This study aimed to investigate the antioxidant and anticancer effects of ethanolic and aqueous extracts of the roots of Ficus beecheyana (EERFB and AERFB) and their phenolic components. In this study, total phenolic content and antioxidant activity of EERFB were higher than those of AERFB. Major phenolic compounds in the extracts were gallic acid, p-hydroxybenzoic acid, caffeic acid, chlorogenic acid, p-coumaric acid, and rutin; which were identified by high-performance liquid chromatography. Flow cytometric analysis of HL-60 cells exposed to EERFB showed that the percentage of apoptotic cells increased in a dose-dependent manner. EERFB treatment resulted in the loss of mitochondrial membrane potential and induced the apoptosis of HL-60 cells through a Fas- and mitochondrial-mediated pathway. Finally, pretreatment with general caspase-9/-3 inhibitors prevented EERFB from inhibiting cell viability in HL-60 cells. Our finding suggests that EERFB is an agent that may have antioxidant activity and inhibit the growth of cancer cells.
The antiobesity effects of quercetin-rich supplement (QRS), which contain quercetin, lycopene, taurine, and litchi flower extract, on a high-fat diet (HFD)-induced obese rats were investigated. The rats that consume HFD with QRS (185 mg/kg rat) have significantly modulated the final body weights [490 ± 11 (HFD) → 441 ± 11 (HFD+QRS) g], total body fat [112.9 ± 4.5 (HFD) → 86.6 ± 5.7 (HFD+QRS) g], liver weights [14.8 ± 0.4 (HFD) → 12.6 ± 0.4 (HFD+QRS) g/rat], and the serum TG [102.5 ± 7.3 (HFD) → 90.7 ± 6.5 (HFD+QRS) mg/dL] to a level that resembled the regular diet-consumed rats (p < 0.05). The excretion of lipid in the faeces augmented in QRS groups as compared with the nonsupplemented HFD group [faecal total lipid: 62.43 ± 2.80 (HFD) → 73.15 ± 0.88 (HFD+QRS) mg/g dried faeces, p < 0.05]. In the histological analysis, quercetin-rich formulation supplemented groups presented a much less lipid accumulation and smaller size of adipocytes. Moreover, a decreased serum thiobarbituric acid reactive substances [1.55 ± 0.17 (HFD) → 0.78 ± 0.04 (HFD+QRS) nmol MDA eq/mL serum] increased levels of serum Trolox equivalent antioxidant capacity [3.89 ± 0.08 (HFD) → 6.46 ± 0.20 (HFD+QRS) μmol/mL serum], and more active hepatic antioxidant enzymes were observed in the supplemented groups (p < 0.05). The result of this work is a good demonstration of how a combination of bioactive compounds could work synergistically and become very effective in disease prevention.
Black garlic (also called aged garlic) is a type of fermented garlic product from fresh garlic that is often used as a food ingredient and a functional food in Asian countries. The aim of this study was to investigate whether black garlic ameliorates obesity induced by a high-fat diet in rats. Male Wistar rats were fed a normal diet or a highfat diet (HFD) (30% lard, w/w) combined with 0, 0.2, 0.6, or 1.2% black garlic (BG) (w/w) for a period of six weeks. The results demonstrated that body weight, tissue weights of liver, peritoneal fat, and epididymal fat, serum triglycerides, and hepatic lipid profiles (total lipids, triglycerides, and cholesterol) in the HFD+BG groups were significantly decreased compared with those in the HFD group. BG also reduced hepatic oxidative stress (reduced GSSG and enhanced TEAC, GSH, GRd, and GPx) in HFD-induced obese rats. These results suggest that black garlic may be useful for the treatment of obesity.
We investigated whether post-exercise capsinoids (CSN) supplementation could enhance muscle glycogen resynthesis via GLUT4/Akt expressions in human skeletal muscle. Nine male college students (aged 21.4±0.2 years, BMI 21.9±1.3 kg/m2, VO2max 47.1±1.8 ml/kg/min) participated in this crossover designed study, and completed a 60-min cycling exercise at 70% VO2max. Immediately after exercise, participants consumed high-carbohydrate diet (2 g carb/kg bodyweight) with CSN (12 mg, single dosage) or placebo. Biopsied muscle samples (vastus lateralis) were obtained immediately (0h) and 3h after exercise. Blood and expired gas samples were collected before and after exercise. We found oral CSN supplementation immediately after exercise was unable to enhance glycogen resynthesis in exercised human skeletal muscle. Despite, CSN could alter the energy reliance on fat oxidation during post-exercise recovery, based on gaseous exchange measurement (NEFA and glycerol). We further identified no significant differences in postprandial glucose/insulin area under curve in both trials. Western blot data showed no significant response of p-Akt/Akt ratio with CSN during post-exercise recovery. Inconsistent with glycogen levels, muscle GLUT4 expression was significantly elevated at 3h in CSN trial. Our findings emphasize the necessity of further evidences to confirm the ergogenic properties of CSN in connection with glycogen recovery in exercised human skeletal muscle.
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