Bitter melon extracts and cucurbitane-type triterpenoid glycosides antagonize lipopolysaccharide-induced inflammation via suppression of NLRP3 inflammasome
| Autor: | Bhimanagouda S. Patil, Yuxiang Sun, Chia S. Wu, Da Mi Kim, Siddanagouda R. Shivanagoudra, Wilmer H. Perera, Guddadarangavvanahally K. Jayaprakasha, Jose L. Perez |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Momordica charantia
Lipopolysaccharide Medicine (miscellaneous) Cucurbitane Inflammasome chemistry.chemical_compound medicine TX341-641 Momordicoside chemistry.chemical_classification Nutrition and Dietetics Momordica biology Nutrition. Foods and food supply Chemistry Macrophages Glycoside PYCARD Triterpenoids biology.organism_classification Metabolic endotoxemia Biochemistry Anti-inflammatory Inflammasome complex Food Science medicine.drug |
| Zdroj: | Journal of Functional Foods, Vol 86, Iss, Pp 104720-(2021) |
| ISSN: | 1756-4646 |
| DOI: | 10.1016/j.jff.2021.104720 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect