جستجوی مقالات مرتبط با کلیدواژه « BDNF » در نشریات گروه « پزشکی »

Melissa officinalis (MO) hydroalcoholic extract has shown neuroprotective effects. We assess the possible therapeutic effects of Melissa officinalis extract (MOE) on blood biochemical and Brain-Derived Neurotrophic Factor (BDNF) levels as well as neurobehavioral consequences of high-fat-diet (HFD)-induced obese rats. Eighty male Wistar rats weighing between 180 and 220 g were divided into two groups at the beginning of the experiment and fed with normal diet (ND) or HFD for 5 weeks. Then, each group was divided into four subgroups (10 rats in each group) and treated daily with MOE (50, 100, 150 mg/kg, intraperitoneal) or vehicle for another two weeks. At the end of the experiments, fasting blood glucose (FBG), blood lipid profile, and serum brain-derived neurotrophic factor (BDNF) levels were measured. The sucrose preference test (anhedonia and depression), open field test (locomotor), elevated plus maze (anxiety), Y-maze (working memory), and Morris water maze test (spatial memory) were done. Feeding with HFD for 7 weeks caused obesity, anhedonia, anxiety, depression and learning and memory disorders in rats and a decrease in serum BDNF level. Administration of MOE at 100 or 150 mg/kg to HFD-fed rats decreased weight gain, FBG, and serum levels of total low-density lipoprotein cholesterol and increased serum BDNF levels. It also improved changes in locomotor activity, anxiety, depression, and learning and memory in HFD-fed rats. The results show that MOE has a therapeutic effect on model rats with HFD-induced metabolic and neurobehavioral abnormalities through regulation of BDNF secretion.

Prenatal stress (PS) can adversely affect cognitive and psychological functions in the offspring. This study aimed to determine the effect of PS and extremely low-frequency electromagnetic field (ELF-EMF) on spatial memory, serum corticosterone, brain-derived neurotrophic factor (BDNF) concentrations, and hippocampal BDNF levels in adult male offspring. 

Female Wistar rats were randomly divided into four groups (n=6): Control, Stress, ELF-EMF (exposure to ELF-EMF), and S+EMF (simultaneous exposure to stress and the ELF-EMF) groups. Animals received interven-tions for 21 days before and 21 days during pregnancy (a total of 42 days). On the offspring’s 90th postnatal day (PND), spatial memory was tested using Morris Water Maze, serum Corticosterone and BDNF levels were measured by the ELISA method, and hippocampal BDNF levels were measured by Western blotting. 

PS did not affect spatial memory in the adult male offspring; however, it significantly (P<0.05) increased se-rum corticosterone levels compared to the control and EMF groups. Simultaneous induction of stress with ELF-EMF disrupted the memory acquisition phase. Serum and hippocampal BDNF levels increased signifi-cantly (P<0.05) in the EMF group compared to the stress group. 

Based on our findings, PS can increase serum corticosterone levels without affecting spatial memory. Howev-er, induction of ELF-EMF with stress has a destructive effect on spatial memory with no change in the corti-costerone levels. Compared to stress, prenatal exposure to ELF-EMF increases serum and hippocampal BDNF levels. Further studies are needed to determine the underlying mechanisms of these findings.

Adult neurogenesis, the process of generating new neurons, continues throughout life. Unfortunately, this process is insufficient in pathological conditions and needs to be promoted. Crocin, the active component of saffron, affects neurogenesis in vivo and in vitro. We aimed to investigate the enhancing effects of crocin on the neurogenesis of adipose-derived mesenchymal stem cells in the presence of retinoic acid, as well as the molecular pathways involved. 

Differentiation capacities and stemness potential of harvested ADSCs were evaluated by differentiating into osteocytes and adipocytes, and expression of mesenchymal CD markers by flow cytometry. The optimum dose of crocin was assessed with an MTT assay. Crocin, retinoic acid, CREB/BDNF, and Notch inhibitors and their combination were added to the culture medium. Jag1, Hes1, Notch, and BDNF gene expression were analyzed by RT-PCR on days 7, 14, and 21, while CREB, DCX, SOX2, and NeuN expression were analyzed by immunofluorescence.

Expression of mesenchymal CD markers as well as adipogenic and osteogenic differentiation confirmed the origin and properties of ADSCs. The optimal dose of crocin was 1 mM. Crocin significantly (P<0.05) increased, while inhibitors (DATP&Naphthol) significantly (P<0.05) decreased Jag1, Hes1, Notch, and BDNF expression. Immunofluorescent assessments showed that expression of DCX, BDNF, NeuN, and Sox2 proteins increased significantly (P<0.05) after crocin administration and decreased significantly (P<0.05) after inhibitor administration.

Crocin can be used as an enhancer for neural differentiation of MSCs in vitro in the presence of retinoic acid. The mechanism is proposed through Notch and CREB/BDNF signaling pathways.

Maternal separation (MS) is a well-characterized model of early life stress, based on the postnatal disruption of the mother-infant interaction. Studies on rodents have demonstrated that MS, as an early adverse life event, leads to spatial memory deficits and lasting changes in brain plasticity. Here, we review data from animal studies regarding the impact of MS on long-term potentiation (LTP). Evidence shows that animal models are useful for evaluating the effects of MS on LTP. Overall, studies suggest that MS impairs LTP.

 Chlorpyrifos (CPF) is an insecticide and has a wide range of applications in the world. The purpose of this research was to investigate the effect of 4-week aerobic exercise and eugenol supplementation on the brain-derived neurotrophic factor/phosphoinositide 3-kinase (BDNF/PI3K) pathway on the skeletal muscle of male rats poisoned with CPF.

 Overall, 12-week-old female rats were used in this experimental research. The rats were randomly divided into 7 groups (8 rats in each group), including healthy control, toxic control, poison solvent, corn oil solvent, poisoned+eugenol, poisoned+aerobic exercise, and poisoned+aerobic exercise+eugenol. Moderate training in the range of 50%-60% VO2max, including 5 training sessions per week (treadmill). Poisoning was performed with CPF poison with a dose of 3 mg/kg. The dose of eugenol was determined to be 250 mg/kg. Finally, a one-way analysis of variance and Tukey’s post hoc test were employed to check the difference between groups.

 The expression of PI3K and BDNF in the poisoned control group was lower than that in the healthy control group (P=0.049 and P=0.001, respectively). In addition, the expression of PI3K and BDNF was higher in the poisoned+eugenol+exercise group compared to the poisoned control group (P=0.009 and P=0.03, respectively). The corn solvent group also had a higher PI3K and BDNF expression in comparison to the poisoned control group (P=0.025 and P=0.01, respectively). Eventually, there was no significant difference among other groups.

 Exercise and eugenol increased PI3K and BDNF expression. It is thought that exercise and consumption of eugenol in poisoned rats reduces damage and improves muscle function and the BDNF/PI3K signaling pathway.

Hypertensive intracerebral hemorrhage (HICH) is a spontaneous cerebrovascular disease occuring in the brain parenchyma.

To characterize the predictive role of miR-155-5p and BDNF in the prognosis of HICH.

All patients with HICH who underwent CT-guided minimally invasive surgery were classified into the good and poor prognosis groups using the modified Rankin Scale (mRS). The level of miR-155-5p was determined by qRT-PCR, and the level of brain-derived neurotrophic factor (BDNF) in serum was determined by ELISA. The relationship between miR-155-5p and BDNF was tested by Pearson correlation and luciferase reporter assay. The logistic regression method was used to determine the risk factors. The ROC curve was drawn to explain the predictive role of miR-155-5p, BDNF, or their combination.

A high level of miR-155-5p and a lower level of BDNF were observed in the poor prognosis group. BDNF level was negatively related to the level of miR-155-5p. BDNF is a target of miR-155-5p. BDNF and miR-155-5p were associated with prognosis. BDNF, miR-155-5p or their combination were predictive biomarkers for the prognosis of HICH.

BDNF and miR-155-5p were associated with the outcome of HICH patients.

 Chronic stress causes a deleterious impact on older adults and accelerates the aging process through different mechanisms, such as increased oxidative stress. Metformin, a drug with pleiotropic effects, exhibited neuroprotective and antioxidant properties.

 Our study aimed to investigate the metformin effects on aging under stress conditions.

 Old male rats (18 months) were divided into 6 experimental groups (N = 8): 1 = control; 2 and 3 = metformin (1 or 10 mg/kg, orally, 40 days); 4 = stress (40 days); 5 and 6 = stress + metformin (1 or 10 mg/kg, orally, 40 days). Chronic variable stress was induced with 7 types of stressors for 40 days. Neurobehavioral functions were evaluated using the Morris water maze, Y-maze, elevated plus maze, open field, forced swimming test, rotarod, and exhausting swimming test. In addition, BDNF level and SOD activity were measured.

 Stress induction increased memory deficits, anxiety, depression, and muscle fatigue in old rats. Metformin (10 mg/kg) enhanced memory performance and muscle strength and diminished anxiety and depression in stressed animals (P < 0.05). Treatment with metformin increased the BDNF brain level and SOD activity (P < 0.05).

 Metformin restored neurobehavioral disruptive changes induced by chronic stress in old rats. The underlying mechanisms could be related to the prevention of oxidative stress and neuronal damage and elevation of BDNF levels in the brain.

Diabetes is a metabolic disorder that affects the development of the central nervous system and plays an important role in learning and memory. Diabetes increases the reactive oxygen species (ROS) level in cells and changes the expression of several genes, including SYP, BDNF, PAX7, and SYNCAM1, through the FOXO transcription factor. This study was done to assess the effect of diabetes on morphometric indexes of the cerebellar cortex and gene expression in mice. Diabetes was induced in twelve adult, male C57BL mice using an injection of streptozotocin. After two months, the mice were dissected, and the cerebellum was stored for further analysis. For the morphometric analysis, tissue sections were stained with cresyl violet and examined with a light microscope. For gene expression analysis, the RNA was extracted, and cDNA was synthesized. The mRNA levels of SYP, BDNF, PAX7, and SYNCAM1 genes were measured by the real-time PCR method. The thickness of the molecular layer and Purkinje layer, and the number of Purkinje and granular cells in the diabetic group were significantly reduced compared to controls P<0.0 1). The area, perimeter, and diameter of Purkinje cells in the diabetic group were significantly reduced compared to controls P<0.0 1). The expression of PAX7, SYP, and BDNF genes of the diabetic group was significantly reduced. However, SYNCAM1 expression in the cerebellum of the diabetic group was significantly increased compared to controls (P<0.05). Induced diabetes in mice can decrease the expression of memory-related genes in the cerebellum. Also, these genes affect the morphology and thickness of the cerebellum.

This research aims to evaluate whether polyethylene glycol (PEG), which can immediately repair neuronal membranes, will have a protective effect against radiation-induced brain injury (RIBI).

Whole brain irradiation (RAD) procedure was performed on 14 of 21 rats included in the study for establishing RIBI. Rats were randomly divided into three groups containing equal numbers of animals: control (RAD not established), placebo (RAD applied, and treated with 1 ml/kg/day of saline that was administered intraperitoneally), and treatment (RAD applied, and treated with 30 mg/kg /day of PEG 3350 that was administered intraperitoneally). Following the end of the 22-day treatments, behavioral tests were performed first, and then magnetic resonance spectroscopy (MRS) was applied to measure brain lactate levels. All rats were sacrificed in order to perform biochemical analysis and histopathological examination of brain tissue.

Compared to the control group, MDA, TNF-α, NF-κB and lactate levels were significantly increased, while BDNF levels were decreased in the placebo group; and RAD-induced changes in all these biochemical markers were reversed by PEG. In MRS performed from the corpus striatum, there was an evident decrease in lactate levels after PEG treatment. Impairment in memory and learning was more limited in PEG-treated rats than in the rats receiving saline therapy. Furthermore, histological examinations from hippocampus and cerebellum exhibited that PEG treatment significantly reduces apoptosis, astrogliosis, and oxidative DNA damage in rats.

Our results support that PEG is very effective in preventing RIBI with its secondary effects on the basis of membrane stabilization.

Preclinical studies have shown that neurotrophic factors, including brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF), are involved in the modulation of biochemical and behavioral adaptations to substance use.

We studied the impact of GDNF and BDNF serum levels on adherence to methadone maintenance treatment (MMT) through cross-sectional research. Participants were clients on MMT (43 males), subjects in remission from opioid use disorder (12 males), and healthy controls (20 males). Adherence and non-adherence to treatment were assessed by the detection of illicit opioids in random urinalysis.

Using t-tests for independent groups and analysis of variance (ANOVA), GDNF serum levels in the adherent patients toMMT were found to be significantly higher than in the non-adherent patients. BDNF serum levels were not different between adherent and non-adherent patients.

Our results suggest the involvement of GDNF as a biological factor in adherence to MMT.

A neurodevelopmental disorder, autism is typically identified with three primary behavioral consequences, such as social impairment, communication problems, and limited or stereotypical behavior. Because of its co-morbidity and lack of therapeutic options, autism is a global economic burden. A short chain of fatty acid, propionic acid is formed biologically by the gut microbiome. Propionic acid levels that are too high can cause leaky intestines, which can lead to autism-like symptoms.

To induce autism, male Albino Wistar rats were given propionic acid (250 mg/kg/po on the 21st, 22nd, and 23rd postnatal days). Rats also received a ryanodine receptor antagonist (Ruthenium red: 3 mg/kg/po; postnatal 21st to 50th day) to see what influence it had on propionic acid-induced autism. Anxiety, social behavior, and repeated behaviors were all assessed, as well as oxidative stress, inflammatory indicators, neuro signaling proteins, and blood-brain barrier permeability.

Ruthenium red was found to counter the propionic acid-induced increases in anxiety, repetitive behavior prefrontal cortex levels of IL-6, TNF-α, TBARS, Evans blue leakage, and water content along with decreases in social behavior, IL-10, and GSH followed by hippocampus CREB and BDNF levels. 

Ryanodine receptor antagonists presented a neuroprotective effect in propionic acid-induced conditions like autism by modulatory effects on social and repetitive behavior, oxidative stress, neuroinflammation, and neuroprotein changes. Ryanodine receptors can be further explored in depth to manage autism as a condition.

Alzheimer’s disease (AD), the most common cause of dementia, is one of the leading causes of morbidity and death in the world. Currently, treatment mostly used to slow down the disease progression. Herbal remedies are considered by many in the community as a natural and safe treatment with fewer side effects. Silibinin, the active ingredient of Silybum marionum, has anti-oxidant, neurotrophic and neuroprotective characteristics. Therefore, here, the effect of different doses of Silibinin extract on oxidative stress and expression of neurotrophic factors was investigated.  Forty eight male Wistar rats were randomly divided into sham, lesion; Aβ1-40 injection, lesion-treatment; Aβ1-40 injection followed by different doses of silibinin (50, 100, 200 mg / kg) through gavage and lesion-vehicle group; Aβ1-40 injection + vehicle of silibinin. Morris water Maze (MWM) was done 28 days after the last treatment. Hippocampal tissue was removed for biochemical analysis. Production of nitric oxide (NO) and reactive oxygen species (ROS), expression of BDNF/VEGF and cell viability were measured using Griess, fluorimetry, Western blotting and MTT techniques.   Different concentrations of silibinin improved behavioral performance in animals. Higher doses of Silibinin could improve memory and learning function through MWM. Also, increasing the concentration of silibinin resulted in decreased ROS and NO production in a dose-dependent manner. Consequently, silibinin may act as a potential candidate for alleviating symptoms of AD.

The development of neurotoxicity in healthy, non-targeted brain tissue exposed to radiation during cranial radiotherapy (RT) is the most frequent event of radiation-induced adverse effects. The 5-hydroxytryptamine-3 (5-HT3) receptor antagonists may also have a range of neuroprotective, anti-inflammatory, and antiphlogistic properties in addition to their anti-emetic effects.

Study groups were formed in the following ways: Group 2: Irradiation (IR)-only (IR+Saline); Group 1: Normal control (orally fed control); Group 3: IR+Granisetron (IR+Granisetron): whole-brain IR and Granisetron 1 mg/kg/day (Merck) administered orally. 15 days of all therapies were given. The 15 days were completed with behavioral testing. In the entire brain IR-only (placebo) group, a substantial deterioration was seen in all studied marker levels and behavioral test results.

Compared to the IR-only group, all of these biochemical indicators significantly improved in the granisetron group (IR+Granisetron), and levels of the control group returned to normal. In behavioral test analyses, a substantial decline in the open field and passive avoidance learning social recognition tests was seen in the IR-only group compared to the healthy control group, whereas an improvement was seen in the IR+Granisetron group. In addition, the IR-only group showed a reduction in hippocampus neurons and Purkinje neurons as well as an increase in hippocampal gliosis, whereas the IR+Granisetron group showed an improvement and a return to the normal control group counts.

In summary, we discovered that granisetron had neuroprotective properties in a rat model of radiation-induced brain damage.