Bitter melon extracts and cucurbitane-type triterpenoid glycosides antagonize lipopolysaccharide-induced inflammation via suppression of NLRP3 inflammasome

[Display omitted] •Bitter melon extracts prevent the expression of various pro-inflammatory genes.•Purified compounds differentially affect the expression of pro-inflammatory genes.•NLRP3 inflammasome related genes are affected by bitter melon treatment.•Molecular docking data suggest momordicoside...

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Bibliographic Details
Published in:Journal of functional foods 2021-11, Vol.86, p.104720, Article 104720
Main Authors: Perez, Jose L., Shivanagoudra, Siddanagouda R., Perera, Wilmer H., Kim, Da Mi, Wu, Chia S., Sun, Yuxiang, Jayaprakasha, G.K., Patil, Bhimanagouda S.
Format: Article
Language:English
Subjects:
Anti-inflammatory
Inflammasome
Macrophages
Metabolic endotoxemia
Momordica charantia
Triterpenoids
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Summary:[Display omitted] •Bitter melon extracts prevent the expression of various pro-inflammatory genes.•Purified compounds differentially affect the expression of pro-inflammatory genes.•NLRP3 inflammasome related genes are affected by bitter melon treatment.•Molecular docking data suggest momordicoside A is a potent inhibitor of NF-κB. Bitter melon (Momordica charantia L.) has been used to manage diabetes and various inflammatory conditions. While studies have explored the use of bitter melon to manage these conditions, the bioactive components and molecular mechanisms mediating the anti-inflammatory effects remain elusive. In the current study, acetone and methanol extracts of bitter melon along with purified compounds (momordicoside A, momordicoside L, karaviloside VI, karaviloside VIII, and charantoside XV) from acetone extract were screened using RAW 264.7 macrophage cells. Acetone and methanol extracts decreased LPS-induced expression of genes related to the formation of the inflammasome complex (NF-κB, NLRP3, Pycard, Casp1). The purified triterpenoids had differential anti-inflammatory effects on the expression of the genes IL-1β, NF-κB, NLRP3, Pycard, Casp1, HMGB1, and HMOX-1. Additionally, molecular docking data suggest that these molecules may be a potent inhibitor of NF-κB. Taken together, the five bioactive compounds exerted anti-inflammatory effects in LPS-induced inflammation, likely via suppression of the NF-κB-NLRP3 pathway.
ISSN:1756-4646
2214-9414
DOI:10.1016/j.jff.2021.104720