Bitter melon or Momordica Charantia is a widely consumed vegetable in South Asia. One of the most notable health benefits of bitter melon is its role in lowering blood glucose as demonstrated in both animal and clinical studies. These effects on glucose appear to be mediated by activation of peroxisome proliferator‐activated receptor (PPAR)‐α and ‐γ, members of the steroid hormone nuclear receptor family involved in the regulation of lipid and glucose homeostasis. The objective of this research was to explore the anti‐inflammatory properties of bitter melon using the RAW 264.7 murine macrophage cell line. Bitter melon was deseeded, the edible portion was blended, and the pulp was separated to obtain the juice. Cells were plated at a density of 10,000 cells/well in a 96‐well plate and then treated with bitter melon at concentrations of 0, 0.125, 0.25, 0.5, 1% (v/v) for 24 hours. Cells were then stimulated with 500 ng/mL of LPS for another 24 hours and the supernatants were collected for determination of nitric oxide (NO), prostaglandin E2 (PGE2) and interleukin (IL)‐6. All experiments were repeated three times and cell viability was assessed using the resazurin‐based assay. Cell viability was not affected by any of the bitter melon juice concentrations used in the study. The LPS‐induced increase in NO production was dose‐dependently down‐regulated by bitter melon. PGE2 and IL‐6 were also elevated by LPS and bitter melon also reduced these inflammatory molecules. Bitter melon, which has been reported to activate both PPAR‐α and PPAR‐γ, suppresses the production of inflammatory mediators brought about by LPS and these anti‐inflammatory effects should be further evaluated using in vivo models. (Supported by College of Human Environmental Sciences, Oklahoma State University)
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