phytoestrogens has been researched along with Encephalitis* in 2 studies
2 other study(ies) available for phytoestrogens and Encephalitis
| Article | Year |
|---|---|
Anti-neuroinflammatory effect of daidzein in human hypothalamic GnRH neurons in an in vitro membrane-based model.
Phytoestrogens can control high-fat diet-induced hypothalamic inflammation that is associated with severe consequences, including obesity, type 2 diabetes, cardiovascular and neurodegenerative diseases. However, the phytoestrogen anti-neuroinflammatory action is poorly understood. In this study, we explored the neuroprotection mediated by daidzein in hypothalamic neurons by using a membrane-based model of obesity-related neuroinflammation. To test the daidzein therapeutic potential a biohybrid membrane system, consisting of hfHypo GnRH-neurons in culture on PLGA membranes, was set up. It served as reliable in vitro tool capable to recapitulate the in vivo structure and function of GnRH hypothalamic tissue. Our findings highlighted the neuroprotective role of daidzein, being able to counteract the palmitate induced neuroinflammation. Daidzein protected hfHypo GnRH cells by downregulating cell death, proinflammatory processes, oxidative stress, and apoptosis. It also restored the proper cell morphology and functionality through a mechanism which probably involves the activation of ERĪ² and GPR30 receptors along with the expression of GnRH peptide and KISS1R. Topics: Anti-Inflammatory Agents; Antioxidants; Apoptosis; Cells, Cultured; Encephalitis; Gonadotropin-Releasing Hormone; Humans; Hypothalamus; Isoflavones; Membranes, Artificial; Models, Biological; Neurons; Neuroprotective Agents; Palmitates; Phytoestrogens; Polylactic Acid-Polyglycolic Acid Copolymer | 2021 |
Biochanin A protects dopaminergic neurons against lipopolysaccharide-induced damage through inhibition of microglia activation and proinflammatory factors generation.
Activation of microglia and consequent release of proinflammatory factors, are believed to contribute to neurodegeneration in Parkinson's disease (PD). Hence, identification of compounds that prevent microglial activation is highly desirable in the search for therapeutic agents for inflammation-mediated neurodegenerative diseases. In this study, we reported that biochanin A, one of the predominant isoflavones in Trifolium pratense, attenuated lipopolysaccharide (LPS)-induced decrease in dopamine uptake and the number of dopaminergic neurons in a dose-dependent manner in rat mesencephalic neuron-glia cultures. Moreover, biochanin A also significantly inhibited LPS-induced activation of microglia and production of tumor necrosis factor-alpha, nitric oxide and superoxide in mesencephalic neuron-glia cultures and microglia-enriched cultures. This study suggested for the first time that biochanin A protected dopaminergic neurons against LPS-induced damage through inhibition of microglia activation and proinflammatory factors generation. Topics: Animals; Animals, Newborn; Cells, Cultured; Coculture Techniques; Dopamine; Dose-Response Relationship, Drug; Encephalitis; Genistein; Gliosis; Inflammation Mediators; Lipopolysaccharides; Microglia; Neurons; Neuroprotective Agents; Nitric Oxide; Parkinson Disease; Phytoestrogens; Rats; Rats, Sprague-Dawley; Substantia Nigra; Superoxides; Tumor Necrosis Factor-alpha | 2007 |