RESUMEN
This study investigated the potential therapeutic properties of fermented ginseng berry extract (GBE) for Alzheimer's disease (AD). Fermented GBE was examined for its ginsenoside content and physiological properties, which have been suggested to have neuroprotective effects and improve cognitive function. The results showed that fermented GBE contains high levels of major active ginsenosides and exhibits antioxidant and acetylcholinesterase inhibitory activities. Post-fermented GBE demonstrated therapeutic potential in AF64A-induced damaged neural stem cells and an animal model of AD. These findings suggest that fermented GBE may hold promise as a candidate for developing new therapeutic interventions for memory deficits and cognitive disorders associated with AD and other neurodegenerative conditions. However, further studies are needed to evaluate the safety, tolerability, and efficacy of fermented GBE in human subjects and to determine its clinical applications. In conclusion, our study provides evidence that fermented GBE has potential as a natural product for the prevention and treatment of AD. The high levels of active ginsenosides and antioxidant and acetylcholinesterase inhibitory activities of fermented GBE suggest that it may be a promising therapeutic agent for improving cognitive function and reducing neurodegeneration.
Asunto(s)
Ginsenósidos , Panax , Animales , Humanos , Ginsenósidos/farmacología , Ginsenósidos/uso terapéutico , Extractos Vegetales/efectos adversos , Antioxidantes/efectos adversos , Frutas , Acetilcolinesterasa , Trastornos de la Memoria/tratamiento farmacológico , Trastornos de la Memoria/prevención & control , Trastornos de la Memoria/inducido químicamente , CogniciónRESUMEN
Pathogenesis-related (PR) proteins produced in plants play a crucial role in self-defense against microbial attacks. Previously, we have identified a novel PR-1-like protein (OPRP) from Oenanthe javanica and examined its pharmacologic relevance and cell signaling in mammalian cells. Purified full-length OPRP protein significantly increased toll-like receptor 4 (TLR4)-dependent expression levels of genes such as inducible nitric oxide synthase (iNOS), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and CD80. We also found that small peptides (OPRP2 and OPRP3) designed from OPRP remarkably upregulated myxovirus resistance (Mx1), 2'-5' oligoadenylate sythetase (OAS), and interferon (IFN) α/ß genes in mouse splenocytes as well as human epithelial cells. Notably, OPRP protein distinctively activated STAT1 phosphorylation and ISGF-3γ. Interestingly, OPRP2 and OPRP3 were internalized to the cytoplasm and triggered dimerization of STAT1/STAT2, followed by upregulation of type I IFN-dependent antiviral cytokines. Moreover, OPRP1 successfully inhibited viral (Pseudo SARS-CoV-2) entry into host cells. Taken together, we conclude that OPRP and its small peptides (OPRP1 to 3) present a new therapeutic intervention for modulating innate immune activity through type I IFN-dependent antiviral signaling and a new therapeutic approach that drives an antiviral state in non-immune cells by producing antiviral cytokines.
Asunto(s)
Antivirales , Inmunidad Innata , Oenanthe , Proteínas de Plantas , Animales , Antivirales/farmacología , Citocinas/metabolismo , Humanos , Interferón-alfa/metabolismo , Interferón beta/metabolismo , Ratones , Oenanthe/metabolismo , Proteínas de Plantas/farmacología , Transducción de SeñalRESUMEN
Pathogenesis-related (PR) proteins are inducible and accumulated in plants upon pathogen challenge for survival. Interest in these proteins has arisen in many fields of research, including areas of protein defense mechanisms and plant-derived allergens. In this study, we cloned a PR protein gene (OJPR) from Oenanthe javanica, which consisted of 465 bp with an approximate molecular mass of 16 kDa. The DNA and deduced amino acid sequences of OJPR were 87% similar to Pimpinella brachycarpa PR-1 together with a glycine-rich loop which is a signature motif of PR-10. In microarray analysis, OJPR-transfected Raw264.7 (OJPR+) upregulated high mobility group box 1 and protein kinase Cα, and downregulated chemokine ligand 3 and interleukin 1ß which are all related to toll-like receptor 4 (TLR4) and inflammation. TAK-242 and PD98059 inhibited the activation by OJPR, suggesting that OJPR transduce TLR4-mediated signaling. Interestingly, OJPR increased anti-viral repertoires, including interferon (IFN)α, IFNγ, OAS1, and Mx1 in CD4+ primary T cells. Taken together, we concluded that OJPR may play a role in modulating host defense responses via TLR signal transduction and provide new insights into the therapeutic and diagnostic advantages as a potential bioactive protein.