Luteolin, apigenin, and chrysin inhibit lipotoxicity–induced NLRP3 inflammasome activation and autophagy damage in macrophages by suppressing endoplasmic reticulum stress

Author:

Lo Chia‐Wen1ORCID,Lii Chong‐Kuei1ORCID,Lin Kuan‐Shuan1,Li Chien‐Chun23ORCID,Liu Kai‐Li23ORCID,Yang Ya‐Chen4ORCID,Chen Haw‐Wen1ORCID

Affiliation:

1. Department of Nutrition China Medical University Taichung Taiwan

2. Department of Nutrition Chung Shan Medical University Taichung Taiwan

3. Department of Nutrition Chung Shan Medical University Hospital Taichung Taiwan

4. Department of Food Nutrition and Health Biotechnology Asia University Taichung Taiwan

Abstract

AbstractLipotoxicity leads to numerous metabolic disorders such as nonalcoholic steatohepatitis. Luteolin, apigenin, and chrysin are three flavones with known antioxidant and anti‐inflammatory properties, but whether they inhibit lipotoxicity‐mediated NLRP3 inflammasome activation was unclear. To address this question, we used J774A.1 macrophages and Kupffer cells stimulated with 100 μM palmitate (PA) in the presence or absence of 20 μM of each flavone. PA increased p‐PERK, p‐IRE1α, p‐JNK1/2, CHOP, and TXNIP as well as p62 and LC3‐II expression and induced autophagic flux damage. Caspase‐1 activation and IL‐1β release were also noted after 24 h of exposure to PA. In the presence of the PERK inhibitor GSK2656157, PA‐induced CHOP and TXNIP expression and caspase‐1 activation were mitigated. Compared with PA treatment alone, Bcl‐2 coupled to beclin‐1 was elevated and autophagy was reversed by the JNK inhibitor SP600125. With luteolin, apigenin, and chrysin treatment, PA‐induced ROS production, ER stress, TXNIP expression, autophagic flux damage, and apoptosis were ameliorated. Moreover, TXNIP binding to NLRP3 and IL‐1β release in response to LPS/PA challenge were reduced. These results suggest that luteolin, apigenin, and chrysin protect hepatic macrophages against PA‐induced NLRP3 inflammasome activation and autophagy damage by attenuating endoplasmic reticulum stress.

Funder

National Science and Technology Council

China Medical University

Publisher

Wiley

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