scholarly journals Adaptogenic potential of Centella lujica supplement in sleep deprived mice

Author(s):  
Anthony T. Eduviere ◽  
Prosper E. Awhin ◽  
Kesiena E. Edje ◽  
Lily O. Otomewo ◽  
Olusegun A. Adeoluwa ◽  
...  

Background: Stress, whether internal or external, has been shown to play a role in the accumulation of oxidative free radicals which leads to cellular modification of normal organ or body function. Centella lujica (C. lujica) is a commonly cultivated herb with therapeutic benefits in various studies. This study aims to evaluate its beneficial effect on the brain and liver of mice exposed to sleep deprivation-induced stress.Methods: Albino mice were treated with distilled water (control), C. lujica (50 and 100 mg/kg) or astaxanthin (50 mg/kg) for seven days. All groups except control were then subjected to three-days of sleep deprivation using the grid suspended over water model beginning from day 4 of treatment. Behavioural assessments followed by biochemical assays and histological analysis were carried out thereafter.Results: Sleep deprivation caused an increase in blood glucose and triglycerides levels but reduced high density lipoproteins. Brain pro-oxidant levels were increased with a concomitant decrease in antioxidants, recognition memory was diminished while depressive-like symptoms were enhanced and neuronal viability of hippocampal CA1 as well as prefrontal cortex cells was reduced in sleep-deprived mice. However, supplementation with C. lujica reversed these effects as significantly as astaxanthin.Conclusions: C. lujica possesses antioxidant property that makes it an effective adaptogen against stress induced responses in mice. 

2017 ◽  
Vol 1 (S1) ◽  
pp. 56-56
Author(s):  
Shaun Evan Gruenbaum ◽  
Roni Dhaher ◽  
Amedeo Rapuano ◽  
Tore Eid

OBJECTIVES/SPECIFIC AIMS: We previously developed a translationally relevant model of temporal lobe epilepsy (TLE) in which glutamine synthetase is irreversibility inhibited by methionine sulfoximine (MSO), resulting in spontaneous seizures and dentate hilar neuron loss. The objective of this study was to determine the effects of chronic BCAA ingestion on neuronal viability in the dentate hilus in the MSO model of TLE. METHODS/STUDY POPULATION: Sixteen rats were randomly divided into 2 groups: 8 rats drank a 4% aqueous solution of all 3 BCAAs (BCAA group) ad libitum for 31 days, and the other 8 rats drank regular water (control group) for the same period. After 10 days of drinking, a microinfusion cannula (Alzet osmotic pump, model 2004) was surgically implanted in the right dentate gyrus to continuously infuse MSO at a rate of 0.625 g/hour for 28 days. After 31 days of drinking, rats were perfused transcardially with 0.9% NaCl followed by 4% paraformaldehyde in phosphate buffer. The brains were removed and fixed, sectioned on a Vibratome at 50-μm thickness, and were mounted on a gelatin-coated slides and stained with NeuN. Neuron counts in the hilar region were performed ipsilateral and contralateral to the infusion site using a stereological technique. RESULTS/ANTICIPATED RESULTS: Rats in the BCAA group had 37% fewer neurons in the ipsilateral dentate hilus than the control group (5.8×10−4±6.8×10−5 vs. 8.9×10−4±5.6×10−5 cells, respectively, p<0.01). Similarly, rats in the BCAA group had 39% fewer neurons in the contralateral dentate hilus than the control group (5.0×10−4±5.8×10−5 vs. 7.0×10−4±3.4×10−5 cells, respectively, p=0.01). DISCUSSION/SIGNIFICANCE OF IMPACT: This study demonstrates that chronic ingestion of BCAAs aggravates hilar neuronal loss in a translationally relevant rodent model of MTLE. This study gives important insight into how BCAAs may affect neuronal viability. Although the role of BCAAs on seizure activity is poorly understood, these results suggest that BCAAs may play an important role in neurochemical modulation and neurotoxicity.


PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40128 ◽  
Author(s):  
Nada M. Porter ◽  
Julia H. Bohannon ◽  
Meredith Curran-Rauhut ◽  
Heather M. Buechel ◽  
Amy L. S. Dowling ◽  
...  

Author(s):  
Xin Qin ◽  
Michael G. Zaki ◽  
Zhicheng Chen ◽  
Elisabet Jakova ◽  
Zhi Ming ◽  
...  

AbstractChronic adenosine A1R stimulation in hypoxia leads to persistent hippocampal synaptic depression, while unopposed adenosine A2AR receptor stimulation during hypoxia/reperfusion triggers adenosine-induced post-hypoxia synaptic potentiation (APSP) and increased neuronal death. Still, the mechanisms responsible for this adenosine-mediated neuronal damage following hypoxia need to be fully elucidated. We tested the hypothesis that A1R and A2AR regulation by protein kinase casein kinase 2 (CK2) and clathrin-dependent endocytosis of AMPARs both contribute to APSPs and neuronal damage. The APSPs following a 20-min hypoxia recorded from CA1 layer of rat hippocampal slices were abolished by A1R and A2AR antagonists and by broad-spectrum AMPAR antagonists. The inhibitor of GluA2 clathrin-mediated endocytosis Tat-GluA2-3Y peptide and the dynamin-dependent endocytosis inhibitor dynasore both significantly inhibited APSPs. The CK2 antagonist DRB also inhibited APSPs and, like hypoxic treatment, caused opposite regulation of A1R and A2AR surface expression. APSPs were abolished when calcium-permeable AMPAR (CP-AMPAR) antagonist (IEM or philanthotoxin) or non-competitive AMPAR antagonist perampanel was applied 5 min after hypoxia. In contrast, perampanel, but not CP-AMPAR antagonists, abolished APSPs when applied during hypoxia/reperfusion. To test for neuronal viability after hypoxia, propidium iodide staining revealed significant neuroprotection of hippocampal CA1 pyramidal neurons when pretreated with Tat-GluA2-3Y peptide, CK2 inhibitors, dynamin inhibitor, CP-AMPAR antagonists (applied 5 min after hypoxia), and perampanel (either at 5 min hypoxia onset or during APSP). These results suggest that the A1R-CK2-A2AR signaling pathway in hypoxia/reperfusion injury model mediates increased hippocampal synaptic transmission and neuronal damage via calcium-permeable AMPARs that can be targeted by perampanel for neuroprotective stroke therapy.


2021 ◽  
Author(s):  
Aleksandra Kuzan ◽  
Emilia Królewicz ◽  
Irena Kustrzeba-Wójcicka ◽  
Karolina Lindner ◽  
Małgorzata Sobieszczańska

Abstract Background: Medical care for geriatric patients is a great challenge, mainly due to overlapping various deficits relevant to physiologic ageing with numerous coexisting diseases, of which the most common are diabetes mellitus and atherosclerosis. In case of diabetes, glycation process is intensified, which accelerates atherosclerosis development and diabetic complications. Our goal was to investigate the relationship between the classical biochemical parameters of diabetes and atherosclerosis (fasting glucose, glycated hemoglobin (HbA1c), low and high density lipoproteins (LDL, HDL), triglycerides, etc.), as well as parameters which may indicate a nephropathy (creatinine, glomerular filtration rate – GFR), and the parameters strictly related to glycation. Methods: We analyzed the patients' serum concentration of fluorescent glycation products, concentration of soluble receptor for advanced glycation products (sRAGE), lipoprotein receptor-1 (LOX-1), galectin 3 (GAL3), scavenger receptor class A (SR-A) and scavenger receptor class B (SR-BI), as well as the level of lipid peroxidation and free amine content. Results: Among the identified correlations, the most interesting are the following : sRAGE with triglycerides (r = 0.47); sRAGE with SR-BI (r=0.47); SR-BI with LOX-1 (r=0.31), and SR-BI with HDL (r=-0.30). It has been shown that pentosidine and fluorescent AGEs as well as reactive free amine contents are significantly higher in elderly patients with ischemic heart disease. Fluorescent AGEs and pentosidine are also significantly higher in patients with arterial hypertension. The influence of diabetes therapy on parameters related to peroxidation and glycation was also analyzed. Malondialdehyde turned to be higher in patients with diabetes mellitus type 2 not treated with insulin or metformin than in those treated with both medications (p=0.052). GAL3 was found to be lower both in persons without diabetes and in diabetics treated with metformin (p=0.005). LOX1 was higher in diabetic patients not treated with metformin or insulin, and lowest in diabetics treated with both insulin and metformin, with the effect of metformin reducing LOX1 levels (p=0.039). Conclusions: Our results were the basis for a discussion about the diagnostic value in clinial practice of LOX-1 and GAL3 in geriatric patients with diabetes and also provide grounds for inferring the therapeutic benefits of insulin and metformin treatment.


2021 ◽  
Vol 10 (4) ◽  
pp. e33910414150
Author(s):  
Lucas Dutra Zani da Silva Souza ◽  
Ariana Ferrari ◽  
Daniele Fernanda Felipe

Several therapeutic benefits of medicinal plants are attributed to antioxidant properties, since antioxidant compounds play an important role in the prevention of various diseases and aging. Many products have synergistic action from combinations of plant extracts that contain natural antioxidants. The present study aimed to evaluate the synergistic effect of Pfaffia glomerata extract with Arrabidaea chica extract for antioxidant action. In the study the extract of the inflorescences of P. glomerata and the extract of the leaves of A. chica were used. The synergism between P. glomerata extract and A. chica extract was evaluated using the ratio between experimental and theoretical antioxidant activity, which was determined using the DPPH method and the potential total reactive antioxidant method (TRAP). The combination of P. glomerata extract and A. chica extract showed a synergistic effect, in which the antioxidant property of this combination was substantially superior to the sum of the individual antioxidant effects. This demonstrates that the combined extracts can be important for the development of products that have a high antioxidant potential.


Geoderma ◽  
1999 ◽  
Vol 89 (1-2) ◽  
pp. 149-175 ◽  
Author(s):  
M.F.P. Bierkens ◽  
P.J.T. Van Bakel ◽  
J.G. Wesseling

2019 ◽  
Vol 39 (34) ◽  
pp. 6613-6625 ◽  
Author(s):  
Giovanna Maria Spano ◽  
Sebastian Weyn Banningh ◽  
William Marshall ◽  
Luisa de Vivo ◽  
Michele Bellesi ◽  
...  

2020 ◽  
Vol 2 (3) ◽  
pp. 325-333
Author(s):  
Jinzi Wu ◽  
Yan Dou ◽  
Warren C. Ladiges

Sleep deprivation is a potent stress factor that disrupts regulatory pathways in the brain resulting in cognitive dysfunction and increased risk of neurodegenerative disease with increasing age. Prevention of the adverse effects of sleep deprivation could be beneficial in older individuals by restoring healthy brain function. We report here on the ability of SS31, a mitochondrial specific peptide, to attenuate the negative neurological effects of short-term sleep deprivation in aging mice. C57BL/6 female mice, 20 months old, were subcutaneously injected with SS31 (3 mg/kg) or saline daily for four days. Sleep deprivation was 4 h daily for the last two days of SS31 treatment. Mice were immediately tested for learning ability followed by collection of brain and other tissues. In sleep deprived mice treated with SS31, learning impairment was prevented, brain mitochondrial ATP levels and synaptic plasticity regulatory proteins were restored, and reactive oxygen species (ROS) and inflammatory cytokines levels were decreased in the hippocampus. This observation suggests possible therapeutic benefits of SS31 for alleviating adverse neurological effects of short-term sleep loss.


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