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Adenophora divaricata Franch. & Sav. Attenuates Particulate Matter-Induced Inflammatory Responses in RAW264.7
Ji-Hye Ha1,2, Ba-Wool Lee1, Da-Hye Yi1
1Functional Biomaterial Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si 56212, Jeollabuk-do, Republic of Korea.
Abstract:
Particulate matter (PM) is a complex mixture of airborne solid particles and liquid droplets originating from various environmental sources, and it has been implicated in the initiation, development, and progression of pulmonary inflammation and respiratory diseases. However, the underlying associated molecular mechanisms remain unclear. Adenophora divaricate Franch. & Sav. (AD) is a medicinal herb classified within the Campanulaceae family and genus Adenophora, with a broad geographic distribution across East Asia, including Korea, Asia, and Russia. In this study, we investigated the mechanisms underlying the effects of AD on PM-induced lung inflammation in both PM-stimulated RAW264.7 cells and PM-exposed mice. Considering that the reactive oxygen species (ROS)-mediated thioredoxin-interacting protein (TXNIP) and NOD-like receptor pyrin domain containing (NLRP3) inflammasome pathway plays a role in PM-induced inflammatory responses, we focused on determining whether AD exerts its anti-inflammatory effects through modulation of this signaling pathway. The anti-inflammatory properties of the methanolic extract of AD were evaluated using PM-stimulated RAW264.7 cells and PM-exposed mice. PM was administered intranasally to mice for 7 days, whereas AD or dexamethasone was orally administered for the same duration. AD treatment significantly attenuated pulmonary inflammation, as evidenced by reduced inflammatory cell counts and decreased cytokine levels in bronchoalveolar lavage fluid. In addition, AD decreased oxidative stress marker (ROS and thiobarbituric acid reactive substances) while increasing glutathione content, leading to suppression of TXNIP/NLRP3 inflammasome expression. Histopathological analysis revealed a marked alleviation of inflammatory responses in lung tissue, characterized by diminished inflammatory cell infiltration and reduced alveolar wall thickening. Collectively, these findings suggest ROS-mediated TXNIP serves as a key regulatory factor, and AD may serve as a potential therapeutic agent for pulmonary inflammation.
Insights
Adenophora divaricate (AD) extract reduces lung inflammation caused by particulate matter (PM) by targeting oxidative stress and the TXNIP/NLRP3 inflammasome pathway, suggesting its therapeutic potential.
Area of Science:
- Environmental Health
- Pharmacology
- Immunology
Background:
- Particulate matter (PM) exposure causes pulmonary inflammation and respiratory diseases through unclear molecular mechanisms.
- The reactive oxygen species (ROS)-mediated thioredoxin-interacting protein (TXNIP) and NOD-like receptor pyrin domain containing (NLRP3) inflammasome pathway is implicated in PM-induced inflammation.
Purpose of the Study:
- To investigate the anti-inflammatory mechanisms of Adenophora divaricate (AD) in particulate matter (PM)-induced lung inflammation.
- To determine if AD modulates the ROS-TXNIP-NLRP3 inflammasome pathway.
Main Methods:
- Evaluated anti-inflammatory properties of AD methanolic extract in PM-stimulated RAW264.7 cells and PM-exposed mice.
- Administered PM intranasally to mice and AD or dexamethasone orally for 7 days.
- Assessed pulmonary inflammation, oxidative stress markers, glutathione content, TXNIP/NLRP3 inflammasome expression, and lung histopathology.
Main Results:
- AD treatment significantly reduced pulmonary inflammation, inflammatory cell counts, and cytokine levels in bronchoalveolar lavage fluid.
- AD decreased oxidative stress markers (ROS, TBARS) and increased glutathione content.
- AD suppressed TXNIP/NLRP3 inflammasome expression and alleviated lung tissue inflammatory responses.
Conclusions:
- ROS-mediated TXNIP is a key regulator in PM-induced lung inflammation.
- Adenophora divaricate (AD) exhibits anti-inflammatory effects by modulating the ROS-TXNIP-NLRP3 inflammasome pathway.
- AD shows potential as a therapeutic agent for pulmonary inflammation.
