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Secoisolariciresinol diglucoside (SDG) has a strong anti-inflammatory effect, which depends partly on the participation of gut microbiota. We studied the effect of SDG on colonic inflammation caused by a common poor diet, high-fat diet (HFD), and the regulation of gut microbiota as well as its metabolites. Considering the difference of sources, prices, and possible bioactivity, we compared the effects of a single compound and the extract of SDG on colon inflammation. The results displayed that both the single compound and the extract ameliorated morphologic damage of the colon and improved intestinal barrier integrity. In addition, SDG suppressed the mRNA expressions of inflammatory cytokines in the colon, and the inhibitory effect of a single compound was stronger than that of the extract. The results of 16S rRNA sequencing showed that SDG altered the diversity and composition of gut microbiota, particularly the abundance of inflammation-related bacteria, and the effect of the extract was greater than that of a single compound. The analysis of short-chain fatty acids (SCFAs) manifested the improved concentration with the intervention of SDG. These results confirmed that SDG, including a single compound and extract, exerted protective effects against colon inflammation, which might be partly explained by the gut microbiome. Our research could provide a positive nutritional intervention for chronic intestinal inflammation.

Inflammatory bowel disease (IBD) is accompanied by some psychiatric disorders, including anxiety and depression. Sesamol has been reported to alleviate colitis symptoms and depression-like behaviors caused by chronic unpredictable mild stress, but its protective effect and underlying neurobiological mechanism on IBD induced by dextran sulfate sodium (DSS) accompanying depression-like and anxiety-like behaviors remains still unclear. Here, we found that a six-week sesamol treatment (100 mg per kg bodyweight per day) for DSS-induced mice predominantly prevented inflammatory response, epithelial barrier dysfunction and depression-like and anxiety-like behaviors

Obesity has been reported to be associated with gut microbiome dysbiosis. seabuckthorn fruits have traditionally been used in Tibetan foods and medicines for thousands of years. Seabuckthorn polysaccharide (SP) is one of the main functional components in seabuckthorn fruits. However, the effects of SP on a high-fat diet (HFD)-induced obesity have not yet been elucidated. The purpose of this study is to explore the amelioration effect of SP on obesity induced by HFD and to reveal its mechanism of gut microbiota and its metabolites. Results showed that 12-week SP (0.1%, w/w) dietary supplementation could significantly reduce body weight gain, serum lipid level and liver triglycerides level in obese mice. Notably, the SP treatment elevated p-AMPKα and PPARα proteins expression stimulated the phosphorylation of ACC1 and inhibited the protein expression of FAS, PPARγ, and CD36 in the mice liver. Further, SP also reorganized the gut microbiome by up-regulating the proportion of

Astaxanthin (AST) has been shown to have neuroprotective effects; however, its bioavailability in vivo is low due to its hydrophobic properties. In this study, lactoferrin (LF) was prepared by heat-treatment at different temperatures, and on this basis, a layer-by-layer self-assembly method was used to construct double-layer emulsions with LF as the inner layer and polysaccharide (beet pectin, BP or carboxymethyl chitosan, CMCS) as the outer layer. Then AST was encapsulated in the emulsions and their physiochemical properties and function were investigated. The results indicated that high temperature heated LF (95 °C) showed a more stable structure than the lower temperature one, and the exposed internal nonpolar groups of LF could give the emulsion an enhanced stability. The rheology results showed that compared with CMCS, the double-layer emulsion formed by BP had a higher viscosity. In addition, the 95 °C LF-AST-BP emulsion showed the best stability among all the bilayer emulsions. The best emulsion was then used as a model drug to investigate its effects on lipopolysaccharide (LPS)-induced neuroinflammation and learning-memory loss in C57BL/6J mice. Through animal behavioral experiments, it was found that dietary supplementation with the AST emulsion could effectively improve the brain cognitive and learning memory impairment caused by inflammation. Transmission electron microscopy, mRNA and western blotting results also illustrated that the AST emulsion could alleviate neuroinflammation caused by LPS. This study provides a feasible scheme for exploring an AST loaded system and may be suitable for food and drug applications.

The inhibition properties of 10 tea polyphenols against α-glucosidase were studied through inhibition assay, inhibition kinetics, fluorescence quenching and molecular docking. It was found that the inhibitory activity of polyphenols with a 3 and/or 3' galloyl moiety (GM) was much higher than that without a GM. The GM could enter into the active site of α-glucosidase and bind with the catalytic amino acid residues through hydrogen bonding and π-conjugation, thus playing an important role in the competitive inhibition of catechins and theaflavins. The positive linear correlations among the constants characterizing the inhibitory activity and binding affinity of tea polyphenols to α-glucosidase indicate that enzyme inhibition by polyphenols is caused by the binding interactions between them, and that the combination of the characterization methods for polyphenol-glucosidase binding is reasonable. In addition, the in vivo hypoglycemic effects of galloylated polyphenols suggest that the GM may be considered as a pharmaceutical fragment for the alleviation of type II diabetes symptoms through α-glucosidase inhibition.

This study aims to evaluate the changes in phenolic acids, lignans and tocopherols of sesame seeds during 0-6 days of germination by monitoring the activities of phenolic metabolism-related enzymes and the expression of key genes in the tocopherol synthesis pathway. Sesamol, which is the most active lignan antioxidant, greatly increased, and most of the phenolic acid contents increased to varying degrees after germination. Correspondingly, the related enzymes, including phenylalanine ammonia-lyase (PAL), cinnamate-4-hydroxylase (C4H), and 4-coumarate:coenzyme A ligase (4CL), were activated. Germination also promoted the conversion of γ-tocopherol to α-tocopherol with the expression of related genes changed. Additionally, there was a high correlation between the tocopherol content and the relative expression levels of key genes. The germination process also increased the bio-accessibility of lignans and tocopherols. Therefore, germination can be utilized to improve the nutritional value of sesame-related products.

Secoisolariciresinol diglucoside (SDG) has positive effects on obesity and its complications. We investigated the effects and mechanism of SDG on high-fat and high-fructose diet (HFFD)-induced hepatic lipid metabolic disorders. Supplementation with 40 mg kg-1 d-1 SDG for 12 weeks significantly reduced the body weight and the ratio of liver and adipose tissue to body weight in HFFD-fed mice. Serum and hepatic TG, TC, HDL-C, and LDL-C levels became normalized, and hepatic lipid metabolic disorders lessened because of the downregulation of lipid synthesis genes and upregulation of lipid oxidation genes. SDG also alleviated endoplasmic reticulum (ER) stress and mitochondrial dysfunction by regulating the ER stress factors Bip, IRE1α, Xbp1, Atf6, Perk, and Chop and mitochondrial function-related genes Cox5b, Cox7a1, Cox8b, and Cycs. Results with HepG2 cells confirmed that SDG regulated lipid metabolic disorders by the ER stress-Ca2+-mitochondrial-associated pathway. Our study provides a strategy for the treatment of obesity and its related comorbidities.

The global rise in obesity and type 2 diabetes has precipitated the need for therapeutic intervention in the arsenal against adiposity. (-)-Epigallocatechin-3-gallate (EGCG), a major nutraceutical component of green tea, has been regarded as a nutraceutical that has powerful antioxidant and anti-obesity bioactivities. In the present study, we showed that EGCG alleviates intracellular lipid accumulation markedly, and the inhibitory effect was largely limited to the early stage of adipocyte differentiation. Consistently, EGCG notably evoked the phosphorylation of AMPK and ACC and blunted the key enzymes of de novo lipogenesis. Interestingly, EGCG elicited iWAT-preadipocyte-derived mature white adipocyte beiging via activating thermogenic gene Ucp1 expression and mitochondrial biogenesis. Furthermore, our results also revealed that EGCG attenuated insulin signaling pathway blockage induced by TNF-α through the abrogation of redox imbalance and mitochondrial dysfunction. These findings indicate that EGCG is capable of suppressing adipogenesis and evoking white adipocyte beiging and therefore it may potentially serve as a novel approach to combat obesity.

As a major nutraceutical component of green tea (-)-epigallocatechin-3-gallate (EGCG) has attracted interest from scientists due to its well-documented antioxidant and antiobesity bioactivities. In the current study, we aimed to investigate the protective effect of EGCG on metabolic misalignment and in balancing the redox status in mice liver and HepG2 cells under insulin resistance condition. Our results indicated that EGCG accelerates the glucose uptake and evokes IRS-1/Akt/GLUT2 signaling pathway via dampening the expression of protein tyrosine phosphatase 1B (PTP1B). Consistently, ectopic expression of PTP1B by Ad-PTP1B substantially impaired EGCG-elicited IRS-1/Akt/GLUT2 signaling pathway. Moreover, EGCG co-treatment stimulated nuclear translocation of Nrf2 by provoking P13K/AKT signaling pathway and thus modulated the downstream expressions of antioxidant enzymes such as HO-1 and NQO-1 in HepG2 cells. Furthermore, knockdown Nrf2 by small interfering RNA (siRNA) notably enhanced the expression of PTP1B and blunt EGCG-stimulated glucose uptake. Consistent with these results, in vivo study revealed that EGCG supplement significantly ameliorated high-fat and high-fructose diet (HFFD)-triggered insulin resistance and oxidative stress by up-regulating the IRS-1/AKT and Keap1/Nrf2 transcriptional pathways. Administration of an appropriate chemopreventive agent, such as EGCG, could potentially serve as an additional therapeutic intervention in the arsenal against obesity.

Acrylamide (ACR) is a chronic neurotoxin that is generated in high-starch foods during heat processing. Alpha-lipoic acid (LA) is an antioxidant that occurs in most plants and animals. The objective of this study was to reveal the mechanism of ACR-triggered neurotoxicity and identify the protective role of LA in SH-SY5Y cells. In this study, LA restored ACR-stimulated depletion of glutathione content and mitochondrial membrane potential, moderated the activation of inflammatory pathways, and recovered the Keap1/Nrf2 pathway. Moreover, LA upregulated the activities of oxidative phosphorylation complexes and diminished ACR-induced variation in AMPK/GSK3β, Ca2+ disturbance, and ATP depletion. The Sirt1/PGC-1α pathway was inhibited by ACR. Notably, autophagy was activated in the mitochondria-mediated apoptosis induced by ACR, which was also blocked by LA. Overall, our study demonstrated the pivotal roles of the mitochondrial energy metabolism and autophagy in the protective effects of LA and cytotoxicity of ACR in SH-SY5Y cells.

Chicoric acid has recently become a hot research topic due to its potent bioactivities. However, there are few studies relevant to this acid's pharmacokinetic characteristics and the pharmacological activities of its metabolites. To compare the abilities of chicoric acid and its metabolites in scavenging free radicals and their effects on the viability of 3T3-L1 preadipocytes, an in vitro study of the metabolism of chicoric acid in rat liver microsomes was performed using liquid tandem mass spectrometry (HPLC-MS/MS). The results indicated that caffeic acid and caftaric acid were the hepatic phase I metabolites of chicoric acid. These three compounds had strong capacities for scavenging free radicals and had been demonstrated to increase intracellular ROS levels in 3T3-L1 preadipocytes, thereby reducing cell vitality. Finally, the pharmacological activities of chicoric acid were significantly stronger than those of its metabolites within a certain concentration range.

Momordin Ic is a natural triterpenoid saponin found in various Chinese and Japanese natural medicines such as the fruit of Kochia scoparia (L.) Schrad. Momordin Ic has been previously demonstrated to induce HepG2 cell apoptosis in a ROS-mediated PI3K and MAPK pathway-dependent manner. In the present study, the underlying mechanisms of PI3K and MAPK pathway-mediated PPARγ, and PGC-1α co-regulator activation, as well as the effects of downstream proteins, COX-2 and FoxO4, on cell apoptosis were investigated. The results demonstrated that momordin Ic activated PPARγ and inhibited COX-2. PGC-1α and FoxO4 expressions were increased by the PI3K or MAPK pathways. Furthermore, PPARγ inhibition decreased p-p38 and FoxO4 expression, and restored COX-2 expression. ROS inhibition exerted little effect on PPARγ, COX-2 and FoxO4 expression but affected PGC-1α expression. These results revealed the involvement of PI3K and MAPK-dependent PPARγ activation in momordin Ic-induced apoptosis, providing more detailed information underlying the pro-apoptotic mechanism of momordin Ic in HepG2 cell apoptosis.