ArticleNeurochemical research2018
Luteolin Could Improve Cognitive Dysfunction by Inhibiting Neuroinflammation.
Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review.Annals of clinical and translational neurology · 2022Pooled it
- Artificial Intelligence for Natural Products Drug Discovery in Neurodegenerative Therapies: A Review.Biomolecules · 2026Review
- Protective Effect of luteolin on CLP-induced Sepsis-associated Encephalopathy via Inhibiting p38 MAPK Signalling in a Rat Model.Molecular neurobiology · 2026Article
- Therapeutic Expedition of Luteolin against Brain-related Disorders: An Updated Review.Combinatorial chemistry & high throughput screening · 2025Review
- Mast Cells in Autism Spectrum Disorder-The Enigma to Be Solved?International journal of molecular sciences · 2024Review
- Anti-Neuroinflammatory Effects of Adaptogens: A Mini-Review.Molecules (Basel, Switzerland) · 2024Review
- Modulation of microglial polarization by sequential targeting surface-engineered exosomes improves therapy for ischemic stroke.Drug delivery and translational research · 2024Article
- A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.Aging · 2024Article
- Hua-Feng-Dan Alleviates LPS-induced Neuroinflammation by Inhibiting the TLR4/Myd88/NF-κB Pathway: Integrating Network Pharmacology and Experimental Validation.Current pharmaceutical design · 2024Article
- Discovery of drug lead compounds for Anti-Alzheimer's disease on the basis of synaptic plasticity.Heliyon · 2023Article
- Potential Role of Moesin in Regulating Mast Cell Secretion.International journal of molecular sciences · 2023Review
- Aged brain and neuroimmune responses to COVID-19: post-acute sequelae and modulatory effects of behavioral and nutritional interventions.Immunity & ageing : I & A · 2023Review
- Article
- A Comprehensive Review of Natural Flavonoids with Anti-SARS-CoV-2 Activity.Molecules (Basel, Switzerland) · 2023Review
- Review
- Luteolin: A promising natural agent in management of pain in chronic conditions.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Humulus japonicus attenuates LPS-and scopolamine-induced cognitive impairment in mice.Laboratory animal research · 2022Article
- Active Compounds in Fruits and Inflammation in the Body.Nutrients · 2022Review
- Mechanism of Huashi Xingyu Qingre recipe in treating oral lichen planus based on network pharmacology and clinical trial verification.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?Molecular neurobiology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Neuroinflammation and oxidative stress play an important role in cognition deficit following chronic cerebral hypoperfusion (CCH). Luteolin, a natural flavonoid found in many plants, is known for a variety of pharmacological activities, such as its anti-inflammatory, anti-allergy, urate, anti-tumor, antibacterial, and antiviral effects. To assess whether luteolin could prevent CCH-induced cognitive dysfunction, through its anti-inflammatory and anti-oxidative-stress effects, we used enzyme-linked immunosorbent assays, enzyme activity assays, behavioral methods, immunohistochemistry, and electrophysiology to detect neuroinflammation and oxidative stress, cognition alterations, and long-term potential (LTP), in a bilateral common carotid arteries ligation (2VO) rat model. We demonstrated that CCH increased tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and malondialdehyde (MDA), and decreased superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels. Further, it caused microglia over-activation and astrogliosis, learning and short-term memory dysfunction, and an LTP deficit. Luteolin treatment reversed CCH-induced changes. Specifically, luteolin prevented the increase of TNF-α and IL-1β, IL-6, and MDA, improved the activity of SOD and GPx, inhibited microglia over-activation and astrogliosis (particularly in the hippocampus and cortex), and ameliorated learning and short-term memory dysfunction, and LTP deficit. Thus, our study suggested that luteolin could be a preferable anti-inflammatory agent to protect cognitive function and synaptic plasticity following CCH. Luteolin could also be putative therapeutic candidate for other inflammation-related brain diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.