Wild bitter gourd (Momordica charantia L. var. abbreviate Seringe), a common vegetable in Asia, is used in traditional medicine to treat various diseases, including inflammation. Extant literature indicates that wild bitter gourds have components that activate PPARα and PPARγ. This research probed the influence of adding wild bitter gourd to diets on inflammation responses in mice with sepsis induced by intraperitoneal injection of LPS. Male BALB/c mice were divided normal, sepsis, positive control, and three experimental groups. The latter ate diets with low (1%), moderate (2%), and high (10%) ratios of wild bitter gourd lyophilized powder. Before mice were sacrificed, with the exception of the normal group, intraperitoneal injection of LPS induced sepsis in each group; positive control group was injected with LPS after PDTC. This experiment revealed starkly lower weights in groups with added wild bitter gourd than those of the remaining groups. Blood lipids (TG, cholesterol, and NEFA) were also lower in comparison to the sepsis group, and blood glucose concentrations recovered and approached normal levels. Blood biochemistry values related to inflammation reactions indicated GOT, GPT, C-RP, and NO concentrations of groups with added wild bitter gourd were all lower than those of the sepsis group. Secretion levels of the spleen pro-inflammatory cytokines IL-1, IL-6, and TNF-α tallied significantly lower in comparison to the sepsis group, whereas secretion levels of IL-10 anti-inflammatory cytokine increased. Expression level of proteins NF-κB, iNOS, and COX-2 were significantly inhibited. Results indicate wild bitter gourd in diets promoted lipid metabolism, reducing fat accumulation, and improving low blood glucose in sepsis. Addition of wild bitter gourd can reduce inflammation biochemical markers or indicators and pro-inflammatory cytokines in the body, hence improving the inflammation responses in mice with sepsis.

Background/Introduction: Wild bitter gourd (Momordica charantia L. var. abbreviate Seringe) common vegetable in Asia, is used in traditional medicine to treat various diseases, including inflammation. Extant literature indicates that wild bitter gourds have components that activate PPARα and PPARγ. This research probed influence of adding wild bitter gourd to diets on inflammation responses in mice with sepsis. Purpose: This study evaluated influence of eating wild bitter gourd on inflammation responses in mice with sepsis. Methods: We injected intraperitoneal LPS to induce sepsis. Male BALB/c mice were divided normal, sepsis, positive control, and three experimental groups. The latter ate diets with low (1%), moderate (2%), and high (10%) ratios of wild bitter gourd lyophilized powder. Before mice were sacrificed, with the exception of the normal group, intraperitoneal injection of LPS induced sepsis in each group; positive control group was injected with LPS after PDTC. Results: This experiment revealed weights in groups with added wild bitter gourd starkly lower than those of the remaining groups. Blood lipids (TG, cholesterol, and NEFA) were also lower in comparison to the sepsis group, and blood glucose concentrations recovered and approached normal levels. Blood biochemistry values related to inflammation reactions indicated GOT, GPT, C-RP, and NO concentrations of groups with wild bitter gourd added all lower than that of the sepsis group. Secretion levels of the spleen pro-inflammatory cytokines IL-1, IL-6, and TNF-α tallied significantly lower in comparison to the sepsis group, whereas secretion levels of IL-10 anti-inflammatory cytokine increased. Expression level of proteins NF-κB, iNOS, and COX-2 were inhibited significantly. Conclusion: Wild bitter gourd in diets promoted lipid metabolism, improved low blood glucose in sepsis, and attenuated inflammatory stress. These findings suggested that this plant food might provide medical benefits for certain persons.

Diabetes is an important chronic disease and the 4th leading cause of death in Taiwan. Hyperglycemia-induced oxidative and inflammatory damage are the main causes of chronic complications in diabetic patients. The red guava (red-fleshed guava cultivar of Psidium guajava L.) is a tropical fruit belonging to the Myrtaceae family and an important commercial crop in Taiwan. In this study, the protective effects of a diet containing red guava on inflammation and oxidative stress in streptozotocin (STZ)-induced diabetic mice were examined. The experimental group was divided into seven subgroups: normal (N), diabetes mellitus (DM), diabetes + red guava 1% (L), 2% (M), and 5% (H), diabetes + 5% red guava + anti-diabetic rosiglitazone (HR), and diabetes + anti-diabetic rosiglitazone (R). The mice were fed for 8 weeks and sacrificed by decapitation. Compared with the DM group, the experimental groups with diets containing red guava as well as rosiglitazone all showed significant improvements in blood glucose control, insulin resistance, creatinine, blood urea nitrogen, triglycerides, non-esterified fatty acids, cholesterol, c-reactive protein, TNF-α, and IL-10. Furthermore, the expression of inflammatory proteins, such as iNOS and NF-κB, was suppressed via activated PPARγ, and the expression levels of GPx3 and ACO increased. In summary, red guava can significantly suppress inflammatory and oxidative damage caused by diabetes and alleviate diabetic symptoms; thus, it exerts protective effects and has potential applications for the development of a dietary supplement.

Background/Introduction: At present, human diet is replete with sugar and fat. Abnormal metabolism and hyperglycemia or hyperlipidemia in the body induces the development of an overactive and continuous inflammatory response, resulting in obesity and metabolic syndromes, including hypertension, hyperlipidemia, and insulin resistance. Torenia concolor Lindley var. formosana Yamazaki (TC), a perennial creeping herbaceous plant, is a traditional Chinese medicinal herb widely used for the treatment of heat stroke, aching muscles and bones, cold, dysentery, and ambustion.Purpose: This study evaluated the influence of TC on inflammation responses and lipid metabolism. Methods: In this study, ground TC powder was extracted with 95% ethanol. The ethanol was removed by vacuum concentration, and the resulting extract was further extracted with a number of solvents of different polarity to produce four final extracts: an ethanol extract (TCEE), an ethyl acetate extract (TCEAE), an n-butanol extract (TCBUE), and a water extract (TCWE). The anti-inflammatory efficacy of the extracts and their capability for lipid metabolism regulation was then explored.Results: TCEE, TCEAE, and TCBUE exhibited good anti-inflammatory efficacy; TCEAE also simultaneously regulated lipid metabolism. In RAW264.7 cells, these three extracts suppressed the expression of iNOS and IL-6 via the signaling pathway activation of the transcription factor peroxisome proliferator activated receptor γ (PPARγ) and thereby showed anti-inflammatory efficacy. In 3T3-L1 cells, these three extracts promoted lipid metabolism and reduced lipid accumulation through the activation of PPARα and the increased expression of adiponectin, thus demonstrating regulation of lipid metabolism.Conclusion: These results indicate that TC possesses anti-inflammatory efficacy and can regulate lipid metabolism through the activation of transcription factor PPARs. We speculate that these nutraceutical effects are attributable to betulin, an active ingredient in this herbal medicine.

Three new benzenoids, 3-isopropenyl-2-methoxy-6-methyl-4,5-methylenedioxy- phenol (1), 2-hydroxy-4,4'-dimethoxy-3,3'-dimethyl-5,6,5',6'-bimethylenedioxybiphenyl (2), 4,4'-dihydroxy-3,3'-dimethoxy-2,2'-dimethyl-5,6,5',6'-bimethylenedioxybiphenyl (3), together with two known benzenoids, 2,3,6-trimethoxy-5-methylphenol (4) and 2,3-methylenedioxy- 4-methoxy-5-methylphenol (5), were isolated from Antrodia camphorata. Our results support that compounds 1–5 potently inhibited LPS (lipopolysaccharide)-induced nitric oxide (NO) production in a dose-dependent manner. The IC₅₀ values of compounds 1, 3 and 5 were 1.8 ± 0.2, 18.8 ± 0.6 and 0.8 ± 0.3 μg/mL, respectively.