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Life sciences · Review
Frontiers in Aging Neuroscience · October 26, 2026
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Background Neuroinflammation serves as a common pathological substrate across various neurological disorders, including neurodegenerative diseases, cerebrovascular diseases, and neuroimmune conditions. Key pathogenic mechanisms underlying these disorders include aberrant microglial activation, sustained release of pro-inflammatory cytokines, and dysregulation of critical signaling cascades, particularly the NLRP3 inflammasome, NF-κB, and Nrf2/HO-1 pathways, all of which collectively contribute to progressive neuronal damage and functional decline. Objectives This review aims to systematically evaluate the preclinical evidence for the neuroprotective effects of Gastrodia elata Blume and its major bioactive constituents—gastrodin, parishin, p-hydroxybenzyl alcohol, and G. elata polysaccharides—in the treatment of Parkinson’s disease, Alzheimer’s disease, acute ischemic stroke, vascular dementia, and epilepsy, with a particular focus on their modulation of inflammation-related signaling pathways. Methods A comprehensive literature search was performed in PubMed, Web of Science, ScienceDirect, China National Knowledge Infrastructure (CNKI), and Wanfang databases from inception to May 2026. Original studies investigating G. elata or its components in animal or cellular models of the aforementioned diseases and reporting inflammatory mechanisms were included. Results G. elata and its active constituents regulate multiple neuroinflammation-associated signaling pathways, including Nrf2/HO-1, NF-κB/NLRP3, JAK2/STAT3, and MAPK, thereby suppressing inflammatory responses. Mechanistically, these effects are primarily manifested as: (1) inhibition of microglial M1 polarization and consequent reduction of pro-inflammatory cytokine release; (2) blockade of inflammation-induced neuronal death through suppression of ferroptosis, pyroptosis, and apoptosis; (3) enhancement of Nrf2 nuclear translocation, leading to upregulation of antioxidant enzymes and attenuation of oxidative stress-mediated inflammation (e.g., ROS-driven cascades); and (4) modulation of the gut microbiota–brain axis to reduce both peripheral and central low-grade chronic inflammation. Conclusion Despite certain limitations in the existing evidence, this review clearly identifies future research priorities, including investigation of non-gastrodin active components, causal validation using gene-knockout models, and development of brain-targeted delivery strategies. These findings provide a valuable reference for the mechanism-guided development of neuroprotective agents derived from G. elata.