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Summary To investigate two-sided functions of tea polyphenols (TP) in antinutrition and energy balance modulation, TP were extracted from Chinese green tea and used to complex porcine pancreas α-amylase (PPA). Changes of PPA in activity and secondary conformations were analysed. Porcine pancreas α-amylase was found sensitive to TP treatment. Tea polyphenols exhibited IC50 at 0.41 mg mL−1 against PPA and maximum inhibitory rate (98.17%) at 3.0 mg mL−1. Tea polyphenols inhibition was concluded as noncompetitive pattern based on its unchanged Km value (0.98 mg mL−1) for soluble starch substrate. Tea polyphenols inhibition arose from pH 1.5 to 10.14, covering gastric and intestinal environments inside body. Circular dichroism spectra analysis revealed regular changes of PPA in secondary conformations (increased proportions of α-helix and β-sheet) prior to its inactivation at low TP concentrations. Tea polyphenols-inhibited PPA had distinct double-negative peaks at 204 nm and 208 nm. Porcine pancreas α-amylase was inactivated by TP in ways of complexation and modification of secondary conformations.

Our previous research found that feruloylated oligosaccharides (FOs) from corn bran modulated the gut microbiota in normal rats. This research aimed to investigate its effect on lipid metabolism and antioxidant activity in the plasma, liver, and heart. The results showed that, compared with the control, oral administration of 300 mg/kg FOs significantly decreased total cholesterol (by 19.8%) and low-density lipoprotein cholesterol (by 29.8%) but did not significantly influence glucose, triacylglycerol, and high-density lipoprotein cholesterol in serum; administration of the dosage to 600 mg/kg did not further change these parameters except for increasing total cholesterol. FOs administration at 300 mg/kg did not influence the content of thiobarbituric acid-reactive substances (TBARS) in plasma, liver, but significantly decreased it and significantly increased glutathione (GSH) in the heart, and superoxide dismutase (SOD) activity in plasma and liver. Interestingly, administration of FOs at 300 and 600 mg/kg decreased nitric oxide (NO) content in the heart but increased it in the plasma and liver. Whether or not the effect of FOs on NO content is beneficial or detrimental warrants further investigation.

In order to study the molecular mechanisms of green tea polyphenols (GTPs) in treatment or prevention of breast cancer, the cytotoxic effects of GTPs on five human cell lines (MCF-7, A549, Hela, PC3, and HepG2 cells) were determined and the antitumor mechanisms of GTPs in MCF-7 cells were analyzed. The results showed that GTPs exhibited a broad spectrum of inhibition against the detected cancer cell lines, particularly the MCF-7 cells. Studies on the mechanisms revealed that the main modes of cell death induced by GTPs were cell cycle arrest and mitochondrial-mediated apoptosis. Flow cytometric analysis showed that GTPs mediated cell cycle arrest at both G1/M and G2/M transitions. GTP dose dependently led to apoptosis of MCF-7 cells via the mitochondrial pathways, as evidenced by induction of chromatin condensation, reduction of mitochondrial membrane potential (ΔΨ m), improvement in the generation of reactive oxygen species (ROS), induction of DNA fragmentation, and activations of caspase-3 and caspase-9 in the present paper.

Three new triterpenoid saponins, polygonoides C (1), D (2), and E (3), were obtained from the ethanolic extract of the rhizome of Polygonatum sibiricum Redoute. On the basis of NMR and ESI-MS spectra, and chemical evidence, the structures of the three new compounds were elucidated as 3-O-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranosyl-(1→4)-β-D-glucopyranosyl-3β,7β,22β-trihydroxy-oleanolic acid (1), 3-O-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranosyl-(1→4)-β-D-glucopyranosyl-3β,7β,22β-trihydroxy-oleanolic acid methyl ester (2), and 3-O-β-D-glucopyranosyl-(1→3)-β-D-glucopyranosyl-(1→4)-[α-L-rhamno-pyranosyl-(1→2)]-β-D-glucopyranosyl-3β,21β-dihydroxy-oleanolic acid 28-O-β-D-glucopyranosyl-(1→3)-β-D-glucopyranosyl-(1→3)-β-D-glucopyranoside (3).