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Article Publish Status: FREE
Abstract Title:

Genipin suppresses NLRP3 inflammasome activation through uncoupling protein-2.

Abstract Source:

Cell Immunol. 2015 Sep ;297(1):40-5. Epub 2015 Jun 16. PMID: 26123077

Abstract Author(s):

Venugopal Rajanbabu, Lakshmi Galam, Jutaro Fukumoto, Juan Enciso, Pratima Tadikonda, Troy N Lane, Sayantani Bandyopadhyay, Prasanna Tamarapu Parthasarathy, Young Cho, Seong Ho Cho, Yong Chul Lee, Richard F Lockey, Narasaiah Kolliputi

Article Affiliation:

Venugopal Rajanbabu

Abstract:

Incomplete clearance of apoptotic cells and reactive oxygen species (ROS) release are known to trigger inflammasome activation causing severe inflammation in acute lung injury and various metabolic and autoimmune diseases. Moreover, it has been reported that apoptotic cell clearance and ROS-mediated apoptosis critically depend on mitochondrial uncoupling protein-2 (UCP2). However, the relationship between UCP2 and inflammasome activation has not been studied. This report investigates the role of UCP2 in the expression and activation of NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome in human macrophages. We found that UCP2 overexpression significantly enhanced the expression levels of NLRP3. The NLRP3 expression levels were significantly suppressed in THP1 cells treated with genipin, a UCP2 inhibitor, compared to controls. In addition, genipin altered adenosine triphosphate (ATP)- and hydrogen peroxide (H2O2)-mediated interleukin-1 beta (IL-1β) secretion and significantly suppressed caspase-1 activity in inflammasome-activated human macrophages. Taken together, our results suggest that genipin modulates NLRP3 inflammasome activation and ATP- or H2O2-mediated IL-1β release.

Study Type : In Vitro Study

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