Brain-derived neurotrophic factor modulator https://greenmedinfo.com/category/keywords/Brain-derived%20neurotrophic%20factor%20modulator en Lotus root might potentially improve neural function through the stimulation of BDNF production in glial cells. https://greenmedinfo.com/article/lotus-root-might-potentially-improve-neural-function-through-stimulation-bdnf- n/a PMID:  J Diet Suppl. 2017 May 9:1-13. Epub 2017 May 9. PMID: 28485986 Abstract Title:  Lotus Root Extract Stimulates BDNF Gene Expression Through Potential Mechanism Depending on HO-1 Activity in C6 Glioma Cells. Abstract:  Polyphenolic compounds have been suggested to be involved in the preservation of neural function via the production of neurotrophic factors in the brain. The nonedible joint part of lotus root (a rhizome of Nelumbo nucifera) has been reported to contain large amounts of polyphenolic compounds and, therefore, is expected to improve neural function by stimulating the production of brain-derived neurotrophic factor (BDNF) in glial cells. The effect of the aqueous extract prepared from the joint part of lotus root on BDNF gene expression was examined in C6 glioma cells as an in vitro model. This extract was shown to increase BDNF messenger ribonucleic acid (mRNA) levels to the elevation of HO-1 mRNA levels in the glioma cells, but failed to cause the elevation of BDNF mRNA levels in the cells pretreated with a HO-1 antisense oligodeoxynucleotide (ODN) or an HO-1 enzyme inhibitor zinc protoporphyrin (ZnPP). These findings strongly suggest that the aqueous extract prepared from the nonedible joint part of lotus root might be able to stimulate BDNF gene expression by enhancing HO-1 activity in the glioma cells, proposing the possibility that the joint part of lotus root might potentially improve neural function through the stimulation of BDNF production in glial cells. https://greenmedinfo.com/article/lotus-root-might-potentially-improve-neural-function-through-stimulation-bdnf-#comments Lotus Brain-derived neurotrophic factor modulator Heme oxygenase-1 up-regulation Brain-derived neurotrophic factor modulator Heme oxygenase-1 up-regulation Lotus Plant Extracts In Vitro Study Wed, 24 May 2017 16:06:20 +0000 greenmedinfo 148175 at https://greenmedinfo.com Melatonin promotes brain-derived neurotrophic factor expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia. https://greenmedinfo.com/article/melatonin-promotes-brain-derived-neurotrophic-factor-expression-and-anti-apopt n/a PMID:  Med Sci Monit. 2017 Dec 16 ;23:5951-5959. Epub 2017 Dec 16. PMID: 29247156 Abstract Title:  Melatonin Promotes Brain-Derived Neurotrophic Factor (BDNF) Expression and Anti-Apoptotic Effects in Neonatal Hemolytic Hyperbilirubinemia via a Phospholipase (PLC)-Mediated Mechanism. Abstract:  BACKGROUND Melatonin therapy shows positive effects on neuroprotective factor brain-derived neurotrophic factor (BDNF) expression and neuronal apoptosis in neonatal hemolytic hyperbilirubinemia. We hypothesized that melatonin promotes BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia through a phospholipase (PLC)-mediated mechanism. MATERIAL AND METHODS A phenylhydrazine hydrochloride (PHZ)-induced neonatal hemolytic hyperbilirubinemia model was constructed in neonatal rats. Four experimental groups - a control group (n=30), a PHZ group (n=30), a PHZ + melatonin group (n=30), and a PHZ + melatonin+U73122 (a PLC inhibitor) group (n=30) - were constructed. Trunk blood was assayed for serum hemoglobin, hematocrit, total and direct bilirubin, BDNF, S100B, and tau protein levels. Brain tissue levels of neuronal apoptosis, BDNF expression, PLC activity, IP3 content, phospho- and total Ca2+/calmodulin-dependent protein kinase type IV (CaMKIV) expression, and phospho- and total cAMP response element binding protein (CREB) expression were also assayed. RESULTS PHZ-induced hemolytic hyperbilirubinemia was validated by significantly decreased serum hemoglobin and hematocrit as well as significantly increased total and direct serum bilirubin (p&lt;0.05). Neonatal bilirubin-induced neurotoxicity was validated by significantly decreased serum BDNF, brain BDNF, and serum S100B, along with significantly increased serum tau protein (p&lt;0.05). PHZ-induced hemolytic hyperbilirubinemia significantly decreased serum BDNF, brain BDNF, and PLC/IP3/Ca2+ pathway activation while increasing neuronal apoptosis levels (p&lt;0.05), all of which were partially rescued by melatonin therapy (p&lt;0.05). Pre-treatment with the PLC inhibitor U73122 largely abolished the positive effects of melatonin on PLC/IP3/Ca2+ pathway activation, downstream BDNF levels, and neuronal apoptosis (p&lt;0.05). CONCLUSIONS Promotion of BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia by melatonin largely operates via a PLC-mediated mechanism. https://greenmedinfo.com/article/melatonin-promotes-brain-derived-neurotrophic-factor-expression-and-anti-apopt#comments Hyperbilirubinemia: Hereditary Melatonin Anti-Apoptotic Brain-derived neurotrophic factor modulator Anti-Apoptotic Brain-derived neurotrophic factor modulator Hyperbilirubinemia: Hereditary melatonin Animal Study Fri, 19 Jan 2018 01:19:50 +0000 greenmedinfo 158582 at https://greenmedinfo.com Spirulina maxima administered together with other therapeutics may induce synergistic effects to ameliorate cognitive dysfunction. https://greenmedinfo.com/article/spirulina-maxima-administered-together-other-therapeutics-may-induce-synergist n/a PMID:  Int J Mol Sci. 2017 Nov 13 ;18(11). Epub 2017 Nov 13. PMID: 29137190 Abstract Title:  Spirulina maxima Extract Ameliorates Learning and Memory Impairments via Inhibiting GSK-3β Phosphorylation Induced by Intracerebroventricular Injection of Amyloid-β 1-42 in Mice. Abstract:  Spirulina maxima, a microalga containing high levels of protein and many polyphenols, including chlorophyll a and C-phycocyanin, has antioxidant and anti-inflammatory therapeutic effects. However, the mechanisms where by Spirulina maxima ameliorates cognitive disorders induced by amyloid-β 1-42 (Aβ1-42) are not fully understood. In this study, we investigated whether a 70% ethanol extract of Spirulina maxima (SM70EE) ameliorated cognitive impairments induced by an intracerebroventricular injection of Aβ1-42 in mice. SM70EE increased the step-through latency time in the passive avoidance test and decreased the escape latency time in the Morris water maze test in Aβ1-42-injected mice. SM70EE reduced hippocampal Aβ1-42 levels and inhibited amyloid precursor protein processing-associated factors in Aβ1-42-injected mice. Additionally, acetylcholinesterase activity was suppressed by SM70EE in Aβ1-42-injected mice. Hippocampal glutathione levels were examined to determine the effects of SM70EE on oxidative stress in Aβ1-42-injected mice. SM70EE increased the levels of glutathione and its associated factors that were reduced in Aβ1-42-injected mice. SM70EE also promotedactivation of the brain-derived neurotrophic factor/phosphatidylinositol-3 kinase/serine/threonine protein kinase signaling pathway and inhibited glycogen synthase kinase-3β phosphorylation. These findings suggested that SM70EE ameliorated Aβ1-42-induced cognitive impairments by inhibiting the increased phosphorylation of glycogen synthase kinase-3β caused by intracerebroventricular injection of Aβ1-42 in mice. https://greenmedinfo.com/article/spirulina-maxima-administered-together-other-therapeutics-may-induce-synergist#comments Alzheimer's Disease Memory Disorders Spirulina Brain-derived neurotrophic factor modulator Neuroprotective Agents Alzheimer's disease Brain-derived neurotrophic factor modulator Memory Disorders Neuroprotective Agents Spirulina Animal Study Thu, 07 Dec 2017 08:55:22 +0000 greenmedinfo 157098 at https://greenmedinfo.com Sulforaphane improves LPS-induced spatial learning and memory dysfunction, likely by upregulating neurogenesis through the BDNF-mTOR pathway. https://greenmedinfo.com/article/sulforaphane-improves-lps-induced-spatial-learning-and-memory-dysfunction-like PMID:  Neuroscience. 2018 09 15 ;388:357-366. Epub 2018 Aug 4. PMID: 30086367 Abstract Title:  Sulforaphane Alleviates Lipopolysaccharide-induced Spatial Learning and Memory Dysfunction in Mice: The Role of BDNF-mTOR Signaling Pathway. Abstract:  Peripheral immune activation could cause neuroinflammation, leading to a series of central nervous system (CNS) disorders, such as spatial learning and memory dysfunction. However, its pathogenic mechanism and therapeutic strategies are not yet determined. The present study aimed to investigate the therapeutic effects of sulforaphane (SFN) on lipopolysaccharide (LPS)-induced spatial learning and memory dysfunction, and tried to elucidate its relationship with the role of hippocampal brain-derived neurotrophic factor (BDNF)-mammalian target of rapamycin (mTOR) signaling pathway. Intraperitoneal injection of LPS for consecutive 7 days to mice caused abnormal behaviors in Morris water maze test (MWMT), while systemic administration of SFN notably reversed the abnormal behaviors. In addition, hippocampal levels of inflammatory cytokines, synaptic proteins, BDNF-tropomyosin receptor kinase B (TrkB) and mTOR signaling pathways were altered in the processes of LPS-induced cognitive dysfunction and SFN&#039;s therapeutic effects. Furthermore, we found that ANA-12 (a TrkB inhibitor) or rapamycin (a mTOR inhibitor) could block the beneficial effects of SFN on LPS-induced cognitive dysfunction, and that hippocampal levels of synaptic proteins, BDNF-TrkB and mTOR signaling pathways were also notably changed. In conclusion, the results of the present study suggest that SFN could elicit improving effects on LPS-induced spatial learning and memory dysfunction, which is likely related to the regulation of hippocampal BDNF-mTOR signaling pathway. <p><a href="https://greenmedinfo.com/article/sulforaphane-improves-lps-induced-spatial-learning-and-memory-dysfunction-like" target="_blank">read more</a></p> https://greenmedinfo.com/article/sulforaphane-improves-lps-induced-spatial-learning-and-memory-dysfunction-like#comments Inflammation Lipopolysaccharide-Induced Toxicity Memory Disorders Sulforaphane Anti-Inflammatory Agents Neurogenesis Brain-derived neurotrophic factor modulator Broccoli Broccoli Sprouts Cruciferous Vegetables Isothiocyanates Animal Study Mon, 29 Jul 2019 21:59:55 +0000 greenmedinfo 192236 at https://greenmedinfo.com The current meta-analysis supports the use of melatonin for anti-nociception. https://greenmedinfo.com/article/current-meta-analysis-supports-use-melatonin-anti-nociception n/a PMID:  Oncotarget. 2017 Nov 21 ;8(59):100582-100592. Epub 2017 Oct 5. PMID: 29246003 Abstract Title:  Exogenous melatonin in the treatment of pain: a systematic review and meta-analysis. Abstract:  Melatonin is an important hormone for regulating mammalian circadian biology and cellular homeostasis. Recent evidence has shown that melatonin exerts anti-nociception effects in both animals and humans. However, according to clinical trials, the anti-nociception effects of melatonin are still controversial. The aim of this meta-analysis was to investigate the anti-nociception effects of melatonin premedication. The primary outcome was the effects of melatonin on pain intensity. The secondary outcomes included the number of patients with analgesic requirements, total analgesic consumption, and brain-derived neurotrophic factor (BDNF) levels. In total, 19 studies were included in the current meta-analysis. The pooling data show that melatonin significantly decreased the pain intensity, as evidenced by the pain scores. Moreover, melatonin administration also reduced the proportion of patients with analgesic requirements and BDNF levels. However, the effects of melatonin on total analgesic consumption still require further confirmation. Collectively, the current meta-analysis supports the use of melatonin for anti-nociception. https://greenmedinfo.com/article/current-meta-analysis-supports-use-melatonin-anti-nociception#comments Chronic Pain Melatonin Antinoceceptive Brain-derived neurotrophic factor modulator Antinoceceptive Brain-derived neurotrophic factor modulator Chronic Pain melatonin Meta Analysis Review Fri, 19 Jan 2018 14:40:04 +0000 greenmedinfo 158587 at https://greenmedinfo.com The data support a promising therapeutic profile for CBD as a new fast-acting antidepressant treatment. https://greenmedinfo.com/article/data-support-promising-therapeutic-profile-cbd-new-fast-acting-antidepressant- n/a PMID:  Mol Neurobiol. 2018 Jun 4. Epub 2018 Jun 4. PMID: 29869197 Abstract Title:  Cannabidiol Induces Rapid and Sustained Antidepressant-Like Effects Through Increased BDNF Signaling and Synaptogenesis in the Prefrontal Cortex. Abstract:  Currently available antidepressants have a substantial time lag to induce therapeutic response and a relatively low efficacy. The development of drugs that addresses these limitations is critical to improving public health. Cannabidiol (CBD), a non-psychotomimetic component of Cannabis sativa, is a promising compound since it shows large-spectrum therapeutic potential in preclinical models and humans. However, its antidepressant properties have not been completely investigated. Therefore, the aims of this study were to investigate in male rodents (i) whether CBD could induce rapid and sustained antidepressant-like effects after a single administration and (ii) whether such effects could be related to changes in synaptic proteins/function. Results showed that a single dose of CBD dose-dependently induced antidepressant-like effect (7-30 mg/kg) in Swiss mice submitted to the forced swim test (FST), 30 min (acute) or 7 days (sustained) following treatment. Similar effects were observed in the Flinders Sensitive and Flinders Resistant Line (FSL/FRL) rats and the learned helplessness (LH) paradigm using Wistar rats. The acute antidepressant effects (30 min) were associated with increased expression of synaptophysin and PSD95 in the medial prefrontal cortex (mPFC) and elevated BDNF levels in both mPFC and hippocampus (HPC). CBD also increased spine density in the mPFC after 30 min, but not 7 days later. Intracerebroventricular injection of the TrkB antagonist, K252a (0.05 nmol/μL), or the mTOR inhibitor, rapamycin (1 nmol/μL), abolished the behavioral effects of CBD. These results indicate that CBD induces fast and sustained antidepressant-like effect in distinct animal models relevant for depression. These effects may be related to rapid changes in synaptic plasticity in the mPFC through activation of the BDNF-TrkB signaling pathway. The data support a promising therapeutic profile for CBD as a new fast-acting antidepressant drug. https://greenmedinfo.com/article/data-support-promising-therapeutic-profile-cbd-new-fast-acting-antidepressant-#comments Cannabidiol Depression Antidepressive Agents Brain-derived neurotrophic factor modulator Antidepressive Agents Brain-derived neurotrophic factor modulator Cannabidiol Depression Animal Study Thu, 07 Jun 2018 00:26:11 +0000 greenmedinfo 165396 at https://greenmedinfo.com The neuroprotective effects of quercetin may be at least partly due to its inducing effects on the expression levels of the BDNF mRNA. https://greenmedinfo.com/article/neuroprotective-effects-quercetin-may-be-least-partly-due-its-inducing-effects n/a PMID:  Bratisl Lek Listy. 2018 ;119(1):28-31. PMID: 29405727 Abstract Title:  Effect of quercetin on the brain-derived neurotrophic factor gene expression in the rat brain. Abstract:  INTRODUCTION: Quercetin is a ubiquitous flavonoid found in many plants. Neuroprotective effects of quercetin have been shown in several in vitro and in vivo studies, but its mechanism of action has not been fully defined yet. Brain-derived neurotrophic factor (BDNF) is a fundamental neurotrophin with vital functions in the survival of neuronal cells. In the present study, we aimed to investigate the effects of quercetin on expression of BDNF mRNA in the hippocampus of rat brain. METHODS: Male rats were daily gavaged with quercetin (10, 20 or 50 mg/kg·bwt) for 30 days. Hippocampal levels of the BDNF transcripts were assessed using quantitative (q) RT-PCR. RESULTS: Quercetin at doses of 20 and 50 mg/kg caused a significant increase in the mRNA expression of BDNF as compared with the control group. Quercetin treatment at a dose of 10 mg/kg failed to cause any significant changes in the levels of BDNF mRNA CONCLUSION: Our findings suggest that the neuroprotective effects of quercetin may be at least partly due to its inducing effects on the expression levels of the BDNF mRNA (Fig. 1, Ref. 40). https://greenmedinfo.com/article/neuroprotective-effects-quercetin-may-be-least-partly-due-its-inducing-effects#comments Quercetin Brain-derived neurotrophic factor modulator Neuroprotective Agents Brain-derived neurotrophic factor modulator Neuroprotective Agents QUERCETIN Animal Study Thu, 08 Feb 2018 04:05:01 +0000 greenmedinfo 159491 at https://greenmedinfo.com