scholarly journals Protective and Antioxidant Effects of a Chalconoid fromPulicaria incisaon Brain Astrocytes

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Anat Elmann ◽  
Alona Telerman ◽  
Hilla Erlank ◽  
Sharon Mordechay ◽  
Miriam Rindner ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Antioxidant Effect ◽  
Desert Plant ◽  
Oxygen Species ◽  
Protective Effects ◽  
Fourfold Increase ◽  
Glial Derived Neurotrophic Factor ◽  
The Brain ◽  
Antioxidant Effects

Oxidative stress is involved in the pathogenesis of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support, such as glial-derived neurotrophic factor (GDNF). Thus, any damage to astrocytes will affect neuronal survival. In the present study, by activity-guided fractionation, we have purified from the desert plantPulicaria incisatwo protective compounds and determined their structures by spectroscopic methods. The compounds were found to be new chalcones—pulichalconoid B and pulichalconoid C. This is the first study to characterize the antioxidant and protective effects of these compounds in any biological system. Using primary cultures of astrocytes, we have found that pulichalconoid B attenuated the accumulation of ROS following treatment of these cells with hydrogen peroxide by 89% and prevented 89% of the H2O2-induced death of astrocytes. Pulichalconoid B exhibited an antioxidant effect bothin vitroand in the cellular antioxidant assay in astrocytes and microglial cells. Pulichalconoid B also caused a fourfold increase inGDNF transcriptionin these cells. Thus, this chalcone deserves further studies in order to evaluate if beneficial therapeutic effect exists.

scholarly journals Antioxidant and Astroprotective Effects of aPulicaria incisaInfusion

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Anat Elmann ◽  
Alona Telerman ◽  
Sharon Mordechay ◽  
Hilla Erlank ◽  
Rivka Ofir
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Brain Injuries ◽  
Desert Plant ◽  
Oxygen Species ◽  
Intracellular Accumulation ◽  
Glial Derived Neurotrophic Factor ◽  
The Brain ◽  
Antioxidant Effects

Oxidative stress is involved in the pathogenesis of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support, such as glial-derived neurotrophic factor (GDNF). Thus, any damage to astrocytes will affect neuronal survival. In the present study, an infusion prepared from the desert plantPulicaria incisa(Pi) was tested for its protective and antioxidant effects on astrocytes subjected to oxidative stress. ThePiinfusion attenuated the intracellular accumulation of ROS following treatment with hydrogen peroxide and zinc and prevented the H2O2-induced death of astrocytes. ThePiinfusion also exhibited an antioxidant effectin vitroand induced GDNF transcription in astrocytes. It is proposed that thisPiinfusion be further evaluated for use as a functional beverage for the prevention and/or treatment of brain injuries and neurodegenerative diseases in which oxidative stress plays a role.

scholarly journals Anticonvulsive and Antioxidant Effects of Pioglitazone on Pilocarpine-induced Seizures in Mice

2021 ◽  
Vol 15 (4) ◽  
pp. 271-278
Author(s):  
Saba Rostamian ◽  
◽  
Samaneh Keshavarz Hedayati ◽  
Sara Khosraviani ◽  
Ehsan Aali ◽  
...  
Keyword(s):  
Action Potentials ◽  
Neuronal Damage ◽  
Antioxidant Properties ◽  
Antioxidant Effect ◽  
Protective Effects ◽  
Seizure Onset ◽  
Ppar Γ ◽  
The Brain ◽  
Antioxidant Effects

Background: Epilepsy is a neurological disorder caused by uncontrollable discharge of action potentials from neurons in the brain. After a seizure, oxidative stress may cause a significant neuronal damage. In the current study, we assessed the anticonvulsant and antioxidant properties of pioglitazone, a peroxisome proliferated activated receptor-γ (PPAR-γ) agonist that is used in type-2 diabetes, on pilocarpine-induced seizure in mice. Methods: Pilocarpine (400 mg/kg) or normal saline was injected intraperitoneally 4 hours after oral administration of Pioglitazone (80 mg/kg). Also, carboxymethyl cellulose was administered orally in control and Pilocarpine groups. After the administration of Pilocarpine all of the mice were observed for 1 hour to measure the seizure latency time. Pilocarpine-induced seizures were categorized using the Racine scale. Then all animals were decapitated, brain was removed and hippocampus was dissected. Finally, the level of Malondialdehyde (MDA) and Catalase (CAT) activity, Superoxide Dismutase (SOD), and Glutathione Reductase (GR) levels were quantified in hippocampus by biochemical methods. Results: Pioglitazone significantly increased the latency to seizure onset of stages 1-4 (P≤0.01-0.001). Also, pioglitazone prevented the development of stage 5 of the pilocarpine-induced seizure. After the seizure, pioglitazone significantly decreased the level of MDA (P<0.01) and elevated the levels of CAT (P<0.01), SOD (P<0.01) and GR (P<0.001) enzymes in the mice hippocampus compared to those in the pilocarpine group. Conclusion: The findings of this study indicate that the antioxidant effect of pioglitazone may play an important role in its protective effects against neuronal damage caused by pilocarpine-induced seizure.

scholarly journals Protective Effects of Scolopendra Water Extract on Trimethyltin-Induced Hippocampal Neurodegeneration and Seizures in Mice

2019 ◽  
Vol 9 (12) ◽  
pp. 369
Author(s):  
Yun-Soo Seo ◽  
Mary Jasmin Ang ◽  
Byeong Cheol Moon ◽  
Hyo Seon Kim ◽  
Goya Choi ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Primary Cultures ◽  
Water Extract ◽  
Model Systems ◽  
Inflammatory Factor ◽  
Dependent Manner ◽  
Protective Effects ◽  
Cell Degeneration

Trimethyltin (TMT) is an organotin compound with potent neurotoxic action characterized by neuronal degeneration in the hippocampus. This study evaluated the protective effects of a Scolopendra water extract (SWE) against TMT intoxication in hippocampal neurons, using both in vitro and in vivo model systems. Specifically, we examined the actions of SWE on TMT- (5 mM) induced cytotoxicity in primary cultures of mouse hippocampal neurons (7 days in vitro) and the effects of SWE on hippocampal degeneration in adult TMT- (2.6 mg/kg, intraperitoneal) treated C57BL/6 mice. We found that SWE pretreatment (0–100 μg/mL) significantly reduced TMT-induced cytotoxicity in cultured hippocampal neurons in a dose-dependent manner, as determined by lactate dehydrogenase and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assays. Additionally, this study showed that perioral administration of SWE (5 mg/kg), from −6 to 0 days before TMT injection, significantly attenuated hippocampal cell degeneration and seizures in adult mice. Furthermore, quantitative analysis of Iba-1 (Allograft inflammatory factor 1)- and GFAP (Glial fibrillary acidic protein)-immunostained cells revealed a significant reduction in the levels of Iba-1- and GFAP-positive cell bodies in the dentate gyrus (DG) of mice treated with SWE prior to TMT injection. These data indicated that SWE pretreatment significantly protected the hippocampus against the massive activation of microglia and astrocytes elicited by TMT. In addition, our data showed that the SWE-induced reduction of immune cell activation was linked to a significant reduction in cell death and a significant improvement in TMT-induced seizure behavior. Thus, we conclude that SWE ameliorated the detrimental effects of TMT toxicity on hippocampal neurons, both in vivo and in vitro. Altogether, our findings hint at a promising pharmacotherapeutic use of SWE in hippocampal degeneration and dysfunction.

scholarly journals Inhibition of cPLA2 and sPLA2 Activities in Primary Cultures of Rat Cortical Neurons by Centella asiatica Water Extract

2012 ◽  
Vol 7 (7) ◽  
pp. 1934578X1200700 ◽  
Author(s):  
Patrícia P. Defillipo ◽  
André H. Raposo ◽  
Alessandra G. Fedoce ◽  
Aline S. Ferreira ◽  
Hudson C. Polonini ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Leaf Extract ◽  
Primary Cultures ◽  
Water Extract ◽  
Centella Asiatica ◽  
Long Time ◽  
Rat Cortical Neurons ◽  
Low Toxicity ◽  
The Brain

Leaf extract of Centella asiatica has been used as an alternative medicine for memory improvement in the Indian Ayurvedic system of medicine for a long time. Although several studies have revealed its effect in ameliorating the cognitive impairment in rat models of Alzheimer's disease, the molecular mechanism of C. asiatica on neuroprotection still remains unexplained. In this study, we investigated the effects of C. asiatica water extract on activity of subtypes of phospholipase A2 (PLA2) in primary cultures of rat cortical neurons and quantified by HPLC a possible molecule responsible for the activity. The cPLA2 and sPLA2 activities were inhibited in vitro by asiaticoside present in the water extract of C. asiatica. This extract may be a candidate for the treatment of neurodegenerative processes because of its pharmacological activity in the brain and its low toxicity, as attested by its long popular use as a natural product.

scholarly journals DHEA Attenuates Microglial Activation via Induction of JMJD3 in Experimental Subarachnoid Haemorrhage

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Tao Tao ◽  
Guang-Jie Liu ◽  
Xuan Shi ◽  
Yan Zhou ◽  
Yue Lu ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Microglial Activation ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Early Brain Injury ◽  
Protective Effects ◽  
In Vivo Models ◽  
The Brain

Abstract Background Microglia are resident immune cells in the central nervous system and central to the innate immune system. Excessive activation of microglia after subarachnoid haemorrhage (SAH) contributes greatly to early brain injury, which is responsible for poor outcomes. Dehydroepiandrosterone (DHEA), a steroid hormone enriched in the brain, has recently been found to regulate microglial activation. The purpose of this study was to address the role of DHEA in SAH. Methods We used in vivo models of endovascular perforation and in vitro models of haemoglobin exposure to illustrate the effects of DHEA on microglia in SAH. Results In experimental SAH mice, exogenous DHEA administration increased DHEA levels in the brain and modulated microglial activation. Ameliorated neuronal damage and improved neurological outcomes were also observed in the SAH mice pretreated with DHEA, suggesting neuronal protective effects of DHEA. In cultured microglia, DHEA elevated the mRNA and protein levels of Jumonji d3 (JMJD3, histone 3 demethylase) after haemoglobin exposure, downregulated the H3K27me3 level, and inhibited the transcription of proinflammatory genes. The devastating proinflammatory microglia-mediated effects on primary neurons were also attenuated by DHEA; however, specific inhibition of JMJD3 abolished the protective effects of DHEA. We next verified that DHEA-induced JMJD3 expression, at least in part, through the tropomyosin-related kinase A (TrkA)/Akt signalling pathway. Conclusions DHEA has a neuroprotective effect after SAH. Moreover, DHEA increases microglial JMJD3 expression to regulate proinflammatory/anti-inflammatory microglial activation after haemoglobin exposure, thereby suppressing inflammation.

scholarly journals Reactivity of Several Reactive Oxygen Species (ROS) with the Sesquiterpene Cacalol

2008 ◽  
Vol 3 (4) ◽  
pp. 1934578X0800300
Author(s):  
Manuel Jiménez-Estrada ◽  
Ricardo Reyes-Chilpa ◽  
Arturo Navarro-Ocaña ◽  
Daniel Arrieta-Báez
Keyword(s):  
Reactive Oxygen Species ◽  
Hydroxyl Radical ◽  
Singlet Oxygen ◽  
Furan Ring ◽  
Reactive Oxygen ◽  
Antioxidant Effect ◽  
Oxygen Species ◽  
Site Reaction ◽  
Hexanedioic Acid ◽  
Antioxidant Effects

To analyze the antioxidant effects of cacalol we determined its reactivity with different reactive oxygen species (ROS). Cacalol gave rise to cacalone by a specific site reaction with a hydroxyl radical. Singlet oxygen reacted only with the double bond of the furan ring, causing its rupture. On the other hand, ozone reacted with all double bonds in cacalol affording 2-methyl-hexanedioic acid as an end product. No reaction was observed with either superoxide or hydrogen peroxide. The potential antioxidant effect of cacalol as a scavenger of hydroxyl radical and singlet oxygen could be related to its function in the plant roots.

Monocarboxylic acid transporters, MCT1 and MCT2, in cortical astrocytes in vitro and in vivo

2000 ◽  
Vol 278 (5) ◽  
pp. C921-C930 ◽  
Author(s):  
Rekha Hanu ◽  
Mary McKenna ◽  
Andrea O'Neill ◽  
Wendy G. Resneck ◽  
Robert J. Bloch
Keyword(s):  
Monocarboxylic Acid ◽  
Primary Cultures ◽  
Cortical Astrocytes ◽  
Immunofluorescence Studies ◽  
Double Label ◽  
Low Levels ◽  
The Brain ◽  
Astrocytic Endfeet

We used sequence-specific antibodies to characterize two monocarboxylic acid transporters, MCT1 and MCT2, in astrocytes. Both proteins are expressed in primary cultures of cortical astrocytes, as indicated by immunoblotting and immunofluorescence. Both MCT1 and MCT2 are present in small, punctate structures in the cytoplasm and at the cell membrane. Cells showing very low levels of labeling for glial fibrillary acidic protein (GFAP) also label more dimly for MCT2, but not for MCT1. In vivo, double-label immunofluorescence studies coupled with confocal microscopy indicate that MCT1 and MCT2 are rare in astrocytes in the cortex. However, they are specifically labeled in astrocytes of the glial limiting membrane and in white matter tracts. Both transporters are also present in the microvasculature. Comparison of labeling for MCT1 and MCT2 with markers of the blood-brain barrier shows that the transporters are not always limited to the astrocytic endfeet in vivo. Our results suggest that the level of expression of monocarboxylic acid transporters MCT1 and MCT2 by cortical astrocytes in vivo is significantly lower than in vitro but that astrocytes in some other regions of the brain can express one or both proteins in significant amounts.

Protective effects of Lactobacillus reuteri and Bifidobacterium infantis in murine models for colitis do not involve the vagus nerve

2008 ◽  
Vol 295 (4) ◽  
pp. R1131-R1137 ◽  
Author(s):  
Hanneke van der Kleij ◽  
Caitlin O'Mahony ◽  
Fergus Shanahan ◽  
Liam O'Mahony ◽  
John Bienenstock
Keyword(s):  
Vagus Nerve ◽  
Lactobacillus Reuteri ◽  
Transfer Model ◽  
Cell Transfer ◽  
Protective Effects ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
T Cell Transfer ◽  
The Brain

The vagus nerve is an important pathway signaling immune activation of the gastrointestinal tract to the brain. Probiotics are live organisms that may engage signaling pathways of the brain-gut axis to modulate inflammation. The protective effects of Lactobacillus reuteri ( LR) and Bifidobacterium infantis ( BI) during intestinal inflammation were studied after subdiaphragmatic vagotomy in acute dextran sulfate sodium (DSS) colitis in BALB/c mice and chronic colitis induced by transfer of CD4+ CD62L+ T lymphocytes from BALB/c into SCID mice. LR and BI (1 × 109) were given daily. Clinical score, myeloperoxidase (MPO) levels, and in vivo and in vitro secreted inflammatory cytokine levels were found to be more severe in mice that were vagotomized compared with sham-operated animals. LR in the acute DSS model was effective in decreasing the MPO and cytokine levels in the tissue in sham and vagotomized mice. BI had a strong downregulatory effect on secreted in vitro cytokine levels and had a greater anti-inflammatory effect in vagotomized- compared with sham-operated mice. Both LR and BI retained anti-inflammatory effects in vagotomized mice. In SCID mice, vagotomy did not enhance inflammation, but BI was more effective in vagotomized mice than shams. Taken together, the intact vagus has a protective role in acute DSS-induced colitis in mice but not in the chronic T cell transfer model of colitis. Furthermore, LR and BI do not seem to engage their protective effects via this cholinergic anti-inflammatory pathway, but the results interestingly show that, in the T cell, transfer model vagotomy had a biological effect, since it increased the effectiveness of the BI in downregulation of colonic inflammation.

Estrogens and progestins: molecular effects on brain cells

2010 ◽  
Vol 4 (3) ◽  
Author(s):  
Paolo Mannella ◽  
Tommaso Simoncini ◽  
Andrea Riccardo Genazzani
Keyword(s):  
Sex Steroids ◽  
Molecular Mechanisms ◽  
Neural Cells ◽  
Protective Effects ◽  
Complete Knowledge ◽  
Molecular Effects ◽  
In Vivo Effects ◽  
The Brain

AbstractSex steroids are known to regulate brain function and their role is so important that several diseases are strictly correlated with the onset of menopause when estrogen-progesterone deficiency makes neural cells much more vulnerable to toxic stimuli. Although in the past years several scientists have focused their studies on in vitro and in vivo effects of sex steroids on the brain, we are still far from complete knowledge. Indeed, contrasting results from large clinical trials have made the entire issue much more complicated. Currently we know that protective effects exerted by sex steroids depend on several factors among which the dose, the health of the cells and the type of molecule being used. In this review, we present an overview of the direct and indirect effects of estrogen and progesterone on the brain with specific focus on the molecular mechanisms by which these molecules act on neural cells.

scholarly journals The Antioxidant Resveratrol Protects against Chondrocyte Apoptosis by Regulating the COX-2/NF-κB Pathway in Created Temporomandibular Osteoarthritis

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Wen Li ◽  
Shiyu Hu ◽  
Xuepeng Chen ◽  
Jiejun Shi
Keyword(s):  
Morphological Changes ◽  
Critical Role ◽  
Chondrocyte Apoptosis ◽  
Optimum Dose ◽  
Protective Effects ◽  
Condylar Cartilage ◽  
Temporomandibular Joint Osteoarthritis ◽  
Cox 2 ◽  
Antioxidant Effects

Temporomandibular joint osteoarthritis (TMJOA) is characterized by chronic inflammatory degradation of mandibular condylar cartilage (MCC). Studies have found a positive correlation between inflammation and cyclooxygenase- (COX-) 2 in OA pathology. NF-κB is a crucial transcription factor of inflammatory and immune responses in the cause of TMJOA pathology. Resveratrol (RES) plays a critical role in antioxidation and anti-inflammation. But, studies on the effects of RES on TMJOA are very limited. So, the purpose of this study is to investigate the antioxidant and protective effects of RES against MCC degradation through downregulating COX-2/NF-κB expression. In vitro studies, the MCC cells were divided into three groups: the NC group, OA group, and RES group. The optimum dose of RES (10 μM) was determined. The TMJOA model of mice was created by injection of collagenase. And mice were injected with RES (100 μg/10 μl) 3 times one week for 4 weeks in the RES group. The expressions of COX-2, P65, MMP1, MMP13, COL2, and ACAN were measured by RT-PCR. Morphological changes of MCC were studied with HE staining. The results showed that inflammation could induce MCC degradation in vitro and vivo, while RES could reverse the degradation. Meanwhile, RES could downregulate COX-2/NF-κB/MMP expression and increase cartilage markers in vitro and vivo studies. The results indicated that RES treatment had antioxidant effects against chondrocyte apoptosis by downregulating the COX-2/NF-κB pathway in created TMJOA.

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