Anti-Neuroinflammatory Potential of Areca Nut Extract and Its Bioactive Compounds in Anthracene-Induced BV-2 Microglial Cell Activation
Issued Date
2024-09-01
Resource Type
eISSN
20726643
Scopus ID
2-s2.0-85203637080
Journal Title
Nutrients
Volume
16
Issue
17
Rights Holder(s)
SCOPUS
Bibliographic Citation
Nutrients Vol.16 No.17 (2024)
Suggested Citation
Janpaijit S., Sukprasansap M., Tencomnao T., Prasansuklab A. Anti-Neuroinflammatory Potential of Areca Nut Extract and Its Bioactive Compounds in Anthracene-Induced BV-2 Microglial Cell Activation. Nutrients Vol.16 No.17 (2024). doi:10.3390/nu16172882 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/101252
Title
Anti-Neuroinflammatory Potential of Areca Nut Extract and Its Bioactive Compounds in Anthracene-Induced BV-2 Microglial Cell Activation
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Abstract
Particulate matter (PM2.5) containing polycyclic aromatic hydrocarbons (PAHs) is of considerable environmental importance worldwide due to its adverse effects on human health, which are associated with neurodegenerative diseases (NDDs). Areca catechu L. (AC) fruit is known to possess various pharmacological properties; however, the anti-neuroinflammatory roles of AC on the suppression of PAH-induced neuroinflammation are still limited. Thus, we focused on the effects and related signaling cascades of AC and its active compounds against anthracene-induced toxicity and inflammation in mouse microglial BV-2 cells. Phytochemicals in the ethanolic extract of AC (ACEE) were identified using LC-MS, and molecular docking was conducted to screen the interaction between compounds and target proteins. Significant bioactive compounds in ACEE such as arecoline, (−)-epicatechin, and syringic acid were evinced through the LC-MS spectrum. The docking study revealed that (−)-epicatechin showed the highest binding affinities against NF-κB. For cell-based approaches, anthracene induced intracellular ROS, mRNA levels of TNF-α, IL-1β, and IL-6, and the release of TNF-α through enhancing JNK, p38, and NF-κB signaling pathways. However, the co-treatment of cells with ACEE or (−)-epicatechin could reverse those anthracene-induced changes. The overall study suggested that ACEE-derived bioactive compounds such as (−)-epicatechin may be developed as a potential anti-neuroinflammatory agent by preventing inflammation-mediated NDDs.
