Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes

Diesel exhaust particulate (DEP) is widely recognized to weaken lung function and skin diseases. When the skin, which defends against external factors, is exposed to PM2.5, various chronic inflammatory diseases occur. When keratinocytes recognize harmful signals, they synthesize the NOD-like recepto...

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Main Authors: Seung Yeon Lee, Gi Ho Lee, Jeonghwan Maeng, Su Yeon Kim, Hwi-Yeol Yun, Gil-Saeng Jeong, Hye Gwang Jeong
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Antioxidants
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Online Access:https://www.mdpi.com/2076-3921/14/5/610
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author Seung Yeon Lee
Gi Ho Lee
Jeonghwan Maeng
Su Yeon Kim
Hwi-Yeol Yun
Gil-Saeng Jeong
Hye Gwang Jeong
author_facet Seung Yeon Lee
Gi Ho Lee
Jeonghwan Maeng
Su Yeon Kim
Hwi-Yeol Yun
Gil-Saeng Jeong
Hye Gwang Jeong
author_sort Seung Yeon Lee
collection DOAJ
description Diesel exhaust particulate (DEP) is widely recognized to weaken lung function and skin diseases. When the skin, which defends against external factors, is exposed to PM2.5, various chronic inflammatory diseases occur. When keratinocytes recognize harmful signals, they synthesize the NOD-like receptor protein 1 (NLRP1) inflammasome. DEP enhances NF-κB signaling and NLRP1 inflammasome expression through the interaction of TXNIP with NLRP1 in keratinocytes. Although many studies have reported the anti-inflammatory and antioxidant characteristics of Impressic acid (IPA), the umbrella consequences of IPA for PM2.5-influenced inflammasomes and the associated mechanisms remain unknown. Therefore, this study aimed to examine the protective function of IPA against inflammation in human keratinocytes. IPA attenuated the NLRP1 expression, caspase-1, IL-1β actuation, and NF-κB and IκB phosphorylation induction by DEP. IPA upregulated the Nrf2, HO-1, and NQO1 expression through CaMKKβ, AMPK, and GSK3β phosphorylation. Also, IPA led to the elevation of p62 and the degradation of the Keap1 protein. ML385 reversed the suppressive effect of IPA on the NLRP1 inflammasome, which was enhanced by DEP, and NAC counteracted the effect of ML385. These findings indicate that IPA can suppress inflammation induced by PM2.5 by expressing antioxidant enzymes through the Keap1/p62/Nrf2-signaling pathway in human keratinocytes.
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spelling doaj-art-04da0a9ca69e466f9d97b4a89a42478d2025-08-20T03:14:39ZengMDPI AGAntioxidants2076-39212025-05-0114561010.3390/antiox14050610Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in KeratinocytesSeung Yeon Lee0Gi Ho Lee1Jeonghwan Maeng2Su Yeon Kim3Hwi-Yeol Yun4Gil-Saeng Jeong5Hye Gwang Jeong6College of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaCollege of Pharmacy, Chungnam National University, Daejeon 34134, Republic of KoreaDiesel exhaust particulate (DEP) is widely recognized to weaken lung function and skin diseases. When the skin, which defends against external factors, is exposed to PM2.5, various chronic inflammatory diseases occur. When keratinocytes recognize harmful signals, they synthesize the NOD-like receptor protein 1 (NLRP1) inflammasome. DEP enhances NF-κB signaling and NLRP1 inflammasome expression through the interaction of TXNIP with NLRP1 in keratinocytes. Although many studies have reported the anti-inflammatory and antioxidant characteristics of Impressic acid (IPA), the umbrella consequences of IPA for PM2.5-influenced inflammasomes and the associated mechanisms remain unknown. Therefore, this study aimed to examine the protective function of IPA against inflammation in human keratinocytes. IPA attenuated the NLRP1 expression, caspase-1, IL-1β actuation, and NF-κB and IκB phosphorylation induction by DEP. IPA upregulated the Nrf2, HO-1, and NQO1 expression through CaMKKβ, AMPK, and GSK3β phosphorylation. Also, IPA led to the elevation of p62 and the degradation of the Keap1 protein. ML385 reversed the suppressive effect of IPA on the NLRP1 inflammasome, which was enhanced by DEP, and NAC counteracted the effect of ML385. These findings indicate that IPA can suppress inflammation induced by PM2.5 by expressing antioxidant enzymes through the Keap1/p62/Nrf2-signaling pathway in human keratinocytes.https://www.mdpi.com/2076-3921/14/5/610diesel exhaust particlesNLRP1 inflammasomeimpressic acidNrf2keratinocytes
spellingShingle Seung Yeon Lee
Gi Ho Lee
Jeonghwan Maeng
Su Yeon Kim
Hwi-Yeol Yun
Gil-Saeng Jeong
Hye Gwang Jeong
Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
Antioxidants
diesel exhaust particles
NLRP1 inflammasome
impressic acid
Nrf2
keratinocytes
title Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
title_full Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
title_fullStr Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
title_full_unstemmed Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
title_short Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes
title_sort anti inflammasome effect of impressic acid on diesel exhaust particulate matter induced nlrp1 inflammasome via the keap1 p62 nrf2 signaling pathway in keratinocytes
topic diesel exhaust particles
NLRP1 inflammasome
impressic acid
Nrf2
keratinocytes
url https://www.mdpi.com/2076-3921/14/5/610
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