Abstract TMP36: Exogenous Oxytocin Confers Significant Neuroprotective Effects and Improves Recovery in Young and Aged Animals After Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Juneyoung Lee ◽  
Yan Xu ◽  
Diego Morales Scheihing ◽  
Louise McCullough ◽  
Venugopal Reddy Venna
Keyword(s):  
Neuroprotective Effect ◽  
Control Group ◽  
Male Mice ◽  
Behavioral Recovery ◽  
Neuroprotective Effects ◽  
Delayed Treatment ◽  
Aged Mice ◽  
Beneficial Effects ◽  
Human Use ◽  
To Receive

Introduction: Oxytocin (OXT) is a highly evolutionary conserved neuropeptide and an important modulator of inflammation in response to stressors such as ischemia. Recent studies have implicated OXT signaling in neuroprotection in young mice after ischemic injury, but it is not known if OXT is efficacious in aged animals. In our ongoing studies, we found that OXT levels decline after stroke and with age. Therefore, we tested if exogenous OXT administration could provide beneficial effects and improve recovery in aged animals. Methods: Aged (18-20m) C57BL/6 male mice were purchased from Jax Labs and aged in house. Stroke was induced by a right MCAO-60min. Mice were randomly assigned to receive OXT or Atosiban, an OXT antagonist (OXTA) (0.5mg/kg) or vehicle. In the first set of experiments, aged mice were pre-treated with OXT, vehicle, or OXTA for 10 days before stroke. Infarcts were quantified 7-days after stroke (n=6-9/grp). In a second set, we tested the efficacy of delayed treatment, at 3hrs after stroke, and OXT was administered intranasally or i.p.. Functional and behavioral recovery and brain infarct size was assessed 7-day post-stroke. OXT levels 24hrs after stroke in human plasma were measured. Results: OXT treatment (0.5mg/kg/i.p. QD) prior to stroke led to significant neuroprotection in aged male mice, whereas OXTA treatment significantly increased infarct (p<0.05, n=6-9/grp) compared to control group (total: 39.4±2.9% control; 20.8±3.1% OXT; 51.3±2.8% OXTA). Importantly, no differences in cerebral blood flow or temperature were seen between groups. Interestingly, the neuroprotective effect of OXT treatment was observed even when treatment was initiated 3hrs (administered either i.p. or nasally) after stroke onset. Also, we observed a significant decrease in circulating OXT levels at 24hrs in stroke patients (n=26) compared to healthy controls, highlighting the translational relevance of this pathway. Conclusions: We found that OXT treatment either before or after stroke is neuroprotective in aged mice and both i.p. and nasal OXT administration improves recovery in parallel to reductions in brain injury. Given that intranasal formulations of OXT are approved for human use, our proposed strategy of supplementing OXT is highly translatable.

scholarly journals Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 985
Author(s):  
Luisa Müller ◽  
Nicole Power Guerra ◽  
Jan Stenzel ◽  
Claire Rühlmann ◽  
Tobias Lindner ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Neuroprotective Effect ◽  
Resonance Spectroscopy ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Positron Emission ◽  
Pet Ct ◽  
Amyloid Aβ ◽  
Β Amyloid

Caloric restriction (CR) slows the aging process, extends lifespan, and exerts neuroprotective effects. It is widely accepted that CR attenuates β-amyloid (Aβ) neuropathology in models of Alzheimer’s disease (AD) by so-far unknown mechanisms. One promising process induced by CR is autophagy, which is known to degrade aggregated proteins such as amyloids. In addition, autophagy positively regulates glucose uptake and may improve cerebral hypometabolism—a hallmark of AD—and, consequently, neural activity. To evaluate this hypothesis, APPswe/PS1delta9 (tg) mice and their littermates (wild-type, wt) underwent CR for either 16 or 68 weeks. Whereas short-term CR for 16 weeks revealed no noteworthy changes of AD phenotype in tg mice, long-term CR for 68 weeks showed beneficial effects. Thus, cerebral glucose metabolism and neuronal integrity were markedly increased upon 68 weeks CR in tg mice, indicated by an elevated hippocampal fluorodeoxyglucose [18F] ([18F]FDG) uptake and increased N-acetylaspartate-to-creatine ratio using positron emission tomography/computer tomography (PET/CT) imaging and magnet resonance spectroscopy (MRS). Improved neuronal activity and integrity resulted in a better cognitive performance within the Morris Water Maze. Moreover, CR for 68 weeks caused a significant increase of LC3BII and p62 protein expression, showing enhanced autophagy. Additionally, a significant decrease of Aβ plaques in tg mice in the hippocampus was observed, accompanied by reduced microgliosis as indicated by significantly decreased numbers of iba1-positive cells. In summary, long-term CR revealed an overall neuroprotective effect in tg mice. Further, this study shows, for the first time, that CR-induced autophagy in tg mice accompanies the observed attenuation of Aβ pathology.

scholarly journals Functional and Structural Effects of Erythropoietin Subconjunctival Administration in Glaucomatous Animals

2018 ◽  
Vol 3 (2) ◽  
pp. 1-11 ◽  
Author(s):  
Ana Paula Resende ◽  
Serge G. Rosolen ◽  
Telmo Nunes ◽  
Berta São Braz ◽  
Esmeralda Delgado
Keyword(s):  
Neuroprotective Effect ◽  
Treated Group ◽  
Retinal Function ◽  
Function Evaluation ◽  
Control Group ◽  
Albino Rats ◽  
Subconjunctival Injection ◽  
Beneficial Effects ◽  
Structural Evaluation ◽  
Retinal Structure

Purpose: The present study aimed to assess functional and structural benefits of erythropoietin (EPO) when administered subconjunctivally in the retina of glaucomatous rats using electroretinography (ERG) and retinal thickness (RT) measurements. Methods: Glaucoma was experimentally induced in 26 Wistar Hannover albino rats. Animals were divided into 2 groups of 13 animals each: a treated group receiving a unique subconjunctival injection of 1,000 IU of EPO and a control group receiving a saline solution. In each group, 7 animals were used for retinal function evaluation (ERG) and 6 animals were used for retinal structural evaluation (histology). RT was measured, dorsally and ventrally, at 500 μm (RT1) and at 1,500 μm (RT2) from the optic nerve. Results: Retinal function evaluation: for both scotopic and photopic conditions, ERG wave amplitudes increased in the treated group. This increase was statistically significant (p < 0.05) in photopic conditions. Structural evaluation: for both locations RT1 and RT2, the retinas were significantly (p < 0.05) thicker in the treated group. Conclusion: Subconjunctival EPO administration showed beneficial effects both on retinal structure and on retinal function in induced glaucoma in albino rats. This neuroprotective effect should be applied in other animal species.

N-Myc Downstream-Regulated Gene 2 (Ndrg2): A Critical Mediator of Estrogen-Induced Neuroprotection Against Cerebral Ischemic Injury

2021 ◽  
Author(s):  
Lixia Zhang ◽  
Yulong Ma ◽  
Min Liu ◽  
Miao Sun ◽  
Jin Wang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Male Mice ◽  
Neuroprotective Effects ◽  
Female Mice ◽  
Ndrg2 Expression ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

Abstract Growing evidence indicates that estrogen plays a pivotal role in neuroprotection against cerebral ischemia, but the molecular mechanism of this protection is still elusive. N-myc downstream‐regulated gene 2 (Ndrg2), an estrogen-targeted gene, has been shown to exert neuroprotective effects against cerebral ischemia in male mice. However, the role of Ndrg2 in the neuroprotective effect of estrogen remains unknown. In this study, we first detected NDRG2 expression levels in the cortex and striatum in both female and male mice with western blot analyses. We then detected cerebral ischemic injury by constructing middle cerebral artery occlusion and reperfusion (MCAO-R) models in Ndrg2 knockout or conditional knockdown female mice. We further implemented estrogen, ERα or ERβ agonist replacement in the ovariectomized (OVX) Ndrg2 knockouts or conditional knockdowns female mice, then tested for NDRG2 expression, glial fibrillary acidic protein (GFAP) expression, and extent of cerebral ischemic injury. We found that NDRG2 expression was significantly higher in female than in male mice in both the cortex and striatum. Ndrg2 knockouts and conditional knockdowns showed significantly aggravated cerebral ischemic injury in female mice. Estrogen and ERβ replacement treatment (DPN) led to NDRG2 upregulation in both the cortex and striatum of OVX mice. Estrogen and DPN also led to GFAP upregulation in OVX mice. However, the effect of estrogen and DPN in activating astrocytes was lost in Ndrg2 knockouts OVX mice and primary cultured astrocytes, but partially retained in conditional knockdowns OVX mice. Most importantly, we found that the neuroprotective effects of E2 and DPN against cerebral ischemic injury were lost in Ndrg2 knockouts OVX mice but partially retained in conditional knockdowns OVX mice. These findings demonstrate that estrogen alleviated cerebral ischemic injury via ERβ upregulation of Ndrg2, which could activate astrocytes, indicating that Ndrg2 is a critical mediator of E2-induced neuroprotection against cerebral ischemic injury.

scholarly journals MiR-137 Boosts the Neuroprotective Effect of Endothelial Progenitor Cell Derived-Exosomes in Oxyhemoglobin Treated SH-SY5Y Cells Partially via COX2/PGE2 Pathway

2020 ◽  
Author(s):  
Yuchen Li ◽  
Jinju Wang ◽  
Shuzhen Chen ◽  
Pei Wu ◽  
Shancai Xu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ischemic Stroke ◽  
Glutathione Peroxidase ◽  
Iron Overload ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Endothelial Progenitor ◽  
Neuroprotective Effects ◽  
Protection Mechanism ◽  
Beneficial Effects

Abstract Background: We have previously verified the beneficial effects of exosomes from endothelial progenitor cells (EPC-EXs) in ischemic stroke. However, the effects of EPC-EXs in hemorrhagic stroke have not been investigated. Additionally, miR-137 is reported to regulate ferroptosis and to be involved in the neuroprotection against ischemic stroke. Hence, the present work explored the effects of miR-137-overexpressing EPC-EXs on apoptosis, mitochondrial dysfunction, and ferroptosis in oxyhemoglobin (oxyHb)-injured SH-SY5Y cells. Methods: The lentiviral miR-137 was transfected into EPCs and then the EPC-EXs were collected. RT-PCR was used to detect the miR-137 level in EPCs, EXs and neurons. The uptake mechanisms of EPC-EXs in SH-SY5Y cells were explored by the co-incubation of Dynasore, Pitstop 2, Ly294002 and Genistein. After the transfection of different types of EPC-EXs, flow cytometry and expression of cytochrome c and cleaved caspase-3 were used to detect the apoptosis of oxyHb-injured neurons. Neuronal mitochondrial function was assessed by reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) depolarization, and cellular ATP content. Cell ferroptosis was measured by lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4. Additionally, recombinational PGE2 was used to detect if activation of COX2/PGE2 pathway could reverse the protection of miR-137 overexpression.Results: The present work showed 1) EPC-EXs could be taken in by SH-SY5Y cells via caveolin-/clathrin-mediated pathways and macropinocytosis; 2) miR-137 was decreased in neurons after oxyHb treatment, and EXsmiR-137 could restore the miR-137 levels; 3) EXsmiR-137 worked better than EXs in reducing the number of apoptotic neurons and pro-apoptotic protein expression after oxyHb treatment; 4) EXsmiR-137 are more effective in improving the cellular MMP, ROS and ATP level; 5) EXsmiR-137, but not EXs, protected oxyHb-treated SH-SY5Y cells against lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4; 6) EXsmiR-137 suppressed the expression of the COX2/PGE2 pathway, and activation of the pathway could partially reverse the neuroprotective effects of EXsmiR-137. Conclusion: MiR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated SH-SY5Y cells. Furthermore, EXsmiR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.

scholarly journals MiR-137 Boosts the Neuroprotective Effect of Endothelial Progenitor Cell Derived-Exosomes in Oxyhemoglobin Treated SH-SY5Y Cells Partially via COX2/PGE2 Pathway

2020 ◽  
Author(s):  
Yuchen Li ◽  
Jinju Wang ◽  
Shuzhen Chen ◽  
Pei Wu ◽  
Shancai Xu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ischemic Stroke ◽  
Glutathione Peroxidase ◽  
Iron Overload ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Endothelial Progenitor ◽  
Neuroprotective Effects ◽  
Protection Mechanism ◽  
Beneficial Effects

Abstract Background: We have previously verified the beneficial effects of exosomes from endothelial progenitor cells (EPC-EXs) in ischemic stroke. However, the effects of EPC-EXs in hemorrhagic stroke have not been investigated. Additionally, miR-137 is reported to regulate ferroptosis and to be involved in the neuroprotection against ischemic stroke. Hence, the present work explored the effects of miR-137-overexpressing EPC-EXs on apoptosis, mitochondrial dysfunction, and ferroptosis in oxyhemoglobin (oxyHb)-injured neurons.Methods: The lentiviral miR-137 was transfected into EPCs and then the EPC-EXs were collected. RT-PCR was used to detect the miR-137 level in EPCs, EXs and neurons. The uptake mechanisms of EPC-EXs in neurons were explored by the co-incubation of Dynasore, Pitstop 2, Ly294002 and Genistein. After the transfection of different types of EPC-EXs, flow cytometry and expression of cytochrome c and cleaved caspase-3 were used to detect the apoptosis of oxyHb-injured neurons. Neuronal mitochondrial function was assessed by reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) depolarization, and cellular ATP content. Cell ferroptosis was measured by lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4. Additionally, recombinational PGE2 was used to detect if activation of COX2/PGE2 pathway could reverse the protection of miR-137 overexpression.Results: The present work showed 1) EPC-EXs could be taken in by SH-SY5Y cells via caveolin-/clathrin-mediated pathways and macropinocytosis; 2) miR-137 was decreased in neurons after oxyHb treatment, and EXs miR-137 could restore the miR-137 levels; 3) EXs miR-137 worked better than EXs in reducing the number of apoptotic neurons and pro-apoptotic protein expression after oxyHb treatment; 4) EXs miR-137 are more effective in improving the cellular MMP, ROS and ATP level; 5) EXs miR-137 , but not EXs, protected oxyHb-treated neurons against lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4; 6) EXs miR-137 suppressed the expression of the COX2/PGE2 pathway, and activation of the pathway could partially reverse the neuroprotective effects of EXs miR-137 .Conclusion: MiR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated neurons. Furthermore, EXs miR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.

scholarly journals Neuroprotective Effects of the Multitarget Agent AVCRI104P3 in Brain of Middle-Aged Mice

2018 ◽  
Vol 19 (9) ◽  
pp. 2615
Author(s):  
Julia Relat ◽  
Julio Come ◽  
Belen Perez ◽  
Pelayo Camps ◽  
Diego Muñoz-Torrero ◽  
...  
Keyword(s):  
Chronic Treatment ◽  
Brain Dysfunction ◽  
Male Mice ◽  
Inhibitory Effects ◽  
Middle Aged ◽  
Neuroprotective Effects ◽  
Aged Mice ◽  
Aβ Aggregation ◽  
Inflammatory Processes ◽  
Inflammatory Proteins

Molecular factors involved in neuroprotection are key in the design of novel multitarget drugs in aging and neurodegeneration. AVCRI104P3 is a huprine derivative that exhibits potent inhibitory effects on human AChE, BuChE, and BACE-1 activities, as well as on AChE-induced and self-induced Aβ aggregation. More recently, cognitive protection and anxiolytic-like effects have also been reported in mice treated with this compound. Now, we have assessed the ability of AVCRI104P3 (0.43 mg/kg, 21 days) to modulate the levels of some proteins involved in the anti-apoptotic/apoptotic processes (pAkt1, Bcl2, pGSK3β, p25/p35), inflammation (GFAP and Iba1) and neurogenesis in C57BL/6 mice. The effects of AVCRI104P3 on AChE-R/AChE-S isoforms have been also determined. We have observed that chronic treatment of C57BL/6 male mice with AVCRI104P3 results in neuroprotective effects, increasing significantly the levels of pAkt1 and pGSK3β in the hippocampus and Bcl2 in both hippocampus and cortex, but slightly decreasing synaptophysin levels. Astrogliosis and neurogenic markers GFAP and DCX remained unchanged after AVCRI104P3 treatment, whereas microgliosis was found to be significantly decreased pointing out the involvement of this compound in inflammatory processes. These results suggest that the neuroprotective mechanisms that are behind the cognitive and anxiolytic effects of AVCRI104P3 could be partly related to the potentiation of some anti-apoptotic and anti-inflammatory proteins and support the potential of AVCRI104P3 for the treatment of brain dysfunction associated with aging and/or dementia.

scholarly journals Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guangqian Li ◽  
LeiQian ◽  
Pan Gu ◽  
Dan Fan
Keyword(s):  
Cardiac Arrest ◽  
Neuroprotective Effect ◽  
Serum Levels ◽  
Spontaneous Circulation ◽  
Cerebral Injury ◽  
Control Group ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Neuroprotective Effects ◽  
Return Of Spontaneous Circulation

Abstract Background Neuroprotection strategies after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR) remain key areas of basic and clinical research. This study was designed to investigate the neuroprotective effects of dexmedetomidine following resuscitation and potential mechanisms. Methods Anesthetized rats underwent 6-min asphyxia-based cardiac arrest and resuscitation, after which the experimental group received a single intravenous dose of dexmedetomidine (25 μg/kg). Neurological outcomes and ataxia were assessed after the return of spontaneous circulation. The serum levels and brain expression of inflammation markers was examined, and apoptotic cells were quantified by TUNEL staining. Results Neuroprotection was enhanced by dexmedetomidine post-conditioning after the return of spontaneous circulation. This enhancement was characterized by the promotion of neurological function scores and coordination. In addition, dexmedetomidine post-conditioning attenuated the serum levels of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α at 2 h, as well as interleukin IL-1β at 2, 24, and 48 h. TUNEL staining showed that the number of apoptotic cells in the dexmedetomidine post-conditioning group was significantly reduced compared with the control group. Further western blot analysis indicated that dexmedetomidine markedly reduced the levels of caspase-3 and nuclear factor-kappa B (NF-κB) in the brain. Conclusions Dexmedetomidine post-conditioning had a neuroprotective effect against cerebral injury following asphyxia-induced cardiac arrest. The mechanism was associated with the downregulation of apoptosis and neuroinflammation.

scholarly journals NEUROPROTECTIVE EFFECTS OF POMEGRANATE JUICE ON LEAD INDUCED NEUROTOXICITY IN MICE

2017 ◽  
Vol 9 (2) ◽  
pp. 207
Author(s):  
Leila Gadouche ◽  
Noureddine Djebli ◽  
Khayra Zerrouki
Keyword(s):  
Drinking Water ◽  
Cerebral Cortex ◽  
Lead Acetate ◽  
Neuronal Degeneration ◽  
Neuroprotective Effect ◽  
Pomegranate Juice ◽  
Total Phenolic ◽  
Control Group ◽  
Histological Structure ◽  
Neuroprotective Effects

<p><strong>Objective: </strong>This study evaluates the potential neuroprotective of the pomegranate juice against chronic intoxication with lead acetate for 3<strong> </strong>months.</p><p><strong>Methods: </strong>Twenty-one female Swiss mice divided into 3 groups were employed in the present investigation. Control group: received drinking water for 90 days, neurotoxic group were exposed to 1000 ppm of lead acetate in the drinking water for 12 weeks, and neurotoxic treated group represents the mice received treatment with juice pomegranate diluted with distilled water (v/v) orally for 4 h / day followed by lead acetate at a dose of 1000 ppm orally for 20 h / day for 90 days. After cessation of treatment, neurobehavioral studies using the open field test, black and white test box and swimming test were made. In the next phase, brain injury was assessed histologically with hematoxylin-eosin staining.</p><p><strong>Results:</strong> Chronic exposure to lead led to significant increase in the level of anxiety, depression and the locomotor activity (P &lt; 0.05). It was confirmed by histopathological alterations in many areas of the cerebral cortex and hippocampus including neuronal degeneration and decrease cell density. Treatment with the juice significantly improve the level of depression, locomotor function (P &lt; 005) and anxiety (P &gt; 0.05) in mice exposed to lead as well as restored the histological structure in cerebral cortex and hippocampus of mice. The total phenolic and flavonoids content in juice of pomegranate was found to be 3809. 8±29.404 mg GAE/l; 2109. 57±18.936 mg QE /l of juice.</p><p><strong>Conclusion: </strong>This finding suggests that phenolic compounds found in pomegranate juice provide a neuroprotective effect on behavioural impairments and histopathological change induced by lead.</p>

scholarly journals Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model

2020 ◽  
Vol 58 (4) ◽  
pp. 461-466
Author(s):  
Seung Hak Lee ◽  
Bong-Kwang Jung ◽  
Hyemi Song ◽  
Han Gil Seo ◽  
Jong-Yil Chai ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Toxoplasma Gondii ◽  
Neuroprotective Effect ◽  
Hypoxia Inducible Factor ◽  
Protozoan Parasite ◽  
Artery Occlusion ◽  
Control Group ◽  
Triphenyltetrazolium Chloride ◽  
Neuroprotective Effects ◽  
Neurobehavioral Function

Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade various organs in the host body, including the central nervous system. Chronic intracranial T. gondii is known to be associated with neuroprotection against neurodegenerative diseases through interaction with host brain cells in various ways. The present study investigated the neuroprotective effects of chronic T. gondii infection in mice with cerebral ischemia experimentally produced by middle cerebral artery occlusion (MCAO) surgery. The neurobehavioral effects of cerebral ischemia were assessed by measurement of Garcia score and Rotarod behavior tests. The volume of brain ischemia was measured by triphenyltetrazolium chloride staining. The expression levels of related genes and proteins were determined. After cerebral ischemia, corrected infarction volume was significantly reduced in T. gondii infected mice, and their neurobehavioral function was significantly better than that of the uninfection control group. Chronic T. gondii infection induced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in the brain before MCAO. T. gondii infection also increased the expression of vascular endothelial growth factor after the cerebral ischemia. It is suggested that chronic intracerebral infection of T. gondii may be a potential preconditioning strategy to reduce neural deficits associated with cerebral ischemia and induce brain ischemic tolerance through the regulation of HIF-1α expression.

scholarly journals Coconut Oil Promotes Greater Satiety and Reduces Blood Cholesterol, But Induces Obesity, Anxiety and Impaired Bone Formation in Adult Wistar Rats

2021 ◽  
Author(s):  
Ítalo Gomes Reis ◽  
Arthur Rocha-Gomes ◽  
Alexandre Alves da Silva ◽  
Mayara Rodrigues Lessa ◽  
Nísia Andrade Villela Dessimoni Pinto ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Caloric Intake ◽  
Coconut Oil ◽  
Blood Cholesterol ◽  
Control Group ◽  
Virgin Coconut Oil ◽  
Total Blood ◽  
Beneficial Effects ◽  
To Receive ◽  
Tibia Length

Background: The aim of this study was to evaluate the nutritional effects of supplementation with virgin coconut oil (VCO) in Wistar rats over a sub-chronic period (6 weeks).Methods: Twelve Wistar rats were used and randomly assigned to receive (n = 6): control - lab chow; coconut oil (CO) - lab chow with added virgin coconut oil (20%). Food and caloric intake, weight gain, food efficiency, body mass index, femur and tibia length, bone mineral composition and blood biochemistry were evaluated.Result: The CO group showed an energy intake closed to control group. Also, the supplementation with VCO generated a decrease in total blood cholesterol as compared to the control group. However, the CO group showed accumulation of fat mass, shorter femur length and anxiogenesis in relation to the control group. These results indicate few beneficial effects from the sub-chronic use of VCO and indicate that its consumption in large quantities for long periods should be questioned.

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