Identification and molecular docking study of sugarcane leaf-derived compounds as potent dipeptidyl peptidase IV, α-glucosidase, and α-amylase inhibitors.

BACKGROUND: Dipeptidyl peptidase-IV (DPP-IV), α-glucosidase, and α-amylase play a prominent role in regulating postprandial blood sugar levels, which are regarded as key targets for the treatment of type 2 diabetes mellitus (T2DM). The present study aimed to characterize bioactive compounds as potent crucial sugar metabolism enzyme inhibitors from sugarcane leaves by virtual screening. In total, 41 sugarcane leaf-derived compounds were used for the screening of multiple targets. Subsequently, the molecular mechanism and activity validation in vitro of the interaction between enzymes and compound were carried out. RESULTS: Flavonoid compound schaftoside was identified by molecular simulation and showed significant DPP-IV (0.1050 ± 1.22 mmol L-1 ), α-glucosidase (0.078 ± 0.06 mmol L-1 ), and α-amylase (0.3067 ± 0.35 mmol L-1 ) inhibitory effects. The residues ARG125 and TYR662 of DPP-IV may play crucial roles in inhibiting the activity of DPP-IV. Multiple hydrogen bonds and electrostatic interactions were exhibited between schaftoside and α-glucosidase. Molecular modeling revealed that schaftoside displays strong binding with the catalytic triad (ASP197, ASP300, and GLU233) of α-amylase. CONCLUSION: Our findings demonstrate that schaftoside from sugarcane leaves might be an edible for T2DM treatment." © 2023 Society of Chemical Industry.

Alginate Oligosaccharides Prevent Dextran-Sulfate-Sodium-Induced Ulcerative Colitis via Enhancing Intestinal Barrier Function and Modulating Gut Microbiota.

Alginate oligosaccharides are degradation products of alginate and have attracted increasing attention due to their versatile biological functions. In the present study, C57BL/6 mice were used to assess the ameliorative effects and mechanisms of guluronate oligosaccharides (GAOS), mannuronic oligosaccharides (MAOS), and heterozygous alginate oligosaccharides (HAOS), which are the three alginate oligosaccharides of dextran sulfate sodium (DSS)-induced ulcerative colitis. The study showed that alginate oligosaccharides alleviated pathological histological damage by slowing down weight loss, inhibiting colonic length shortening, and reducing disease activity index (DAI) and histopathological scores. Alginate oligosaccharides modulated the colonic inflammatory response by reducing colonic MPO levels and downregulating the expression of IL-6 and IL-1ß. Alginate oligosaccharides reduced intestinal permeability and reversed intestinal barrier damage by increasing the number of goblet cells, decreasing LPS levels, downregulating Bax protein levels, upregulating Bcl-2 protein levels, and enhancing the expression of the E-cadherin. Furthermore, alginate oligosaccharides modulated the composition of the gut microbiota and restored the production of short-chain fatty acids (SCFAs), especially acetate and butyrate. In conclusion, our study provides a scientific basis for the role of alginate oligosaccharides in relieving ulcerative colitis.

Colon and gut microbiota greatly affect the absorption and utilization of astaxanthin derived from Haematococcus pluvialis.

Astaxanthin has been widely favored as a health food supplement by individuals but its absorption in the body seems not to be satisfactory. In addition, the peak time of astaxanthin derived from Haematococcus pluvialis in the plasma was much longer than other carotenoids found in our previous research. Thus, it is necessary to explore the process that affects the absorption of astaxanthin in order to potentially find a novel approach to improve the absorption in the future. In this study, we confirmed that the colon has an ability to absorb astaxanthin and conducted acute feeding experiments with the treatment of antibiotics in C57BL/6J mice and chronic feeding experiments in germ-free (GF) mice to detect the relationship between the gut microbiota and the absorption of astaxanthin. Our study showed that the decrease of gut microbiota led to a less oral absorbability, which might be related to the decreased expression of SR-BI in the small intestine and the reduction of free form and Z-astaxanthin converted by the gut microbiota found in the vitro culture. The experiments of anaerobic culture also implied that Lactobacillus might play an important role in the absorption of astaxanthin.

The risk of carrageenan-induced colitis is exacerbated under high-sucrose/high-salt diet.

As a common used food additive, the threat of carrageenan to colon health is controversial, and is inseparable from personal eating habits. However, no detailed descriptions are available concerning the influence of different dietary patterns on the risk of carrageenan-induced colitis. In this study, we explored the risk of κ-carrageenan-induced colitis under high-sucrose or high-salt diet in mice. Intervention with carrageenan under high-sucrose diet significantly reduced colon length and induced more serious deepening of the crypts. In addition, the intake of carrageenan under high-sucrose/high-salt diet induced more serious goblet cell reduction and increased intestinal permeability. 16S rRNA sequencing and LC-MS based metabonomic approaches were conducted to explore the changes of gut microbiota and metabolites. It was found that the intake of carrageenan under high-sucrose/high-salt diet significantly reduced the abundance of anti-inflammatory bacterium and increased the abundance of harmful bacterium, which was significantly related to the decrease of anti-inflammatory metabolites in colon, such as methyl caffeate, spermine, oleanolic acid and senecionine. Overall, high-sucrose or high-salt diet increased the risk of carrageenan-induced colitis. This reminds us to maintain good eating habits, do not prefer high-sugar or high-salt foods, and try not to consume large amounts of carrageenan continuously to maintain gut health.