Fermented bitter gourd extract differentially regulates lipopolysaccharide-induced cytokine gene expression through nuclear factor-κB and interferon regulatory factor-1

Abstract

Bitter gourd is the fruit of a tropical vine in Asia, Africa, and South America where it is commonly used in traditional medicine. Our study tested the effects of a fermented extract of the bitter gourd on the inflammatory activities of the human monocytic leukemia cell line, THP-1. Treatment with the extract resulted in the suppression of phagocytic as well as lipopolysaccharide (LPS)-induced adhesion activity. Interestingly, the LPS-induced expression of matrix metalloproteinase-9 (MMP-9) and tumor necrosis factor-α (TNF-α) was suppressed by the extract while the expression of Interleukin-8 (IL-8) was upregulated. The extract inhibited the LPS-induced activation of p38 mitogen-activated protein kinase (MAPKs) and nuclear factor-κB (NF-κB), both of which are well known to be required for the expression of MMP-9 and TNF-α. In contrast, the expression of interferon regulatory factor (IRF) 1, a transcription factor involved in the expression of IL-8, but not TNF-α, was enhanced by the extract. Suppression of IRF-1 expression resulted in the elimination of the extract's interleukin-8 (IL-8) enhancing effect. These results indicate that the fermented bitter gourd extract has general anti-inflammatory effects, with a differential effect on the expression of cytokines through modulation of NF-κB and IRF-1 activities.

Transcriptome and metabolome changes induced by bitter melon (Momordica charantia)- intake in a high-fat diet induced obesity model

“… 111 , 112 , 113 Reports have shown bitter melon increased superoxide dismutase activity 114 and attenuated pro-inflammatory signaling in myocardial infarction, mitochondrial oxidation and HFD or other biological agents (ethanol, lipopolysaccharide, bacterial) induced neuroinflammation, and macrophage/mast cell infiltration in mice. 17 , 26 , 115 , 116 , 117 , 118 Briefly, our results show BMJ intervention has an expansive influence on immunity signaling as indicated by its targeting of innate/adaptive (GO 0045087, GO 0002460), humoral immune (GO 0006959) and general immune activation (GO 0002253) responses to combat pro-inflammatory mediators involved in adipocytokine signaling. Specifically, our study results showed that BMJ leads to inhibition of pro-inflammatory cytokine ( Ccl2 ), and higher levels of DG(40:1) (adipocytokine-associated metabolite).…”

Glucocorticoid-mediated anti-inflammatory effect through NFκB is preserved in the absence of Dexras1

“…Cell culture media were composed of DMEM supplemented with 10% FBS, penicillin (100 U/mL), and streptomycin (100 μg/mL). To instigate an inflammatory state, bacterial LPS (100 ng/ml) was added to the media for 4 hrs (Jang et al 2015). siRNA RAW264.7 cells were plated into 100-mm-diameter dishes 18-24 h prior to transfection.…”