◽  
Acid Oxidation ◽  
Clinical Biomarkers

Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids. Several clinical biomarkers and techniques have been used to detect the antioxidant status and oxidative stress/oxidative nucleic acid damage associated with long-term complications such as inflammation, atherosclerosis, amyloidosis, and malignancy in CKD patients. Antioxidant therapies have been studied to reduce the oxidative stress and nucleic acid oxidation in patients with CKD, including alpha-tocopherol, N-acetylcysteine, ascorbic acid, glutathione, folic acid, bardoxolone methyl, angiotensin-converting enzyme inhibitor, and providing better dialysis strategies. This paper provides an overview of radical production, antioxidant defence, pathogenesis and biomarkers of oxidative stress in patients with CKD, and possible antioxidant therapies.

scholarly journals Novel Antidepressant-Like Activity of Caffeic Acid Phenethyl Ester Is Mediated by Enhanced Glucocorticoid Receptor Function in the Hippocampus

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Mi-Sook Lee ◽  
Young Han Kim ◽  
Bo-ram Lee ◽  
Seung-Hae Kwon ◽  
Won-Jin Moon ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Caffeic Acid ◽  
Behavioral Assessment ◽  
Caffeic Acid Phenethyl Ester ◽  
Mitogen Activated Protein Kinase ◽  
Antidepressant Effect ◽  
Chronic Unpredictable Stress ◽  
Western Blots ◽  
Corticosterone Secretion ◽  
Mitogen Activated Protein

Caffeic acid phenethyl ester (CAPE) is an active component of propolis that has a variety of potential pharmacological effects. Although we previously demonstrated that propolis has antidepressant-like activity, the effect of CAPE on this activity remains unknown. The present study assessed whether treatment with CAPE (5, 10, and 20 µmol/kg for 21 days) has an antidepressant-like effect in mice subjected to chronic unpredictable stress via tail suspension (TST) and forced swim (FST) tests. CAPE administration induced behaviors consistent with an antidepressant effect, evidenced by decreased immobility in the TST and FST independent of any effect on serum corticosterone secretion. Western blots, conducted subsequent to behavioral assessment, revealed that CAPE significantly decreased glucocorticoid receptor phosphorylation at S234 (pGR(S234)), resulting in an increased pGR(S220/S234) ratio. We also observed negative correlations between pGR(S220)/(S234) and p38 mitogen-activated protein kinase (p38MAPK) phosphorylation, which was decreased by CAPE treatment. These findings suggest that CAPE treatment exerts an antidepressant-like effect via downregulation of p38MAPK phosphorylation, thereby contributing to enhanced GR function.

scholarly journals The Metabolite Urolithin-A Ameliorates Oxidative Stress in Neuro-2a Cells, Becoming a Potential Neuroprotective Agent

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 177 ◽  
Author(s):  
Guillermo Cásedas ◽  
Francisco Les ◽  
Carmen Choya-Foces ◽  
Martín Hugo ◽  
Víctor López
Keyword(s):  
Oxidative Stress ◽  
Enzyme Inhibitor ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Monoamine Oxidase A ◽  
Mitochondrial Activity ◽  
Radical Scavenger ◽  
Dependent Manner ◽  
Urolithin A ◽  
Ic50 Values

Urolithin A is a metabolite generated from ellagic acid and ellagitannins by the intestinal microbiota after consumption of fruits such as pomegranates or strawberries. The objective of this study was to determine the cytoprotective capacity of this polyphenol in Neuro-2a cells subjected to oxidative stress, as well as its direct radical scavenging activity and properties as an inhibitor of oxidases. Cells treated with this compound and H2O2 showed a greater response to oxidative stress than cells only treated with H2O2, as mitochondrial activity (MTT assay), redox state (ROS formation, lipid peroxidation), and the activity of antioxidant enzymes (CAT: catalase, SOD: superoxide dismutase, GR: glutathione reductase, GPx: glutathione peroxidase) were significantly ameliorated; additionally, urolithin A enhanced the expression of cytoprotective peroxiredoxins 1 and 3. Urolithin A also acted as a direct radical scavenger, showing values of 13.2 μM Trolox Equivalents for Oxygen Radical Absorbance Capacity (ORAC) and 5.01 µM and 152.66 µM IC50 values for superoxide and 2,2-diphenyss1-picrylhydrazyl (DPPH) radicals, respectively. Finally, inhibition of oxidizing enzymes, such as monoamine oxidase A and tyrosinase, was also detected in a dose-dependent manner. The cytoprotective effects of urolithin A could be attributed to the improvement of the cellular antioxidant battery, but also to its role as a direct radical scavenger and enzyme inhibitor of oxidases.

The Onset and Rate of the Antidepressant Effect of Electroconvulsive Therapy

1993 ◽  
Vol 162 (6) ◽  
pp. 725-732 ◽  
Author(s):  
Allan I. F. Scott ◽  
Lawrence J. Whalley
Keyword(s):  
Electroconvulsive Therapy ◽  
Royal College ◽  
Mode Of Action ◽  
Depressive Disorders ◽  
Practical Interest ◽  
Antidepressant Effect ◽  
Rapid Improvement ◽  
Research Committee ◽  
Biological Studies ◽  
Antidepressant Effects

This annotation is concerned with how soon and at what rate antidepressant effects become apparent over a course of electroconvulsive therapy (ECT). The first question is of importance in the design and interpretation of biological studies of the mode of action of ECT. The second question is of practical interest to the treating psychiatrist when we ask how the speed of recovery is influenced by what the psychiatrist prescribes, that is, the number and frequency of treatments. These questions are little better answered now than 20 years ago. This may come as a surprise to many readers, who have been advised to use ECT when “seeking rapid improvement” in depressive disorders (ECT Sub-Committee of the Research Committee of the Royal College of Psychiatrists, 1989). This lack of progress is attributable to a dearth of appropriately designed ECT studies.

scholarly journals Curcumin Acts as a Chemosensitizer for Leiomyosarcoma Cells In Vitro But Fails to Mediate Antioxidant Enzyme Activity in Cisplatin-Induced Experimental Nephrotoxicity in Rats

2019 ◽  
Vol 18 ◽  
pp. 153473541987281 ◽  
Author(s):  
Irida Dhima ◽  
Stelios Zerikiotis ◽  
Panagiotis Lekkas ◽  
Yannis V. Simos ◽  
Maria Gkiouli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Side Effects ◽  
Antioxidant Enzyme ◽  
Mitochondrial Function ◽  
Intraperitoneal Administration ◽  
Relative Weight ◽  
Antioxidant Enzyme Activity ◽  
Dose Finding ◽  
In Vivo Model

Background. Cisplatin (cis-diamminedichloroplatinum) is a widely used chemotherapeutic agent for the treatment of various cancers. Although it represents an effective regimen, its application is accompanied by side effects to normal tissues, especially to the kidneys. Cisplatin generates free radicals and impairs the function of antioxidant enzymes. Modulation of cisplatin-induced oxidative stress by specific antioxidant molecules represents an attractive approach to minimize side effects. Methods. We studied the ability of curcumin to sensitize leiomyosarcoma (LMS) cells to cisplatin. Assays for cell proliferation, mitochondrial function, induction of apoptosis, and cell cycle arrest were performed using various concentrations of cisplatin and a concentration of curcumin that caused a nonsignificant reduction in cell viability. Moreover, the effect of curcumin was examined against cisplatin-induced experimental nephrotoxicity. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen (BUN), and the kidney’s relative weight. Oxidative stress was measured by means of enzymatic activities of superoxide dismutase and glutathione peroxidase in the rats’ blood and malondialdehyde levels in rats’ urine. Results. In our study, we found that curcumin sensitizes LMS cells to cisplatin by enhancing apoptosis and impairing mitochondrial function. In an in vivo model of cisplatin-induced experimental nephrotoxicity, intraperitoneal administration of curcumin failed to preserve blood’s antioxidant enzyme activity and decrease lipid peroxidation. Nevertheless, curcumin was able to protect nephrons’ histology from cisplatin’s toxic effect. Conclusion. Our results showed that curcumin can act as chemosensitizer, but its role as an adjunctive cisplatin-induced oxidative stress inhibitor requires further dose-finding studies to maximize the effectiveness of chemotherapy.

scholarly journals Indomethacin Ameliorates Trimethyltin-Induced Neuronal Damage in Vivo by Attenuating Oxidative Stress in the Dentate Gyrus of Mice

2011 ◽  
Vol 34 (12) ◽  
pp. 1856-1863 ◽  
Author(s):  
Nguyen Quynh Huong ◽  
Yukary Nakamura ◽  
Nobuyuki Kuramoto ◽  
Masanori Yoneyama ◽  
Reiko Nagashima ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dentate Gyrus ◽  
Neuronal Damage

The Role of Oxidative Stress in Depressive Disorders

2012 ◽  
Vol 18 (36) ◽  
pp. 5890-5899 ◽  
Author(s):  
Tanja Maria Michel ◽  
Dietrich Pulschen ◽  
Johannes Thome
Keyword(s):  
Oxidative Stress ◽  
Depressive Disorders

THYROID FUNCTION AND ADRENAL WEIGHT IN THE RABBIT

1958 ◽  
Vol 17 (2) ◽  
pp. 197-200 ◽  
Author(s):  
K. BROWN-GRANT
Keyword(s):  
Young Adult ◽  
Thyroid Function ◽  
Adult Male ◽  
Adrenal Glands ◽  
Relative Weight ◽  
Adrenal Weight ◽  
Absolute Weight ◽  
Young Adult Male ◽  
The Mean ◽  
The Absolute

SUMMARY Young adult male rabbits were thyroidectomized or treated with methylthiouracil and adrenal weights determined after 3 or 6 weeks. No significant changes were seen following thyroidectomy. After 3 weeks of methylthiouracil treatment the mean absolute weight of the adrenal glands, but not the relative weight, was reduced. After 6 weeks both the absolute and relative weights were increased above the control levels, but the differences were not statistically significant. The results are compared with those obtained by other workers for rabbits and for other species.

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