scholarly journals Centella asiaticaPrevents Increase of Hippocampal Tumor Necrosis Factor-αIndependently of Its Effect on Brain-Derived Neurotrophic Factor in Rat Model of Chronic Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Mawaddah Ar Rochmah ◽  
Ika Murti Harini ◽  
Dian Eurike Septyaningtrias ◽  
Dwi Cahyani Ratna Sari ◽  
Rina Susilowati
Keyword(s):  
Chronic Stress ◽  
Neuroprotective Effect ◽  
Centella Asiatica ◽  
Sirtuin 1 ◽  
Male Rats ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Neurotropic Factor ◽  
The Relationship

Centella asiaticaameliorates memory impairment and induces expression of hippocampal brain-derived neurotropic factor (BDNF) in chronically stressed rats. The relationship between the anti-inflammatory effect ofCentella asiaticaon hippocampal BDNF and the involvement of sirtuin-1, a BDNF expression regulator, in neuroprotective mechanisms ofCentella asiaticawarrants an investigation. We investigated the effect ofCentella asiaticaethanolic extracts (CA) on TNF-α, IL-10, and SIRT1 levels and whether these predicted BDNF expression in rat hippocampus after chronic stress. For the experiments, thirty male rats (Sprague Dawley) were divided into six groups: nonstressed-control, stressed-control, nonstressed +CA 300mg/kg/d, stressed +CA 150 mg/kg/d, stressed +CA 300 mg/kg/d, and stressed +CA 600 mg/kg/d. On day 28, rats were sacrificed and hippocampus was dissected out. Hippocampal TNF-α, IL-10, SIRT1, and BDNF were measured by enzyme-linked immunosorbent assay. Hippocampal TNF-αlevel was significantly higher in the stressed-control compared to nonstressed-control groups. Across all stress conditions, rats receiving the highest dose of CA had the lowest mean TNF-αand highest mean BDNF. There were no significant differences in IL-10 and SIRT1 levels between groups. Hippocampal TNF-αdid not predict hippocampal BDNF in a regression analysis. In conclusion, lower TNF-αand higher BDNF in the hippocampus support the hypothesis that these factors independently contribute toCentella asiatica’s neuroprotective effect in chronically stressed rats.

scholarly journals THE EFFECTS OF ETHANOL EXTRACTS OF Centella asiatica LEAF ON SERIAL SERUM BRAIN DERIVED NEUROTROPHIN FACTOR (BDNF) CONCENTRATION OF RATS (SPRAGUE DAWLEY) FOLLOWING CHRONIC STRESS

2015 ◽  
Vol 2 (1) ◽  
pp. 159 ◽  
Author(s):  
Dwi Cahyani Ratna Sari ◽  
Mawaddah Ar Rochmah
Keyword(s):  
Chronic Stress ◽  
Centella Asiatica ◽  
Male Rats ◽  
Control Group ◽  
Sprague Dawley ◽  
Electrical Stress ◽  
Significant Difference ◽  
Before And After ◽  
Ethanol Extracts ◽  
Serum Bdnf

<p>Centella asiatica is considered herbal plant for increasing memory performance. Brain-derived neurotrophin factor (BDNF) has a significant role in memory formation process, while stress causes memory impairment. Objective: This study aimed to investigate the effects of ethanol extracts of Centella asiatica leaf on serum BDNF concentration of rats that was taken serially before and after chronic electrical stress. Materials and Methods : Twenty male rats (Sprague Dawley) were divided into four groups: control/aquades group and groups treated with different doses (mg/kg) of Centella asiatica :150 (CA150), 300 (CA300) and 600 (CA600). Each rat underwent memory exercise for nine days before and after electrical stress and oral administration of ethanol extracts of Centella asiatica for twenty-eight days. Blood sampling was taken serially from rats’ tail for four times : (1) before memory exercise, (2) after memory exercise (before stress), (3) after chronic stress, and (4) after memory exercise (following chronic stress). Concentration of serum BDNF was assessed using ELISA. Results: There was no significant difference in serum BDNF concentration between groups in first and second serum sampling, which was prior to chronic stress and administration of different treatments. However, there was significant difference in third and fourth serum sampling between groups. Mean concentration of serum BDNF (ng/ml) in third and fourth sampling for control group, CA150, CA300, and CA600, respectively were 1.88+0.21 &amp;1.93+0.24; 2.29+0.13 &amp; 2.01+0.22; 2.29+0.08 &amp;1.86+0.11; 2.71+0.70 and 2.99+0.27 (p&lt;0.05). Conclusion: Ethanol extracts of Centella asiatica leaf increases serum BDNF concentration in rats after chronic stress. <br /><strong></strong></p><p><strong>Keywords</strong>: stress, memory, Centella asiatica, BDNF</p>

Effects of hyperbaric oxygen pretreatment on brain antioxidant capacity in rats with decompression sickness

2021 ◽  
pp. 287-295
Author(s):  
Ya Li ◽  
◽  
Xiaona Xu ◽  
Junxiang Bao Bao ◽  
Wenlan Wang ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Decompression Sickness ◽  
Neuroprotective Effect ◽  
Male Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Rat Models ◽  
Metal Elements ◽  
Flame Atomic Absorption ◽  
Brain Tissues

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.

scholarly journals BIOCHEMICAL STUDIES OF HIPPOCAMPAL GENE EXPRESSION OF BRAIN-DERIVED NEUROTROPIC FACTOR AND TOLL-LIKE RECEPTOR-4 IN DIABETIC RATS EXPOSED TO CHRONIC STRESS: EFFECTS OF ANTIDEPRESSANT DRUGS

2018 ◽  
Vol 11 (1) ◽  
pp. 271
Author(s):  
Sawsan Aboul-fotouh ◽  
Doaa Mohamed Hassan ◽  
Mohamed Zaki Eldeen Habib ◽  
Ahmed Ibrahim Amin ◽  
Samar K. Kassim ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Antidepressant Drugs ◽  
Chronic Administration ◽  
Diabetic Rats ◽  
Toll Like Receptor ◽  
Bdnf Expression ◽  
Toll Like Receptor 4 ◽  
Inflammatory State ◽  
Neurotropic Factor ◽  
Factor Α

  Objective: Depression and diabetes are closely associated in a reciprocal manner, leading to significant morbidity and mortality with an evidence of a pro-inflammatory state underlying pathophysiology of both diseases. Unfortunately, little information is available about the effects of antidepressant drugs on hippocampal brain-derived neurotrophic factor (BDNF) and toll-like receptor-4 (TLR-4) expression in diabetes.Methods: We investigated the effect of chronic administration of fluoxetine (FLU) and imipramine (IMIP) on behavioral, metabolic, and inflammatory abnormalities in diabetic and non-diabetic rats exposed to chronic restraint stress (CRS).Results: Both diabetes and CRS induced depressive-like behavior which was more prominent in diabetic/depressed rats; this was reversed by chronic treatment with FLU and IMIP. Diabetic and non-diabetic rats exposed to CRS showed a significant increase in hippocampal expression of TLR-4 and pro-inflammatory cytokines alongside a decrease in BDNF expression. FLU and IMIP ameliorated these inflammatory abnormalities.Conclusion: Diabetes mellitus (DM) and chronic stress induced a depressive-like behavior associated with an increase in hippocampal expression of TLR-4, tumor necrosis factor-α, and interleukin-1ß with a significant correlation to decreased BDNF expression. FLU and IMIP showed comparable effects regards the improvement of depressive and inflammatory abnormalities associated with DM.

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

scholarly journals 7,8-Dihydroxyflavone Enhances Cue-Conditioned Alcohol Reinstatement in Rats

2020 ◽  
Vol 10 (5) ◽  
pp. 270 ◽  
Author(s):  
Samuel J. Hogarth ◽  
Elvan Djouma ◽  
Maarten van den Buuse
Keyword(s):  
Body Weight ◽  
Progressive Ratio ◽  
Ethanol Exposure ◽  
Ethanol Solution ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Self Administration ◽  
Bdnf Expression ◽  
Sprague Dawley Rats

Alcohol use disorder (AUD) is a detrimental disease that develops through chronic ethanol exposure. Reduced brain-derived neurotrophic factor (BDNF) expression has been associated with AUD and alcohol addiction, however the effects of activation of BDNF signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown. We therefore trained male and female Sprague Dawley rats in operant chambers to self-administer a 10% ethanol solution. Following baseline acquisition and progressive ratio (PR) analysis, rats were split into drug and vehicle groups during alcohol lever extinction. The animals received two weeks of daily IP injection of either the BDNF receptor, TrkB, agonist, 7,8-dihydroxyflavone (7,8-DHF), or vehicle. During acquisition of alcohol self-administration, males had significantly higher absolute numbers of alcohol-paired lever presses and a higher PR breakpoint. However, after adjusting for body weight, the amount of ethanol was not different between the sexes and the PR breakpoint was higher in females than males. Following extinction, alcohol-primed reinstatement in male rats was not altered by pretreatment with 7,8-DHF when adjusted for body weight. In contrast, in female rats, the weight-adjusted potential amount of ethanol, but not absolute numbers of active lever presses, was significantly enhanced by 7,8-DHF treatment during reinstatement. Analysis of spontaneous locomotor activity in automated photocell cages suggested that the effect of 7,8-DHF was not associated with hyperactivity. These results suggest that stimulation of the TrkB receptor may contribute to reward craving and relapse in AUD, particularly in females.

scholarly journals Central Sirt1 Regulates Body Weight and Energy Expenditure Along With the POMC-Derived Peptide α-MSH and the Processing Enzyme CPE Production in Diet-Induced Obese Male Rats

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 961-974 ◽  
Author(s):  
Nicole E. Cyr ◽  
Jennifer S. Steger ◽  
Anika M. Toorie ◽  
Jonathan Z. Yang ◽  
Ronald Stuart ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Obese Individual ◽  
Nutrient Sensing ◽  
Sirtuin 1 ◽  
Male Rats ◽  
Sprague Dawley ◽  
Phosphorylated Akt ◽  
Central Inhibition

Abstract In the periphery, the nutrient-sensing enzyme Sirtuin 1 (silent mating type information regulation 2 homolog 1 [Sirt1]) reduces body weight in diet-induced obese (DIO) rodents. However, the role of hypothalamic Sirt1 in body weight and energy balance regulation is debated. The first studies to reveal that central Sirt1 regulates body weight came from experiments in our laboratory using Sprague-Dawley rats. Central inhibition of Sirt1 decreased body weight and food intake as a result of a forkhead box protein O1 (FoxO1)-mediated increase in the anorexigenic proopiomelanocortin (POMC) and decrease in the orexigenic Agouti-related peptide in the hypothalamic arcuate nucleus. Here, we demonstrate that central inhibition of Sirt1 in DIO decreased body weight and increased energy expenditure at higher levels as compared with the lean counterpart. Brain Sirt1 inhibition in DIO increased acetylated FoxO1, which in turn increased phosphorylated FoxO1 via improved insulin/phosphorylated AKT signaling. Elevated acetylated FoxO1 and phosphorylated FoxO1 increased POMC along with the α-melanocyte-stimulating hormone (α-MSH) maturation enzyme carboxypeptidase E, which resulted in more of the bioactive POMC product α-MSH released into the paraventricular nucleus. Increased in α-MSH led to augmented TRH levels and circulating T3 levels (triiodothyronine, thyroid hormone). These results indicate that inhibiting hypothalamic Sirt1 in DIO enhances the activity of the hypothalamic-pituitary-thyroid axis, which stimulates energy expenditure. Because we show that blocking central Sirt1 causes physiological changes that promote a negative energy balance in an obese individual, our results support brain Sirt1 as a significant target for weight loss therapeutics.

Electrically evoked local muscle contractions cause an increase in hippocampal BDNF

2018 ◽  
Vol 43 (5) ◽  
pp. 491-496 ◽  
Author(s):  
Takahiro Maekawa ◽  
Riki Ogasawara ◽  
Arata Tsutaki ◽  
Kihyuk Lee ◽  
Satoshi Nakada ◽  
...  
Keyword(s):  
Muscle Contractions ◽  
Triceps Surae ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Custom Made ◽  
Fibronectin Type Iii ◽  
Systemic Factors ◽  
Triceps Surae Muscles ◽  
Neurotropic Factor ◽  
Fibronectin Type Iii Domain

High-intensity exercise has recently been shown to cause an increase in brain-derived neurotropic factor (BDNF) in the hippocampus. Some studies have suggested that myokines secreted from contracting skeletal muscle, such as irisin (one of the truncated form of fibronectin type III domain-containing protein 5 (FNDC5)), play important roles in this process. Thus, we hypothesized that locally evoked muscle contractions may cause an increase of BDNF in the hippocampus through some afferent mechanisms. Under anesthesia, Sprague–Dawley rats were fixed on a custom-made dynamometer and their triceps surae muscles were made to maximally contract via delivery of electric stimulations of the sciatic nerve (100 Hz with 1-ms pulse and 3-s duration). Following 50 repeated maximal isometric contractions, the protein expressions of BDNF and activation of its receptor in the hippocampus significantly increased compared with the sham-operated control rats. However, the expression of both BDNF and FNDC5 within stimulated muscles did not significantly increase, nor did their serum concentrations change. These results indicate that local muscular contractions under unconsciousness can induce BDNF expression in the hippocampus. This effect may be mediated by peripheral reception of muscle contraction, but not by systemic factors.

The Protective Effect of Notoginsenoside R1 on Isoflurane-Induced Neurological Impairment in the Rats via Regulating miR-29a Expression and Neuroinflammation

2021 ◽  
pp. 1-7
Author(s):  
Meijing Wang ◽  
Hongyan Liu ◽  
Lufeng Xu ◽  
Mengmeng Li ◽  
Ming Zhao
Keyword(s):  
Protective Effect ◽  
Neuroprotective Effect ◽  
Neurological Impairment ◽  
Morris Water Maze Test ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spatial Learning And Memory ◽  
Sprague Dawley ◽  
Real Time Quantitative Pcr ◽  
Rat Pups ◽  
Tnf Α

<b><i>Introduction:</i></b> Isoflurane inhalation leads to apoptotic neurodegeneration and further results in learning and cognitive dysfunction. Notoginsenoside R1 (NGR1), a major ingredient from Radix notoginseng, has been reported to exert neuroprotective effect during brain or neuron injury. This study aimed to investigate the effect of NGR1 on neurological impairment. <b><i>Methods:</i></b> Sixty-four male Sprague Dawley rat pups (15–20 g) of postnatal day 7 were recruited. Spatial learning and memory were assessed by the Morris water maze test, and the neurological severity score was determined. Real-time quantitative PCR was used to detect the expression levels of microRNA (miR)-29a. Enzyme-linked immunosorbent assay was applied to estimate the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the hippocampal tissues. <b><i>Results:</i></b> NGR1 attenuated neurological impairment induced by isoflurane, shown by the decrease in neurological function score and escape latency and the increase in staying time in the original quadrant in rats. NGR1 reversed the downregulation of miR-29a expression induced by isoflurane treatment. After the treatment of NGR1, the elevated levels of IL-6, TNF-α, and IL-1β induced by isoflurane were all decreased significantly in the hippocampal tissues of rats. Additionally, the repressive action of NGR1 in neurological impairment and neuroinflammation was eliminated by downregulating miR-29a in rats. <b><i>Conclusion:</i></b> NGR1 protects against isoflurane-induced neurological impairment. The protective effect of NGR1 might be achieved by promoting the expression of miR-29a and preventing inflammatory response.

Physical fatigue and the morfofunctional state of myocardium in experimental chronic stress

2019 ◽  
Vol 485 (2) ◽  
pp. 247-250
Author(s):  
M. V. Kondashevskaya ◽  
V. E. Tseylikman ◽  
M. V. Komelkova ◽  
M. S. Lapshin ◽  
A. P. Sarapultsev ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Male Rats ◽  
Structural Components ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
First Time ◽  
The Relationship

The relationship between skeletal muscle fatigue and morpho-functional alterations in the myocardium was analyzed for the first time in Wistar male rats exposed to chronic stress. Post traumatic stress disorder (PTSD) was associated with signs of increased oxidative stress, which apparently induced the changes in cardiomyocyte structural components and the acceleration of skeletal and muscular fatigue.

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