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)
CAP37 is an inflammatory mediator that plays a key role in innate immunity. Recently, we showed that CAP37 is present in the vasculature of patients with Alzheimer's disease (AD) and that it is a potent regulator of microglial functions. The objective of this study was to extend these observations to determine the role of CAP37 as an inflammatory mediator in AD. Tissue was obtained from temporal, parietal, midbrain, and hippocampus from 10 AD patients, patients diagnosed with Pick's disease, Diffuse Lewy Body Dementia with AD‐aging, vascular dementia with no AD pathology, and sex‐ and age‐matched controls. Immunohistochemistry showed that in addition to the previously observed endothelial expression of CAP37 in AD patients, CAP37 was expressed in hippocampal neurons including dentate gyrus as well as pyramidal neurons of regions CA1–4 and the subiculum. Tissues obtained from patients with other neurodegenerative diseases and age‐ and sex‐matched controls lacked staining for CAP37. In vitro studies demonstrated that CAP37 is expressed in a dose‐ and time‐dependent fashion in HCN‐1A neurons in response to beta‐amyloid peptide 1–40 and tumor necrosis factor‐alpha but not interleukin 1‐beta. These findings lead us to hypothesize that CAP37 induced in neurons in AD patients activates microglia resulting in the exacerbation of the inflammatory cascade leading to neuronal death. Support: Alzheimer's Association.
Green tea has been widely consumed as a healthful beverage and its active constituent, EGCG, is a potent antioxidant and anti‐inflammatory agent. This study aimed to elucidate the effects of green tea or EGCG (0.39, 0.78, 1.56, 3.13, 6.25, 12.5, 25, or 50μg/mL) on nitric oxide production in murine macrophage cells following lipopolysaccharide (LPS) challenge. Different concentrations of green tea in media (0.15, 0.3, 0.63, 1.25, 2.5, 5, 10, or 20%) were prepared from a stock (2.12 g of green tea leaves brewed in 240mL of H2O). RAW 264.7 murine macrophages were cultured in DMEM supplemented with 10% fetal bovine serum and 1% penicillin. Following a 24‐hour treatment with green tea or EGCG, cells were challenged with LPS (500ng/mL) for the next 24 hours and cell viability (resazurin assay) and nitrite concentrations (Griess reaction) were measured. In comparison to the control (LPS), 10% and 20% green tea caused a significant reduction in nitrite levels (49.7±5.1, 27.3±4.3, & 13.1±2.3 μg/mL, respectively; P ≤ 0.05). In case of EGCG, significant inhibitions were noted at 25 & 50μg/mL, versus control (22.4±2.6, 3.4±0.64, & 47.7±4.93 μg/mL, respectively; P ≤ 0.05). Both green tea and EGCG at their highest concentrations (20% & 50μg/mL, respectively) affected cell viability versus controls, whereas, no differences were noted among the other groups. Thus, green tea and EGCG inhibit nitric oxide production at higher doses, which may explain their anti‐inflammatory effects, and warrants further research as a therapeutic strategy in clinical practice. This study was funded by CHES, OSU.
Regular consumption of fruits and vegetables may protect against many chronic diseases due to its anti‐inflammatory and anti‐oxidative flavonoids. Proanthocyanidins are a subclass of flavonoids with powerful anti‐oxidative and anti‐inflammatory effects and are found in Vaccinium berries such as cranberries. In this study, we have investigated the in vitro anti‐inflammatory effects of cranberry juice. RAW 264.7 murine macrophage cells were treated with different concentrations of cranberry juice (0, 2.5, 5, 10, and 20%, v/v) for 24 h and then stimulated with 500 ng/mL of E. coli lipopolysaccharide (LPS) for another 24 h to induce inflammation. Cell viability, nitric oxide (NO), cytokines, and protein levels of cyclooxygenase‐2 (COX‐2) and inducible nitric oxide synthase (iNOS) were assessed. Cranberry juice at concentration of 20% significantly reduced iNOS expression, NO, and prostaglandin E2 secretion (P<0.05). Western blot data showed that cranberry juice did not affect protein levels of COX‐2. Cranberry juice has no effect on interleukin‐6 (IL6) and tumor necrosis factor‐α (TNF‐α) concentrations. The results from this study indicate that cranberry juice effectively inhibits pro‐inflammatory markers such as NO and PGE2 but has little effect on TNF‐α and IL‐6, and warrants further investigations as a component of medical nutrition therapy for chronic diseases. (Supported by College of Human Environmental Sciences, Oklahoma State University)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.