Extractions, Contents, Antioxidant Activities and Compositions of Free and Bound Phenols from Kidney Bean Seeds Represented by 'Yikeshu' Cultivar in Cold Region.

To thoroughly understand the profile of phenolic phytochemicals in kidney bean seeds cultivated in a cold region, the extractions, contents, antioxidant activities, compositions of free and bound phenols in the seed coat and cotyledon, and also relevant color attributes, were investigated. The results indicated that ultrasound-assisted extraction was an efficient method for free phenols. The bound phenols in seed coat and cotyledon were released more efficiently by alkali-acid and acid-alkali sequential hydrolysis, respectively. Under the optimized extractions, total phenols (TPC), flavonoids (TFC), and anthocyanins (TAC) ranged in 7.81-32.89 mg GAE/g dw, 3.23-15.65 mg RE/g dw, and 0-0.21 mg CE/g dw in the whole seeds of the five common kidney beans. There was a big difference in phenolic distribution between red and white seeds. From whole seed, the phenols in the four red cultivars mainly existed in free state (78.84%) and seed coat (71.56%), while the phenols in the white 'Sark' divided equally between free (51.18%) and bound (48.82%) states and consisted chiefly in cotyledon (81.58%). The correlation analyses showed that the antioxidant activities were significantly and positively correlated with TPC and TFC. The phenolic attributes were closely associated with the color of the seed coat. Red seeds had higher total contents of phenols than white seeds. TAC had a positively significant correlation with redness. Brightness and yellowness showed a negatively significant correlation with TPC, TFC, and antioxidant capacities, which were necessarily linked with redness degree and spot in red seeds. The spotted red 'Yikeshu' with the most outstanding performance on phenolic attributes was selected to analyze phenolic compounds with UHPLC-QE-MS. Among the 85 identified phenolics, 2 phenolic acids and 10 flavonoids were dominant. The characteristic phenolics in free and bound states were screened in both seed coat and cotyledon, respectively. The available information on the phenolic profile may expand the utilization of kidney beans as a nutritional ingredient in the food industry.

Anti-diabetic effect of red quinoa polysaccharide on type 2 diabetic mellitus mice induced by streptozotocin and high-fat diet.

The purpose of this study was to explore the mechanism of red quinoa polysaccharide (RQP) in alleviating type 2 diabetes (T2D) through in vivo and in vitro experiments. Results of HPLC and FITR showed that RQP was a complex polysaccharide and contained more glucose, galactose and acarbose. In vitro experiments, RQP showed strong antioxidant capacity and inhibition on α-amylase and α-glucosidase. In vivo experiments, RQP was proved to induce a significant improvement of diabetes after 4 weeks of ingestion, including the abilities of lowering blood glucose, regulating lipid metabolism, anti-oxidation and promoting secretion of SCFAs. Furthermore, 16S rRNA study demonstrated that RQP transformed the intestinal microbiota composition in diabetic mice, decreased the abundance of norank_f_Muribaculaceae and Lachnospiraceae_NK4A136_group, and increased the relative abundance of Akkermansia, unclassified_f_Lachnospiraceae, norank_f_Eubacterium_coprostanoligenes_group, unclassified_f_Atopobiaceae and norank_f_Lachnospiraceae. The biosynthetic pathways, metabolic pathways and intestinal microbiome phenotypes in mice also changed accordingly. In conclusion, this study suggests that RQP can inhibit the development of diabetes by correcting the imbalance of intestinal flora.

Anti-diabetic effects of natural and modified 'Ganzhou' navel orange peel pectin on type 2 diabetic mice via gut microbiota.

Pectin, a kind of dietary fiber, has attracted much attention owing to its beneficial effect on human health in recent years. In this study, the effects of both 'Ganzhou' navel orange peel pectin (GOP) and modified GOP (MGOP) on type 2 diabetes (T2DM) were investigated. The results indicated that GOP and MGOP intervention had positive effects on T2DM in C57BL/6 mice. After modification, pectin can be changed into low methoxy pectin (LMP) and the content of GalA can increase, which endow MGOP with significant effects on improving lipid metabolism (TC, TG, and LDL-C decreased by 30.46%, 50%, and 37.56%, respectively, and HDL-C increased by 56%) and OGTT, further reducing insulin resistance (insulin decreased by 74.35%). In addition, MGOP was superior to GOP in improving oxidative stress (GSH and GSH-Px increased by 52.05% and 29.08% respectively, and MDA decreased by 84.02%), inhibiting inflammation and promoting SCFA synthesis. 16S rRNA analysis showed that MGOP changed the composition of intestinal microbiota in diabetic mice, decreased the abundance of Alistipes, Helicobacter and Oscillibacter, and increased the relative abundance of Dubosiella, Akkermansiaceae, and Atopobiaceae. The phenotypes of the gut microbiome also changed accordingly, which showed that MGOP significantly inhibited the growth of Gram-negative bacteria and potential pathogenic bacteria and reversed the related complications. Taken together, our findings revealed that MGOP intake regulated lipid metabolism and oxidative stress and improved the gut health of mice, with promising effects against T2DM and related complications.

Anti-diabetic effect of modified 'Guanximiyou' pummelo peel pectin on type 2 diabetic mice via gut microbiota.

This study aimed to investigate the mechanisms of nature and modified 'Guanximiyou' pummelo peel pectin (GGP and MGGP) in alleviating T2DM through in vitro and in vivo. After modification, pectin was transformed from high methoxy pectin (HMP) to low methoxy pectin (LMP), and the content of galacturonic acid was increased. These made MGGP have stronger antioxidant capacity and better inhibition effect on corn starch digestion in vitro. In vivo experiments have shown that both GGP and MGGP inhibited the development of diabetes after 4 weeks of ingestion. However, MGGP can more effectively reduce blood glucose and regulate lipid metabolism, and has significant antioxidant capacity and the ability to promote SCFAs secretion. In addition, 16S rRNA analysis showed that MGGP changed the composition of intestinal microbiota in diabetic mice, decreased the abundance of Proteobacteria, and increased the relative abundance of Akkermansia, Lactobacillus, Oscillospirales and Ruminococcaceae. The phenotypes of the gut microbiome also changed accordingly, indicating that MGGP can inhibit the growth of pathogenic bacteria, alleviate intestinal functional metabolic disorders and reverse the potential risk of related complications. Altogether, our findings demonstrate that MGGP, as a dietary polysaccharide, may inhibit the development of diabetes by reversing the imbalance of gut microbiota.

Effects of highland barley ß-glucan on blood glucose and gut microbiota in streptozotocin-induced, diabetic, C57BL/6 mice on a high-fat diet.

OBJECTIVES: This study aimed to investigate the hypoglycemic effect of highland barley ß-glucan (HBG) on mice with type 2 diabetes (T2D), and determine whether the hypoglycemic effects are related to modulations of the gut microbiota. METHODS: T2D was induced with a high-fat diet and streptozotocin in the mice. HBG was orally administered to mice with T2D for 4 wk, and biochemical indices were analyzed in the serum and liver. Fecal samples were collected and analyzed with high-throughput 16S ribosomal RNA sequencing. RESULTS: Intake of HBG for 4 wk suppressed the body weight, as well as liver and heart indices, and regulated the levels of fasting blood glucose, serum insulin, blood lipid, oxidative damage, and inflammatory reaction in mice with T2D. Furthermore, HBG reversed the gut microbiota dysbiosis in mice with T2D by increasing the abundance of Lachnospiraceae_UCG-006, Streptococcaceae, and Eggerthellaceae, and by decreasing the abundance of Parasutterella. CONCLUSIONS: Our findings indicate that the antidiabetic abilities of HBG might be related to the improvement of gut microbiota imbalance.

Quality Characteristics and Anthocyanin Profiles of Different Vitis amurensis Grape Cultivars and Hybrids from Chinese Germplasm.

To evaluate the important Vitis amurensis germplasm, the quality characteristics and anthocyanin profiles of the ripe berries of 20 V. amurensis grapes and 11 interspecific hybrids in two consecutive years were analysed. Compared with the V. vinifera grapes, V. amurensis grapes had small berries with low total soluble solids and high titratable acids, and were richer in phenolic compounds except for flanan-3-ols in their skins but had lower phenolic contents in their seeds and showed lower antioxidant activities. An outstanding feature of the V. amurensis grapes was their abundant anthocyanin contents, which was 8.18-fold higher than the three wine grapes of V. vinifera. The anthocyanin composition of V. amurensis was characterized by an extremely high proportion of diglucoside anthocyanins (91.71%) and low acylated anthocyanins (0.04%). Interestingly, a new type of speculated 3,5,7-O-triglucoside anthocyanins was first identified and only detected in V. amurensis grapes and hybrids. Based on the total phenolic and anthocyanin characteristics, V. amurensis grapes were set apart from V. vinifera cultivars and the interspecific hybrids, for the same qualities, fell between them, as assessed by principal component analysis.

Molecular mechanisms of quinalizarin induces apoptosis and G0/G1 cell cycle of human esophageal cancer HCE-4 cells depends on MAPK, STAT3, and NF-κB signaling pathways.

Quinalizarin (Quina) is one of the main components of many herbal medicines and has good anti-tumor activity. However, the exact mode of cytotoxic action and signaling pathways on Quina in human esophageal cancer has not yet been confirmed. In this study, we explored the anticancer effect of Quina against human esophageal cancer HCE-4 cells and the underlying mechanisms. The results of the Cell Counting Kit-8 (CCK-8) assay showed that Quina inhibited the viability of human esophageal cancer HCE-4 cells in a dose-dependent and time-dependent manner. It also inhibited HCE-4 cells proliferation and induced apoptosis by increasing the levels of Bad, caspase-3, and PARP, decreasing the level of Bcl-2. The results of the cell cycle analysis suggested that Quina arrested HCE-4 cells in the G0/G1 cycle by downregulating cyclin-dependent (CDK) 2/4, cyclin D1/E and upregulating the levels of p21 and p27. We also found that Quina activated mitogen-activated protein kinase (MAPK) and inhibited the signal transducer and activator of transcription-3 (STAT3) and nuclear factor kappa B (NF-κB) signaling pathways. Furthermore, Quina significantly increased intracellular reactive oxygen species (ROS) level. The pretreatment of N-acetyl-L-cysteine (NAC) blocked the apoptosis induced by Quina and inhibited the activities of MAPK, STAT3, and NF-κB signaling pathways. These results indicate that Quina induces the apoptosis in HCE-4 cells, which is via accumulating ROS generation and regulating MAPK, STAT3, and NF-κB. In conclusion, this study demonstrated that Quina have good therapeutic effects on human esophageal cancer cells.

Quinalizarin induces ROS­mediated apoptosis via the MAPK, STAT3 and NF­κB signaling pathways in human breast cancer cells.

Quinalizarin has been demonstrated to exhibit potent antitumor activities in lung cancer and gastric cancer cells, but currently, little is known regarding its anticancer mechanisms in human breast cancer cells. The aim of the present study was to investigate the apoptotic effects of quinalizarin in MCF­7 cells and to analyze its molecular mechanisms. The MTT assay was used to evaluate the viability of human breast cancer cells that had been treated with quinalizarin and 5­fluorouracil. Flow cytometric analyses and western blotting were used to investigate the effects of quinalizarin on apoptosis and cycle arrest in MCF­7 cells with focus on reactive oxygen species (ROS) production. The results demonstrated that quinalizarin exhibited significant cytotoxic effects on human breast cancer cells in a dose­dependent manner. Accompanying ROS, quinalizarin induced MCF­7 cell mitochondrial­associated apoptosis by regulating mitochondrial­associated apoptosis, and caused cell cycle arrest at the G2/M phase in a time­dependent manner. Furthermore, quinalizarin can activate p38 kinase and JNK, and inhibit the extracellular signal­regulated kinase, signal transducer and activator of transcription 3 (STAT3) and NF­κB signaling pathways. These effects were blocked by mitogen­activated protein kinase (MAPK) inhibitor and N­acetyl­L­cysteine. The results from the present study suggested that quinalizarin induced G2/M phase cell cycle arrest and apoptosis in MCF­7 cells through ROS­mediated MAPK, STAT3 and NF­κB signaling pathways. Thus, quinalizarin may be useful for human breast cancer treatment, as well as the treatment of other cancer types.

Glycitein induces reactive oxygen species-dependent apoptosis and G0/G1 cell cycle arrest through the MAPK/STAT3/NF-κB pathway in human gastric cancer cells.

Glycitein is an isoflavone that reportedly inhibits the proliferation of human breast cancer and prostate cancer cells. However, its anti-cancer molecular mechanisms in human gastric cancer remain to be defined. This study evaluated the antitumor effects of glycitein on human gastric cancer cells and investigated the underlying mechanisms. We used MTT assay, flow cytometry and western blotting to investigate its molecular mechanisms with focus on reactive oxygen species (ROS) production. Our results showed that glycitein had significant cytotoxic effects on human gastric cancer cells. Glycitein markedly decreased mitochondrial transmembrane potential (ΔΨm) and increased AGS cells mitochondrial-related apoptosis, and caused G0/G1 cell cycle arrest by regulating cycle-related protein. Mechanistically, accompanying ROS, glycitein can activate mitogen-activated protein kinase (MAPK) and inhibited the signal transducer and activator of transcription 3 (STAT3) and nuclear factor-kappaB (NF-κB) signaling pathways. Furthermore, the MAPK signaling pathway regulated the expression levels of STAT3 and NF-κB upon treatment with MAPK inhibitor and N-acetyl-L-cysteine (NAC). These findings suggested that glycitein induced AGS cell apoptosis and G0/G1 phase cell cycle arrest via ROS-related MAPK/STAT3/NF-κB signaling pathways. Thus, glycitein has the potential to a novel targeted therapeutic agent for human gastric cancer.

Cryptotanshinone induces reactive oxygen species­mediated apoptosis in human rheumatoid arthritis fibroblast­like synoviocytes.

The present study investigated the mechanisms of apoptosis induced by cryptotanshinone (CT) in human rheumatoid arthritis fibroblast­like synoviocytes (RA­FLSs). Cell Counting kit­8 assay was performed to determine the cytotoxic effects of CT in human RA­FLSs, including primary RA­FLS, HFLS­RA and MH7A cells, and in HFLS cells derived from normal synovial tissue. Annexin V­FITC/PI staining was used to detect the apoptotic effects of CT in HFLS­RA and MH7A cells. Flow cytometry was performed to detect the apoptotic and reactive oxygen species (ROS) levels induced by CT in HFLS­RA cells. Western blotting was used to assess the expression levels of proteins associated with apoptosis and with the mitogen­activated protein kinase (MAPK), protein kinase B (Akt), and signal transducer and activator of transcription­3 (STAT3) signaling pathways. The results demonstrated that CT treatment significantly suppressed HFLS­RA and MH7A cell growth, whereas no clear inhibitory effect was observed in normal HFLS cells. CT exposure downregulated the expression levels of B­cell lymphoma 2 (Bcl­2), p­Akt, p­extracellular signal­related kinase and p­STAT3, while it upregulated the expression levels of Bcl­2­associated death promoter (Bad), caspase­3, poly (ADP­ribose) polymerase (PARP), p­p38 and p­c­Jun N­terminal kinase. Following ROS scavenging, the CT­induced apoptosis and altered expression levels of Bcl­2, Bad, cleaved caspase­3 and cleaved PARP were restored. Furthermore, the Akt, MAPK and STAT3 signaling pathways were regulated by intracellular ROS. These results suggest that ROS­mediated Akt, MAPK and STAT3 signaling pathways serve important roles in the CT­induced apoptosis of RA­FLSs.

Novel 1,4­naphthoquinone derivatives induce reactive oxygen species­mediated apoptosis in liver cancer cells.

Derivatives of 1,4­naphthoquinone have excellent anti­cancer effects, but their use has been greatly limited due to their serious side effects. To develop compounds with decreased side effects and improved anti­cancer activity, two novel types of 1,4­naphthoquinone derivatives, 2,3­dihydro­2,3­epoxy­2­propylsulfonyl­5,8­dimethoxy­1,4­naphthoquinone (EPDMNQ) and 2,3­dihydro­2,3­epoxy­2­nonylsulfonyl­5,8­dimethoxy­1,4­naphthoquinone (ENDMNQ) were synthesized and their anti­tumor activities were investigated. The effects of EPDMNQ and ENDMNQ on cell viability, apoptosis and accumulation of reactive oxygen species (ROS) in liver cancer cells were determined by MTT cell viability assay and flow cytometry. The expression levels of mitochondrial, mitogen activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3) signaling pathway­associated proteins in Hep3B liver cancer cells were analyzed by western blot analysis. The results demonstrated that EPDMNQ and ENDMNQ inhibited the proliferation of liver cancer Hep3B, HepG2, and Huh7 cell lines but not that of normal liver L­02, normal lung IMR­90 and stomach GES­1 cell lines. The number of apoptotic cells and ROS levels were significantly increased following treatment with EPDMNQ and ENDMNQ, and these effects were blocked by the ROS inhibitor N­acetyl­L­cysteine (NAC) in Hep3B cells. EPDMNQ and ENDMNQ induced apoptosis by upregulating the protein expression of p38 MAPK and c­Jun N­terminal kinase and downregulating extracellular signal­regulated kinase and STAT3; these effects were inhibited by NAC. The results of the present study demonstrated that EPDMNQ and ENDMNQ induced apoptosis through ROS­modulated MAPK and STAT3 signaling pathways in Hep3B cells. Therefore, these novel 1,4­naphthoquinone derivatives may be useful as anticancer agents for the treatment of liver cancer.

Protective effects of dietary kaempferol glycoside components from unripe soybean (Edamame, Glycine max L. Merrill. 'Jindai') leaves and their serous metabolite on carbon tetrachloride-induced liver injury mice.

The study investigated the protective effects of kaempferol galactoside (KG) components in mice, which were separated from Jindai soybean leaves (JDL) and mainly composed by two kaempferol galactosides. Further, KG-related metabolites in serum of mice were identified by Tof-MS. Results showed that both JDL and KG prevented the CCl4-induced increases in serum aspartate aminotransferase and serum alanine aminotransferase. Additionally, mice treated with KG had significantly decreased TBARS and TNF-alpha levels, compared to CCl4-treated mice. Serous analysis showed that kaempferol, glucuronidated kaempferol and methylated kaempferol with a glucuronic acid moiety were identified in the serum of mice fed unripe soybean leaves or kaempferol galactosides isolated from the leaves. The results indicated that kaempferol 3-O-galactoside connected to other glycosides via galactose might be hydrolyzed in the gastro-intestinal tract and/or epithelium cells to release kaempferol, followed by glucuronidation and/or methylation in the liver to contribute to a reduction in liver injury. The use of raw leaves containing kaempferol galactosides as food materials may contribute to a reduction in oxidation-related diseases.

Quinalizarin exerts an anti-tumour effect on lung cancer A549 cells by modulating the Akt, MAPK, STAT3 and p53 signalling pathways.

Quinalizarin may be a potential chemical agent for cancer therapy, as it exerts anti­tumour effects against a variety of different types of cancer. However, the underlying regulatory mechanism and signalling pathways of quinalizarin in lung cancer cells remains unknown. The present study sought to investigate the effects of quinalizarin on proliferation, apoptosis and reactive oxygen species (ROS) generation in lung cancer. MTT assays were used to evaluate the effects of quinalizarin on the viability of lung cancer A549, NCI­H460 and NCI­H23 cells. Flow cytometry was employed to evaluate the effects of quinalizarin on the cell cycle, apoptosis and ROS generation in A549 cells. Western blotting was performed to detect cell cycle and apoptosis­associated protein expression levels in A549 cells. Quinalizarin inhibited A549, NCI­H460 and NCI­H23 cell proliferation and induced A549 cell cycle arrest at the G0/G1 phase. Quinalizarin induced apoptosis by upregulating the expression of B­cell lymphoma 2 (Bcl­2)­associated agonist of cell death, cleaved­caspase­3 and cleaved­poly (adenosine diphosphate­ribose) polymerase, and downregulating the expression of Bcl­2. Furthermore, quinalizarin activated mitogen­activated protein kinase (MAPK) and p53, and inhibited the protein kinase B and signal transducer and activator of transcription­3 (STAT3) signalling pathways. In addition, quinalizarin increased ROS generation. The ROS scavenger N­acetyl­L­cysteine restored quinalizarin­induced cell apoptosis, and inactivated the MAPK and STAT3 signalling pathways. The results of the present study demonstrated that quinalizarin induces G0/G1 phase cell cycle arrest and apoptosis via ROS mediated­MAPK and STAT3 signalling pathways.

Cryptotanshinone induces ROS-mediated apoptosis in human gastric cancer cells.

Cryptotanshinone (CT), isolated from the plant Salvia miltiorrhiza Bunge, has been reported to have potential anticancer effects on human prostate and breast cancer cells. However, the mechanisms of action of CT on gastric cancer (GC) cells are not well understood. Here we investigated the antitumor effects of CT on GC cells and its possible molecular mechanism. We found CT suppressed viability of twelve GC cell lines in a dose-dependent manner. CT induced cell cycle arrest at the G2/M phase and mitochondrial apoptosis accompanying the accumulation of reactive oxygen species (ROS). Pretreatment with ROS inhibitor N-acetyl-L-cysteine (NAC) blocked CT-induced apoptosis. CT increased p-JNK and p-p38, and decreased p-ERK and p-STAT3 protein expression, these effects were prevented by NAC. Furthermore, a xenograft assay showed that CT significantly inhibited MKN-45 cell-induced tumor growth in vivo by increasing expression of pro-apoptotic proteins (p-JNK, p-38 and cleaved-caspase-3) and reducing expression of anti-apoptotic proteins (p-ERK and p-STAT3) without adverse effects on nude mice weight. In conclusion, CT induced apoptosis and cell cycle arrest in GC cells via ROS-mediated MAPK and AKT signaling pathways, and this CT may be a useful compound for the developing anticancer agents for GC.

Antioxidant and hepatoprotective activity of kaempferol 3-O-ß-d- (2,6-di-O-α-l-rhamnopyranosyl)galactopyronoside against carbon tetrachloride-induced liver injury in mice.

This study aims to investigate the antioxidant and hepatoprotective effects of kaempferol 3-O-ß-d- (2,6-di-O-α-l-rhamnopyranosyl)galactopyronoside (KG) isolated from unripe soybean leaves. Carbon tetrachloride (CCl4)-induced hepatotoxic ddY mice were used in the study. The mice were divided into three groups, namely the control group, the CCl4 group (CCl4, CCl4 injected), and the KG group (KG, CCl4 injected with KG administration). Hepatic injury markers of serum and liver were analyzed. The results show that serum ALT, AST activities, hepatic glutathione, superoxide dismutase, catalase, and glutathione peroxidase activities were normalized in mice pretreated with KG. Furthermore, the liver thiobarbituric acid reactive substances levels were found to be improved by pretreatment with KG, indicating that KG is available to alleviate liver injury, this may be due to its antioxidant properties. This study suggests that unripe soy leaves could be used as functional food materials.

Anti-diabetic effects of luteolin and luteolin-7-O-glucoside on KK-A(y) mice.

Anti-diabetic potential of luteolin (LU) and luteolin-7-O-glucoside (LUG) were investigated in the amount of equimolar on KK-A(y) mice. The results showed that both of LU and LUG significantly improved blood glucose, HbA1c, insulin, and HOMR-IR levels. Anti-inflammatory and anti-oxidative effects of the LU and LUG were also proved. Furthermore, TGs in serum and liver were significantly decreased in the LU and LUG groups, as well as the mRNA expression of fat acid expression-related genes (SREBP-1c), compared to the basal diet group (CON). When compared the effects between the LU and LUG groups, TGs of the LU group were lower than those of the LUG group, accompanied with significantly decreased FAS activity and SREBP-1c expression in liver. These results suggested that both LU and LUG had positive effects of anti-diabetes on KK-A(y) mice, but LU more potently ameliorated diabetes than LUG, which might be attributed to the inhibitory of lipid synthesis.

The anti-obesity and anti-diabetic effects of kaempferol glycosides from unripe soybean leaves in high-fat-diet mice.

The present study investigated the anti-obesity and anti-diabetic effects of kaempferol glycoside (KG) fractions which were composed of four kaempferol glycosides and purified from unripe Jindai-soybean (Edamame) leaves in C57BL/6J mice. High fat-fed mice treated with 0.15% dietary KG for 92 days had reduced body weight, adipose tissue and TG levels compared to the high fat-fed control group. KG-treatment also decreased fasting blood glucose, serum HbA1c (hemoglobin A(1c)) levels and improved insulin resistance. Gene expression analysis of the liver showed that KG decreased peroxisome proliferator-activated receptor (PPAR-γ) and sterol regulatory element-binding protein (SREBP-1c) expression. These results suggest that KG reduced the accumulation of adipose tissue, improving hyperlipidemia as well as diabetes in obese mice by increasing lipid metabolism through the downregulation of PPAR-γ and SREBP-1c. Thus, KG may have an anti-obesity and anti-diabetic potential.

Anti-obese and anti-diabetic effects of a mixture of daidzin and glycitin on C57BL/6J mice fed with a high-fat diet.

We investigated the effects of a mixture of daidzin and glycitin, which are the glycoside-form isoflavones of daidzein and glycitein, respectively, on body weight, lipid levels, diabetic markers, and metabolism in a high-fat diet (HF) fed C57BL/6J mice for 92 days. The mice were divided into basic diet group (CON), HF group, and HF companied with the isoflavone mixture group (HFISO). Results showed that mice in HFISO had a significantly lower body weight and adipose tissue compared to HF group. Blood glucose, serum HbA1c, and serum insulin also showed lower levels in HFISO group. In addition, higher hepatic GSH level and lower serum 8-hydroxy-2'-deoxyguanosine (8-OHdG) level were found in HFISO group mice. This suggests that the regulation of oxidative stress by daidzin and glycitin was closely related to the suppression of adipose tissue and the progression of diabetes.

Effects of adding urea on fermentation quality of pruned persimmon branch silage and its digestibility, preference, nitrogen balance and rumen fermentation in beef cattle.

Four cattle were used in a 4 × 4 Latin square design experiment to study digestibility, ruminal fermentation, nitrogen retention and preference of ensiling pruned persimmon branch (PPB) chips treated with urea. After 60 days of ensiling, urea-treated PPB showed higher (P < 0.05) pH, acetic acid and ammonia-N levels than no-urea PPB. Both urea-treated PPB and rice straw diets showed higher (P < 0.05) apparent digestibility and digestible nutrient content in cattle than no-urea PPB diet. Neither mold nor yeast was detected in any urea-treated PPB. Urinary and fecal excretion as well as nitrogen retention in cattle fed urea-treated PPB were higher (P < 0.05) than in those fed no-urea PPB and rice straw. With the exception that ruminal ammonia-N levels in cattle fed urea-treated PPB were higher (P < 0.05) than in those given no-urea PPB and rice straw, ruminal pH, volatile fatty acid concentrations, and the acetic : propionic acid ratio of rumen content were unaffected by diets. The rank order of preference was rice straw > low-urea > no-urea > high-urea. The results suggested that urea treatment of PPB inhibited growth of mold and yeast during silage storage, enhanced its digestibility and had nutritive value almost equivalent to that of rice straw.

Anti-diabetic effects of a kaempferol glycoside-rich fraction from unripe soybean (Edamame, Glycine max L. Merrill. 'Jindai') leaves on KK-A(y) mice.

The anti-diabetic effects of a kaempferol glycoside-rich fraction (KG) prepared from leaves of unripe Jindai soybean (Edamame) and kaempferol, an aglycone of kaempferol glycoside, were determined in genetically type 2 diabetic KK-A(y) mice. The hemoglobin A(1c) level was decreased and tended to be decreased by respectively feeding KG and kaempferol (K). The area under the curve (AUC) in the oral glucose tolerance test (OGTT) tended to be decreased by feeding K and KG. The liver triglyceride level and fatty acid synthase activity were both decreased in the mice fed with KG and K when compared to those parameters in the control mice. These results suggest that KG and K would be useful to improve the diabetes condition. The major flavonoids in KG were identified as kaempferol 3-O-ß-D-glucopyranosyl(1→2)-O-[α-L-rhamnopyranosyl(1→6)]-ß-D-galactopyranoside, kaempferol 3-O-ß-D-glucopyranosyl(1→2)-O-[α-L-rhamnopyranosyl(1→6)]-ß-D-glucopyranoside, kaempferol 3-O-ß-D-(2-O-ß-D-glucopyranosyl) galactopyranoside and kaempferol 3-O-ß-D-(2,6-di-O-α-L-rhamnopyranosyl) galactopyronoside, suggesting that these compounds or some of them may be concerned with mitigation of diabetes.