ArticleLaboratory animal research2020
Brain Factor-7® improves learning and memory deficits and attenuates ischemic brain damage by reduction of ROS generation in stroke in vivo and in vitro.
Article in Laboratory animal research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Stabilization of CXCL12 (SDF-1α) via silk fibroin films enhances stem cell migration/retention and functional recovery after stroke.Regenerative biomaterials · 2026Article
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- Resistance to Degradation of Silk Fibroin Hydrogels Exposed to Neuroinflammatory Environments.Polymers · 2023Article
- Nrf2-mediated activation of HO-1 is required in the blocking effect of compound K, a ginseng saponin metabolite, against oxidative stress damage in ARPE-19 human retinal pigment epithelial cells.Journal of ginseng research · 2023Article
- Activation of Nrf2/HO-1 antioxidant signaling correlates with the preventive effect of loganin on oxidative injury in ARPE-19 human retinal pigment epithelial cells.Genes & genomics · 2023Article
- Silk fibroin carriers with sustained release capacity for treating neurological diseases.Frontiers in pharmacology · 2023Review
- Effects of Brain Factor‑7® against motor deficit and oxidative stress in a mouse model of MPTP‑induced Parkinson's disease.Experimental and therapeutic medicine · 2022Article
- Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and HAntioxidants (Basel, Switzerland) · 2022Article
- Effects of Silk Fibroin Enzyme Hydrolysates on Memory and Learning: A Review.Molecules (Basel, Switzerland) · 2022Review
- Fermented Mentha arvensis administration provides neuroprotection against transient global cerebral ischemia in gerbils and SH-SY5Y cells via downregulation of the MAPK signaling pathway.BMC complementary medicine and therapies · 2022Article
- Fisetin Attenuated Oxidative Stress-Induced Cellular Damage in ARPE-19 Human Retinal Pigment Epithelial Cells Through Nrf2-Mediated Activation of Heme Oxygenase-1.Frontiers in pharmacology · 2022Article
- Antimicrobial protein REG3A and signaling networks are predictive of stroke outcomes.Journal of neurochemistry · 2022Article
- Therapeutic Effects of Decursin andMolecules (Basel, Switzerland) · 2021Article
- Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking CaInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain Factor-7® (BF-7), silk fibroin peptide, is known to be effective in improvement of memory and learning ability. In this study, the effects of BF-7 (10 mg/kg, p.o., pre-treatment for 7 days and post-treatment for 7 days) on neuroprotection and memory and learning functions were investigated in a rat model of transient focal cerebral ischemia and a gerbil model of transient global forebrain ischemia. Furthermore, to find the mechanism of BF-7, we examined the neuroprotective and antioxidative effects of BF-7 in vitro using neuroblastoma (SH-SY5Y) cells. In vivo model, treatment with BF-7 significantly reduced the number of errors in 8-arm maze test and significantly increased latency time in passive avoidance test at 7 days after focal ischemia compared to those in the vehicle-treated group. In addition, treatment with BF-7 significantly decreased the infarct size or neuronal death at 7 day following transient ischemia compared to that in the vehicle-treated group. In vitro model, 10 or 20 μg/ml of BF-7 treatment significantly increased cell viability in dose-dependent manner. In addition, oxidative stress was significantly attenuated in the ischemic cells, showing that 10 or 20 μg/ml of BF-7 treatment significantly reduced the generation of reactive oxygen species (ROS) compared to that in the ischemic cells. These results indicate that BF-7 treatment can attenuate ischemic damages and improve memory deficits via reduction of ROS generation.
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