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This study evaluated and compared the nutritional components and antioxidant activities of Abelmoschus esculentus (L.) Moench (AM) extracts processed using hot air and freeze-drying methods. The results showed that hot air and freeze-dried AM extracts were mainly composed of carbohydrates and crude protein. Both hot air and freeze-dried AM had a high content of saturated fatty acids (palmitic acid). Also, both these extracts had a high content of unsaturated fatty acids (oleic acid and linoleic acid). The ratio of essential amino acids (EAA)/amino acids (AA) was higher in the hot air dried AM extract compared to the freeze-dried AM extract. Both the drying methods resulted in high content of potassium (K), followed by calcium (Ca) and magnesium (Mg) in decreasing order. Freeze-dried AM extract showed higher total polyphenol content compared to hot air dried AM extract. Total flavonoid content was significantly higher in hot-air dried AM extract compared to freeze-dried AM extract. The IC50 value for 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity with hot-air dried and freeze-dried AM extract was found to be 0.78 and 0.69 mg/mL, respectively. The IC50 value for 2,2‘-azinobis-(3-ethylbenzothiazoline-6-sulfonate) (ABTS) and the reducing power of freeze-dried AM extract were lower than that of hot-air dried AM extract. Ferric reducing antioxidant power (FRAP) was significantly higher in the freeze-dried AM extract than in the hot air dried AM extract. According to our results, it appears that AM extracts possess higher nutritional and antioxidant activities.

Isoliquiritigenin (isoLQ), a chalcone found in licorice, has shown a variety of biological activity including anti-inflammatory and antioxidative effects, and the distribution of isoLQ in gastrointestinal tract was higher than any other tissues. Thus, we evaluated whether or not isoLQ attenuated the dextran sulfate sodium (DSS)-induced colitis by observing the physiological changes (body weight loss, diarrhea, bleeding stool, overall disease activity index (DAI) scores, colon length), histopathological analysis and myeloperoxidase (MPO) activities of esophagus and colon. Also, the MAPK pathways including phosphorylation of ERK1/2, p38, and AKT, and the activation of NK-κB were evaluated in colon tissue. Interestingly, the reduction of body weight and colon length, increase of diarrhea, bloody stool, DAI scores and MPO activity, and histologic disturbances in DSS-induced colitis were recovered by isoLQ treatment. Also, isoLQ treatment suppressed the phosphorylation of ERK1/2 and p38, and the activation of NK-κB compared to those in DSS-induced colitis mice. In addition, the distributions of isoLQ in colon were relatively higher in DSS-induced colitis models. All of these results suggested that isoLQ has potential activity to ameliorate the DSS-induced colitis through the inhibition of MAPK pathway.

Isoliquiritigenin, a chalcone found in licorice has shown a variety of biological activities including antioxidative, anti-inflammatory, estrogenic, chemopreventive and antitumor effects. Thus, pharmacokinetics of isoliquiritigenin and its metabolites [liquiritigenin, glucuronidated isoliquiritigenin (M1), and glucuronidated liquiritigenin (M2)] after intravenous and oral administration of isoliquiritigenin was evaluated in rats. The pharmacokinetics of isoliquiritigenin, liquiritigenin, M1, and M2 showed no dose dependence after both intravenous and oral administration of isoliquiritigenin. Although approximately 92.0 % of the oral isoliquiritigenin was absorbed, the extent of the absolute bioavailability value was only 11.8 % of the oral dose. The low absolute bioavailability value of isoliquiritigenin might be due to the considerable metabolism of isoliquiritigenin in the small intestine and liver. This was supported by the facts that the ratios of AUCM1/AUCisoLQ and AUCM2/AUCisoLQ were high (over 0.25), isoliquiritigenin disappeared, and M1 and M2 were formed mainly in S9 fractions of the liver and small intestine. The affinities of liquiritigenin, isoliquiritigenin, M1, and M2 were high in the liver, small intestine, large intestine, and/or kidney.

Previous studies have shown that α-mangostin (α-MG) suppresses intracellular fat accumulation and stimulation of lipolysis in in vitro systems. Together with the relatively high distribution of α-MG in liver and fat, these observations made it possible to propose a plausible hypothesis that an α-MG supplement may regulate hepatic steatosis and obesity. An α-MG supplement (50 mg/kg) reduced the body weight gain (13.8%) and epidymal and retroperitoneal fat mass accumulation (15.0 and 11.3%, respectively), as well as the biochemical serum profiles such as cholesterol [TC (26.9%), LDL-C (39.1%), and HDL-C (15.3%)], glucose (30.2%), triglyceride (29.7%), and fatty acid (30.3%) levels in high-fat fed mice compared with the high-fat diet-treated group, indicating that α-MG may regulate lipid metabolism. In addition, an α-MG supplement up-regulated hepatic AMPK, SirT1, and PPARγ levels compared with the high-fat diet states, suggesting that α-MG regulates hepatic steatosis and obesity through the SirT1-AMPK and PPARγ pathways in high-fat diet-induced obese mice.