AI Article Synopsis
- Neuroinflammation is linked to neurodegenerative diseases like Alzheimer's and Parkinson's, and this study investigates the effects of Andalucin (ADL) on microglial cells.
- ADL effectively inhibited pro-inflammatory mediators and cytokines release in LPS-activated BV2 cells and downregulated specific genes associated with inflammation.
- The study revealed that ADL activates the Nrf2/HO-1 signaling pathway while suppressing the NF-κB pathway, highlighting its regulatory role in the interaction between Nrf2 and p65.
Article Abstract
Background: Neuroinflammation plays an important role in many neurodegenerative conditions such as Alzheimer's disease (AD) and Parkinson disease (PD). Andalucin (ADL), a sesquiterpene lactone from Artemisia lannta, has been reported to exhibit NO inhibition in vitro. However, the effect of ADL on microglia-mediated neuroinflammation has not been investigated.
Purpose: This study was designed to determine the anti-neuroinflammatory effect of ADL against LPS-activated BV2 microglial cells and to explore the underlying mechanisms.
Methods: The production of pro-inflammatory mediators and cytokines were measured by ELISA. The relevant mechanisms were analyzed by qRT-PCR, Luciferase assay, Western blot and Co-immunoprecipitation Assay.
Results: ADL inhibited the LPS-induced release of NO, PGE, TNF-α, IL-6 and IL-1β. In addition, ADL reduced the mRNA and protein levels of iNOS and COX-2. Mechanism studies found that ADL activated Nrf2/HO-1 signaling pathway and suppressed NF-κB signaling pathway. Further investigation showed that the stimulative effect of ADL on Nrf2 transcriptional activity and the inhibitory effect of ADL on RelA transcriptional activity were due to its regulation on p300-Nrf2/p65 interaction.
Conclusion: ADL displayed anti-neuroinflammatory activity in LPS-activated BV2 cells. The mechanism concerns its regulatory effect on the crosstalk between Nrf2 and p65.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.phymed.2018.06.014 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Anti-neuroinflammatory and Neuroprotective Effects of T-006 on Alzheimer's Disease Models by Modulating TLR4-Mediated MyD88/ NF-κB Signaling.
CNS Neurol Disord Drug Targets
January 2025
School of Medicine, Foshan University, Foshan, 528000, China.
Introduction: Neuroinflammation derived from the activation of the microglia is considered a vital pathogenic factor of Alzheimer's Disease (AD). T-006, a tetramethylpyrazine derivative, has been found to alleviate cognitive deficits via inhibiting tau expression and phosphorylation in AD transgenic mouse models. Recently, T-006 has been proven to dramatically decrease the levels of total Amyloid β (Aβ) peptide and Glial Fibrillary Acidic Protein (GFAP) and suppress the expression of ionized calcium binding adaptor molecule-1 (Iba-1) in APP/PS1 mice.
View Article and Find Full Text PDFSynthesis and biological evaluation of lappaconitine analogues as potential anti-neuroinflammatory agents by side chain modification and scaffold hopping strategy.
Bioorg Med Chem
January 2025
School of Life Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China; Key Laboratory of Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University, Chengdu 610031, China; School of Life Science and Engineering, Yibin Institute of Southwest Jiaotong University, Yibin 644000, China. Electronic address:
Article Synopsis
- - Neuroinflammation caused by microglia is a major factor in neurodegenerative diseases, and Lappaconitine (LA), derived from a plant, has been found to reduce certain inflammatory responses in cells.
- - Researchers synthesized and tested LA analogues for their ability to inhibit nitric oxide production in microglia, with one compound (compound 10) showing the strongest effect.
- - Compound 10 works by inhibiting a specific inflammatory pathway in microglia and appears to be safer than LA in toxicity tests, suggesting it could be a promising candidate for treating neuroinflammation.
Anti-Inflammatory Effects of Honeysuckle Leaf Against Lipopolysaccharide-Induced Neuroinflammation on BV2 Microglia.
Nutrients
November 2024
Department of Pharmacology, School of Korean Medicine, Wonkwang University, 460 Iksan-daero, Iksan 54538, Republic of Korea.
Background/objectives: Neurodegenerative disorders have emerged as a major global public health concern, and the burden is predicted to increase over time. Modulating neuroinflammation and microglial activity is considered a promising target for improving neurodegenerative disorders. The leaf of honeysuckle (LH), which has anti-inflammatory properties, has long been collected, regardless of the season, and used for medicinal purposes.
View Article and Find Full Text PDFExosomes Derived from DPA-treated UCMSCs Attenuated Depression-like Behaviors and Neuroinflammation in a Model of Depression Induced by Chronic Stress.
J Neuroimmune Pharmacol
October 2024
Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang, 524088, China.
Depression is characterized by both neuroinflammation and neurodegeneration. Exosomes (Exo) have been shown to function as inhibitors of inflammation and promoters of neurogenesis. Omega-3 polyunsaturated fatty acids, such as eicosapentaenoic acid, can combat depression by increasing levels of docosapentaenoic acid (DPA).
View Article and Find Full Text PDFAntidepressant effects of sulforaphane (SFN) and its derivatives SLL-III-9 and SLL-III-120 and their potential underlying mechanisms based on the microbiota-gut-brain axis.
Food Funct
October 2024
College of Life Science, Liaoning University, Shenyang, 110036, China.
Article Synopsis
- Broccoli contains sulforaphane (SFN), which has beneficial properties such as anti-inflammatory, antioxidant, and anti-cancer effects, and researchers developed SFN derivatives for potential antidepressant benefits.
- The study identified SLL-III-9 and SLL-III-120 as effective SFN derivatives that improved depression-like behaviors in mice and influenced gut bacteria composition, suggesting a link to the microbiota-gut-brain axis.
- SFN and its derivatives were shown to enhance protective proteins, increase levels of neurotransmitters and brain-derived neurotrophic factor, and reduce inflammatory factors, indicating their potential as safe antidepressant agents.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!