Coeloglossum viride var. bracteatum extract improves learning and memory of chemically-induced aging mice through upregulating neurotrophins BDNF and FGF2 and sequestering neuroinflammation

Ginsenoside Rg1 ameliorates the cognitive deficits in D-galactose and AlCl3-induced aging mice by restoring FGF2-Akt and BDNF-TrkB signaling axis to inhibit apoptosis

“…However, compelling evidence has supported the longevity effect through the inhibition of mTOR activity [37]. Therefore, a moderate activity of Akt is required to prevent neural apoptosis and anti-toxic inflammation [12]. In other words, neurotrophins such as BDNF (brain-derived neurotrophic factor) or chemokine like FGF2 activated TrkB and Akt signaling axis to inhibit apoptosis and preserve the integrity of neurons and synapse plasticity is essential for brain functions.…”

“…In the nucleus, Akt enhances the transcription of anti-apoptotic genes such as Bcl-2 but inhibits the transcription factors promoting the expression of cell apoptosis-related genes. Moderate activity and healthy response of FGF2-PI3K/Akt signaling axis are essential for neural homeostasis and functions [12].…”

“…Western blotting of hippocampal and prefrontal cortex proteins was performed as described previously [12,19]. The antibodies used in the experiments were included as following, Goat anti-mouse IgG-HRP (#ZDR-5307, dilution 1:5000) and goat anti-rabbit IgG-HRP (#ZDR-5306, dilution 1:5000) antibodies were purchased from ZSGB-BIO.…”

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

“…combination of D-galactose and aluminum chloride-induced aging mouse (i) Improved learning and memory in aging mouse[275] (ii) Upregulated mRNA expression of BDNF and fibroblast growth factor 2 (FGF2) in the hippocampus of aging mouse (iii) Inhibited mRNA expression of neuroinflammatory factors (TNF-α, IL-6, IL-1β, and NOS-2) in the hippocampus of aging mouse (iv) Activated PI3K/Akt signaling pathway(v) Inhibited the canonical caspase-3 apoptosis pathways Methanolic extract of Cinnamomum camphora leaves Maximal electroshock-induced seizures in albino Wistar rats (i) Exhibited the anticonvulsant activity in maximal electroshock-induced seizures by reducing epileptic seizures [276] (ii) Increased gamma-aminobutyric acid (GABA) release (iii) Decreased lipid peroxidation and acetylcholinesterase activity (iv) Increased GSH level Phragmanthera austroarabica extract Pentylenetetrazol-kindled mouse (i) Reduced seizures and cortical malondialdehyde level [277] (ii) Enhanced cortical GSH (iii) Reduced the percentage of pyknotic neurons in the hippocampus (iv) Increased the percentage of viable neurons Parawixin 10, a compound isolated from Parawixia bistriata spider venom A rat excitotoxicity model of brain injury by kainic acid, N-methyl-D-aspartate, and pentylenetetrazol (i) Decreased glial proliferation in all hippocampal subfields studied, as well as the preservation of cell layers [278, 279] (ii) Prevented the onset of seizures induced with kainic acid, N-methyl-D-aspartate, and pentylenetetrazol (iii) Increased the latency to the onset of kainic acid-, pentylenetetrazol-, and N-methyl-Daspartate-induced seizures White rose (Rosa hybrida) petal extract Kainic acid-induced mouse and in HB1.F3 human neural stem cells (i) Exhibited radical scavenging activities [280] (ii) Inhibited lipid peroxidation (iii) Decreased scores of epileptiform seizures (iv) Decreased hippocampal pyramidal neuronal loss (v) Downregulated mRNA expressions of antioxidant enzymes (vi) Downregulated mRNA and protein expressions of inflammatory mediators Rosemary extract Kainic acid-induced rats (i) Decreased neuronal loss in CA3 hippocampal region [281] (ii) Decreased spatial memory and learning impairment Walnut extract Lipopolysaccharide-induced neurotoxicity in rat microglial cell line (i) Downregulated iNOS and Iba-1 expressions [273] (ii) Upregulated calmodulin expression…”

2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside eliminates staurosporine-induced cytotoxicity by restoring BDNF-TrkB/Akt signaling axis

“…Indeed, the typical neurotrophic factor BDNF and its receptor TrkB is essential for neural survival and synaptic activity. Inappropriate expression of BDNF and dysfunctions of its associated signaling axis were frequently observed in a number of neural diseases [8,10,23]. In light of this statement, we concentrated on the regulation of BDNF and its regulated signaling pathway in THSG mediated neuroprotective functions.…”