scholarly journals Modulation of Brain-Derived Neurotrophic Factor (BDNF) Signaling Pathway by Culinary Sage (Salvia officinalis L.)

2021 ◽  
Vol 22 (14) ◽  
pp. 7382
Author(s):  
Nancy Chiang ◽  
Shahla Ray ◽  
Jade Lomax ◽  
Sydney Goertzen ◽  
Slavko Komarnytsky ◽  
...  

Culinary sage (Salvia officinalis L.) is a common spice plant in the mint family (Lamiaceae) well known for its distinctive culinary and traditional medicinal uses. Sage tea has been used traditionally as a brain-enhancing tonic and extracts from sage have been reported to have both cognitive and memory enhancing effects. Brain-derived neurotrophic factor (BDNF) is an endogenous signaling molecule involved in cognition and memory function. In this study, activity-guided fractionation employing preparative reverse-phase high performance liquid chromatography (RP-HPLC) of culinary sage extracts led to the discovery of benzyl 6-O-β-D-apiofuranosyl-β-D-glucoside (B6AG) as a natural product that upregulates transcription of neurotrophic factors in C6 glioma cells. Purified B6AG showed a moderate dose response, with upregulation of BDNF and with EC50 at 6.46 μM. To better understand the natural variation in culinary sage, B6AG was quantitated in the leaves of several commercial varieties by liquid chromatography-mass spectrometry (LC-MS). The level of B6AG in dried culinary sage was found to range from 334 ± 14 to 698 ± 65 μg/g. This study provided a foundation for future investigations, including quantitative inquiries on the distribution of B6AG within the different plant organs, explorations in optimizing post-harvest practices, and aid in the development of sage varieties with elevated levels of B6AG.

Author(s):  
O. P. Oladosu ◽  
N. R. Isu ◽  
I. M. Aboh ◽  
S. E. Okhale ◽  
A. T. Orishadipe ◽  
...  

The emergence of multi-drug resistance in bacteria has led to call for research and development of new leads as antibiotics from medicinal plants. Acacia nilotica (Linn) is a plant of multipurpose medicinal uses, three bioactive flavonoids (methyl gallate, gallic acid and catechin) were isolated from its fruit pulps through a bioassay guided fractionation technique and characterized based on High Performance Liquid Chromatography, Liquid Chromatography-Mass Spectra and Nuclear Magnetic Resonance spectra. Antibacterial activity of these compounds was determined by microplate tetrazolium dye assay of broth microdilution technique against Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli, and clinical isolates of Salmonella typhi, Klebsiella pneumonia, Candida albicans and Bacillus subtilis. Catechin, methyl gallate and gallic acid at 19.5, 39 and 39 µg/ml respectively caused a significant bio-reduction in cells of test organisms. Time kill kinetic study of the extract shows that there was percentage of growth reduction in test organisms at 2, 4, 6, 8 and 12 hrs of contact. The extent and rate of killing of the organism by the extract at 2 x MIC followed the same trend as rate of killing was time dependent. Antibacterial effects of these compounds are within the breakpoint of control drug chloramphenicol and could serve as leads in new drug development.


2002 ◽  
Vol 22 (7) ◽  
pp. 843-851 ◽  
Author(s):  
Brian J. D'Cruz ◽  
Kristofer C. Fertig ◽  
Anthony J. Filiano ◽  
Shawn D. Hicks ◽  
Donald B. DeFranco ◽  
...  

Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest. After resuscitation, rats were maintained either at normal temperature (37°C) or cooled to mild hypothermia (33°C, beginning 60 minutes after resuscitation). After 12 or 24 hours, neurotrophin levels in hippocampus were measured by immunoblotting. Ischemia and reperfusion increased hippocampal levels of BDNF. Induction of hypothermia during reperfusion potentiated the increase in BDNF after 24 hours, but not after 12 hours. Levels of NGF were not increased by postresuscitation hypothermia. Hypothermia also increased tissue levels and tyrosine phosphorylation of TrkB, the receptor for BDNF. Increased BDNF levels were correlated with activation of the extracellularly regulated kinase (ERK), a downstream element in the signal transduction cascade induced by BDNF. In contrast to the many deleterious processes during ischemia and reperfusion that are inhibited by induced hypothermia, increasing BDNF levels is a potentially restorative process that is augmented. Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest.


2019 ◽  
Author(s):  
Henry L. Hallock ◽  
Henry M. Quillian ◽  
Yishan Mai ◽  
Kristen R. Maynard ◽  
Julia L. Hill ◽  
...  

AbstractBrain-derived neurotrophic factor (BDNF) signaling regulates synaptic plasticity in the hippocampus (HC) and prefrontal cortex (PFC), and has been extensively linked with fear memory expression in rodents. Notably, disrupting BDNF production from promoter IV-derived transcripts enhances fear expression in mice, and decreases fear-associated HC-PFC synchrony, suggesting that Bdnf transcription from promoter IV plays a key role in HC-PFC function during fear memory retrieval. To understand how promoter IV-derived BDNF affects fear expression and HC-PFC connectivity, we generated a viral construct that selectively targets cells expressing promoter IV-derived Bdnf transcripts (“p4-cells”) for tamoxifen-inducible Cre-mediated recombination (AAV8-p4Bdnf-ERT2CreERT2-PEST). Using this construct, we found that ventral (vHC) p4-cells are recruited during fear expression, and that activation of these cells causes exaggerated fear expression that co-occurs with disrupted vHC-PFC synchrony in mice. Our data highlight how this novel construct can be used to interrogate genetically-defined cell types that selectively contribute to BDNF-dependent behaviors.


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