Neuroprotective effects of protocatechuic acid on sodium arsenate induced toxicity in mice: Role of oxidative stress, inflammation, and apoptosis

2021 ◽  
Vol 337 ◽  
pp. 109392
Author(s):  
Zhaoxia Li ◽  
Yujuan Liu ◽  
Fang Wang ◽  
Zhuanglei Gao ◽  
Mohamed A. Elhefny ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protocatechuic Acid ◽  
Sodium Arsenate ◽  
Neuroprotective Effects

scholarly journals Benefits under the Sea: The Role of Marine Compounds in Neurodegenerative Disorders

Marine Drugs ◽  
2021 ◽  
Vol 19 (1) ◽  
pp. 24
Author(s):  
Mariano Catanesi ◽  
Giulia Caioni ◽  
Vanessa Castelli ◽  
Elisabetta Benedetti ◽  
Michele d’Angelo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorders ◽  
Extreme Temperature ◽  
Bioactive Molecules ◽  
Neuroprotective Effects ◽  
Physical Conditions ◽  
Adjuvant Therapies ◽  
Marine Habitats ◽  
Marine Compounds

Marine habitats offer a rich reservoir of new bioactive compounds with great pharmaceutical potential; the variety of these molecules is unique, and its production is favored by the chemical and physical conditions of the sea. It is known that marine organisms can synthesize bioactive molecules to survive from atypical environmental conditions, such as oxidative stress, photodynamic damage, and extreme temperature. Recent evidence proposed a beneficial role of these compounds for human health. In particular, xanthines, bryostatin, and 11-dehydrosinulariolide displayed encouraging neuroprotective effects in neurodegenerative disorders. This review will focus on the most promising marine drugs’ neuroprotective potential for neurodegenerative disorders, such as Parkinson’s and Alzheimer’s diseases. We will describe these marine compounds’ potential as adjuvant therapies for neurodegenerative diseases, based on their antioxidant, anti-inflammatory, and anti-apoptotic properties.

scholarly journals Carnosine Prevents Aβ-Induced Oxidative Stress and Inflammation in Microglial Cells: A Key Role of TGF-β1

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 64 ◽  
Author(s):  
Giuseppe Caruso ◽  
Claudia Fresta ◽  
Nicolò Musso ◽  
Mariaconcetta Giambirtone ◽  
Margherita Grasso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Microglial Cells ◽  
Neuronal Cultures ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Aβ Oligomers ◽  
Endogenous Antioxidant ◽  
Tgf Β1

Carnosine (β-alanyl-L-histidine), a dipeptide, is an endogenous antioxidant widely distributed in excitable tissues like muscles and the brain. Carnosine is involved in cellular defense mechanisms against oxidative stress, including the inhibition of amyloid-beta (Aβ) aggregation and the scavenging of reactive species. Microglia play a central role in the pathogenesis of Alzheimer’s disease, promoting neuroinflammation through the secretion of inflammatory mediators and free radicals. However, the effects of carnosine on microglial cells and neuroinflammation are not well understood. In the present work, carnosine was tested for its ability to protect BV-2 microglial cells against oligomeric Aβ1-42-induced oxidative stress and inflammation. Carnosine prevented cell death in BV-2 cells challenged with Aβ oligomers through multiple mechanisms. Specifically, carnosine lowered the oxidative stress by decreasing NO and O2−• intracellular levels as well as the expression of iNOS and Nox enzymes. Carnosine also decreased the secretion of pro-inflammatory cytokines such as IL-1β, simultaneously rescuing IL-10 levels and increasing the expression and the release of TGF-β1. Carnosine also prevented Aβ-induced neurodegeneration in mixed neuronal cultures challenged with Aβ oligomers, and these neuroprotective effects were completely abolished by SB431542, a selective inhibitor of the type-1 TGF-β receptor. Our data suggest a multimodal mechanism of action of carnosine underlying its protective effects on microglial cells against Aβ toxicity with a key role of TGF-β1 in mediating these protective effects.

The comprehensive mechanistic insight into the effects of vitamin D on dementia – a review

2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Jaber Jafarzadeh ◽  
Laleh Payahoo ◽  
Mohammad Yousefi ◽  
Ali Barzegar
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Bone Mineralization ◽  
Serum Levels ◽  
Skeletal Maturation ◽  
Micronutrient Deficiencies ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Modifiable Factors

Purpose This paper aims to depict the mechanistic role of vitamin D on dementia prevention, relief of the severity and the complication of the disease. All papers indexed in scientific databases, including Scopus, Elsevier, PubMed, Embase and Google Scholar between 2000 and 2021 were extracted and discussed. To present the mechanistic role of vitamin D in declining the severity of dementia, keywords including dementia, vitamin D, oxidative stress, inflammation, amyloid beta-Peptides were used. Design/methodology/approach Dementia is a prevalent cognitive disorder worldwide, especially in elderly people, which is accompanied by serious disabilities. Besides genetic, biological and lifestyle factors are involved in the incidence of dementia. An unhealthy diet along with micronutrient deficiencies are among modifiable factors. Vitamin D is one of the important micronutrients in brain health. Besides the involvement in gene expression, bone mineralization, apoptosis, inflammation, skeletal maturation, neurotropic action and hemostasis of phosphate and calcium, vitamin D also exerts neuroprotective effects via genomic and non-genomic pathways. Findings Vitamin D up-regulates the expression of various genes involved in dementia incidence via various mechanisms. Decreasing oxidative stress and the neuro-inflammatory cytokines levels, regulation of the expression of alternated Proteins including Tau and Amyloid-ß, calcium homeostasis in the central nervous system and also vascular are considered main mechanisms. Originality/value Considering the importance of diet in preventing dementia, adherence to a healthy diet that provides essential nutrients to brain function seems to be urgent. Controlling serum levels of vitamin D periodically and providing vitamin D by related sources or supplements, if there is a deficiency, is recommended. Future studies are needed to clarify other related mechanisms.

Role of the inhibition of oxidative stress and inflammatory mediators in the neuroprotective effects of hydroxytyrosol in rat brain slices subjected to hypoxia reoxygenation

2013 ◽  
Vol 24 (12) ◽  
pp. 2152-2157 ◽  
Author(s):  
Susana Cabrerizo ◽  
José Pedro De La Cruz ◽  
Juan Antonio López-Villodres ◽  
Javier Muñoz-Marín ◽  
Ana Guerrero ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Inflammatory Mediators ◽  
Brain Slices ◽  
Neuroprotective Effects ◽  
Hypoxia Reoxygenation

scholarly journals Neuroprotective effects of α-lipoic acid on the development of oxidative stress and astrogliosis in the brain of STZ-diabetic rats

2014 ◽  
Vol 5 (2) ◽  
pp. 143-147
Author(s):  
S. Kyrychenko ◽  
I. Prishchepa ◽  
V. Lagoda ◽  
M. Velika ◽  
V. Nedzvetsky
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipoic Acid ◽  
Diabetic Rats ◽  
Alpha Lipoic Acid ◽  
Neuroprotective Effects ◽  
Neuronal Markers ◽  
The Brain ◽  
Polypeptide Band

The aim of this study was to examine whether the antioxidant alpha-lipoic acid protects neurons from diabetic-reperfusion injury. The streptozotocin (STZ) rat model was used to study the glial reactivity and prevention of gliosis by alpha-lipoic acid (alpha-LA) administration. The expression of glial fibrillary acidic protein (GFAP) was determined, as well as lipid peroxidation (LPO) and glu-tathione (GSH) levels in some brain tissues. We observed significant increasing of lipid peroxidation products in both hippocampus and cortex. Changesof polypeptide GFAP were observed in hippocampus and cortex. Both soluble and filamentous forms of GFAP featured the increase in hippocampus of rat with hyperthyreosis. In the filamentfractions, increase in the intensity of 49 kDa polypeptide band was found. In the same fraction of insoluble cytoskeleton proteins degraded HFKB polypeptides with molecular weight in the range of 46–41 kDa appeared. Markedincrease of degraded polypeptides was found in the soluble fraction of the brain stem. The intensity of the intact polypeptide – 49 kDa, as well as in the filament fraction, significantly increased. It is possible that increasing concentrations of soluble subunits glial filaments may be due to dissociation of own filaments during the reorganization of cytoskeleton structures. Given the results of Western blotting for filament fraction, increased content of soluble intact 49 kDa polypeptide is primarily the result of increased expression of HFKB and only partly due to redistribution of existing filament structures. Calculation and analysis of indicators showed high correlation between the increase in content and peroxidation products of HFKB.These results indicate the important role of oxidative stress in the induction of astroglial response under conditions of diabet encefalopathia. Administration of alpha-LA reduced the expression both of glial and neuronal markers. In addition, alpha-LA significantly prevented the increase in LPO levels found in diabetic rats. GSH levels increased by the administration of alpha-LA. This study suggests that alpha-LA prevents neural injury by inhibiting oxidative stress and suppressing reactive gliosis. All these changes were clearly counteracted by alpha-lipoic acid. The results of this study demonstrate that alpha-lipoic acid provides for protection to the GFAP, as a whole, from diabet -reperfusion injuries. 

Role of heme oxygenase-1 protein in the neuroprotective effects of cyclopentenone prostaglandin derivatives under oxidative stress

2003 ◽  
Vol 17 (11) ◽  
pp. 2249-2255 ◽  
Author(s):  
Takumi Satoh ◽  
Megumi Baba ◽  
Daisaku Nakatsuka ◽  
Yasuyuki Ishikawa ◽  
Hiroyuki Aburatani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Neuroprotective Effects ◽  
Cyclopentenone Prostaglandin

Sulfur – Containing Amino Acids in Seizures: Current State of the Art

2018 ◽  
Vol 25 (3) ◽  
pp. 378-390 ◽  
Author(s):  
Dragan Hrncic ◽  
Aleksandra Rasic-Markovic ◽  
Duro Macut ◽  
Dusan Mladenovic ◽  
Veselinka Susic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Experimental Models ◽  
Neuroprotective Effects ◽  
Homocysteine Thiolactone ◽  
Current State ◽  
Sulfur Containing ◽  
And Oxidative Stress

Background: Homocysteine and taurine are non-proteinogenic sulfur-containing amino acids with numerous important physiological roles. Homocysteine and taurine are considered to be neurotransmitters and neuromodulators, the first showing clear hyperexcitability role, while the second is known by its inhibitory and neuroprotective properties. Objective: In this article we addressed the role of homocysteine and its related metabolite homocysteine thiolactone in the development of seizures, focusing on its experimental models in vivo, potential mechanisms of proepileptogenic activity via interactions with glutamatergic neurotransmission, sodium pump activity, oxidative stress, cholinergic system and NO-mediated neuronal signaling, as well as the pharmacological and non-pharmacological approaches to modulate its proconvulsive activity. Additionally, herein we will focus on taurine neuroprotective effects linked with its anticonvulsive properties and mediated by taurine interactions with GABA-ergic and glutamatergic system and oxidative stress.

Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 723 ◽  
pp. 137969 ◽  
Author(s):  
Ebtesam M. Al Olayan ◽  
Abeer S. Aloufi ◽  
Ohoud D. AlAmri ◽  
Ola H. El-Habit ◽  
Ahmed E. Abdel Moneim
Keyword(s):  
Oxidative Stress ◽  
Protocatechuic Acid

Protective role of protocatechuic acid in sevoflurane-induced neuron apoptosis, inflammation and oxidative stress in mice

2020 ◽  
Vol 38 (4) ◽  
pp. 323-331
Author(s):  
Yuhua Gao ◽  
Liping Ma ◽  
Tao Han ◽  
Meng Wang ◽  
Dongmei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Apoptosis ◽  
Protocatechuic Acid ◽  
Protective Role ◽  
Continuous Treatment ◽  
Tunel Staining ◽  
Neuroprotective Effects ◽  
Tnf Α ◽  
Pre Treatment ◽  
And Oxidative Stress

Background: In neonatal mice, sevoflurane, inspired through the nasal cavity to act as anesthesia, triggers neuronal apoptosis, inflammation and oxidative injury that can hamper cognitive functions in the growth of the central nervous system in the later stages of life. Objective: Our study aimed to explore the potential neuroprotective effects of protocatechuic acid (PCA) to ameliorate neonatal sevoflurane-induced neurotoxicity. Methods: Male mice were pretreated with PCA (10 or 20 mg/kg) for half an hour before continuous treatment for 6 h with 3 % sevoflurane. TUNEL staining was performed to examine the apoptotic cells to record their count. ELISA was performed to evaluate the expressions of the proteins - IL-1β, IL-18 and TNF-α. Analysis of the Western blot and test of the Morris maze was determined and the results analyzed. Results: TUNEL findings assay showed a significant reduction with sevoflurane in neuronal apoptosis treated with PCA at 20 mg/kg. The expression of protein Caspase-3 showed significant changes in the group SEV + PCA (20 mg/kg). ELISA analysis showed that the levels of IL-18 and TNF-α were significantly reduced in the SEV + PCA (20 mg/kg) group as compared to SEV + PCA (10 mg/kg) group. MDA, ROS and SOD levels were noted to decrease significantly only in the SEV + PCA group (20 mg/kg) while IL-1β levels decreased in both SEV + PCA groups (10 or 20 mg/kg) respectively. Conclusions: Our findings imply that apoptosis, inflammation, and oxidative stress in the hippocampal region of neonatal mouse brain were significantly reduced by pre-treatment with PCA before sevoflurane exposure. Therefore, suggesting a role for PCA as a novel therapeutic agent in the treatment of sevoflurane anesthesia-induced neurobehavioral dysfunction.

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