Polysaccharide from Mulberry Fruit (Morus alba L.) Protects against Palmitic-Acid-Induced Hepatocyte Lipotoxicity by Activating the Nrf2/ARE Signaling Pathway.

This study was aimed to investigate the protective effects of three different mulberry fruit polysaccharide fractions (MFP-I, MFP-II, and MFP-III) against palmitic acid (PA)-induced hepatocyte lipotoxicity and characterize the functional polysaccharide fraction using gel permeation chromatography, high-performance liquid chromatography, Fourier transform infrared spectroscopy, and nuclear magnetic resonance analyses. MFP-I, MFP-II, and MFP-III were isolated from mulberry fruit by stepwise precipitation with 30, 60, and 90% ethanol, respectively. MFP-II at 0.1 and 0.2 mg/mL dramatically attenuated PA-induced hepatic lipotoxicity, while MFP-I and MFP-III showed weak protection. It was demonstrated that MFP-II not only increased nuclear factor erythroid-2-related factor 2 (Nrf2) phosphorylation and its nuclear translocation, thereby activating the Nrf2/ARE signaling pathway, but also enhanced heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, and γ-glutamate cysteine ligase gene expressions and promoted catalase and glutathione peroxidase activities, which protected hepatocytes against PA-induced oxidative stress and lipotoxicity. Further investigation indicated that the molecular weight of MFP-II was 115.0 kDa, and MFP-II mainly consisted of galactose (30.5%), arabinose (26.2%), and rhamnose (23.1%). Overall, our research might provide in-depth insight into mulberry fruit polysaccharide in ameliorating lipid metabolic disorders.

Pelargonidin-3-O-glucoside Derived from Wild Raspberry Exerts Antihyperglycemic Effect by Inducing Autophagy and Modulating Gut Microbiota.

Increasing evidence indicates that anthocyanins exert beneficial effects on type 2 diabetes (T2D), but the underlying mechanism remains unclear. Herein, the hyperglycemia-lowering effect of Pg3G derived from wild raspberry was investigated on high-glucose/high-fat (HG+HF)-induced hepatocytes and db/db diabetic mice. Our results indicated that Pg3G promoted glucose uptake in HG+HF-induced hepatocytes. Moreover, Pg3G induced autophagy, whereas autophagy inhibitors blocked the hypoglycemic effect of Pg3G. Transcriptional factor EB (TFEB) was found to be linked to Pg3G-induced autophagy. In vivo study showed that Pg3G treatment contributed to the improvement of glucose tolerance, insulin sensitivity, and induction of autophagy. Furthermore, Pg3G not only modified the gut microbiota composition, as indicated by an increased abundance of Prevotella, and elevated Bacteroidetes/Firmicutes ratio, but also strengthened the intestinal barrier integrity. This study unveils a novel mechanism that Pg3G attenuates hyperglycemia through inducing autophagy and modulating gut microbiota, which implicates a potential nutritional intervention strategy for T2D.

In vitro gastrointestinal digestion promotes the protective effect of blackberry extract against acrylamide-induced oxidative stress.

Acrylamide (AA)-induced toxicity has been associated with accumulation of excessive reactive oxygen species. The present study was therefore undertaken to investigate the protective effect of blackberry digests produced after (BBD) in vitro gastrointestinal (GI) digestion against AA-induced oxidative damage. The results indicated that the BBD (0.5 mg/mL) pretreatment significantly suppressed AA-induced intracellular ROS generation (56.6 ± 2.9% of AA treatment), mitochondrial membrane potential (MMP) decrease (297 ± 18% of AA treatment) and glutathione (GSH) depletion (307 ± 23% of AA treatment), thereby ameliorating cytotoxicity. Furthermore, LC/MS/MS analysis identified eight phenolic compounds with high contents in BBD, including ellagic acid, ellagic acid pentoside, ellagic acid glucuronoside, methyl-ellagic acid pentoside, methyl-ellagic acid glucuronoside, cyanidin glucoside, gallic acid and galloyl esters, as primary active compounds responsible for antioxidant action. Collectively, our study uncovered that the protective effect of blackberry was reserved after gastrointestinal digestion in combating exogenous pollutant-induced oxidative stress.

Blackberry subjected to in vitro gastrointestinal digestion affords protection against Ethyl Carbamate-induced cytotoxicity.

Ethyl Carbamate (EC) was detected in many fermented foods. Previous studies indicated that frequent exposure to ethyl carbamate may increase the risk to suffer from cancers. Blackberry is rich in polyphenols and possesses potent antioxidant activity. This study aims to investigate the protective effect of blackberry homogenates produced before (BH) and after in vitro simulated gastrointestinal digestion (BD) on EC-induced toxicity in Caco-2 cells. Our results showed that blackberry homogenates after digestion (BD) was more effective than that before digestion (BH) in ameliorating EC-induced toxicity in Caco-2 cells. Further investigation revealed that BD remarkably attenuated EC-induced toxicity through restoring mitochondrial function, inhibiting glutathione depletion and decreasing overproduction of intracellular reactive oxygen species. Additionally, LC-MS result implied that the better protective capacity of BD may be related to the increased content of two anthocyanins (cyanidin-3-glucoside and cyanidin-3-dioxalyglucoside). Overall, the present study may give implication to prevent EC-induced health problem.

Antimicrobial effect of bayberry leaf extract for the preservation of large yellow croaker (Pseudosciaena crocea).

BACKGROUND: Chemical preservatives have been widely used to keep large yellow croaker fresh. However, the potential harm to human health cannot be ignored. This study was undertaken to investigate the antimicrobial effect of bayberry leaf extract and to evaluate the efficacy of this natural product on the preservation of large yellow croaker. RESULTS: The minimum inhibitory concentration (MIC) values of bayberry leaf extract against bacteria were 1.0 mg mL⁻¹ for Micrococcus luteus, 0.5 mg mL⁻¹ for Staphylococcus aureus, 0.25 mg mL⁻¹ for Escherichia coli, 0.5 mg mL⁻¹ for Pseudomonas aeruginosa, 0.0625 mg mL⁻¹ for Vibrio parahaemolyticus, and 0.03125 mg mL⁻¹ for Listeria monocytogenes, respectively. This result was confirmed by the diameters of inhibition zone (DIZ) assay. Further studies showed that the bacterial growth was significantly retarded when large yellow croaker was pretreated with bayberry leaf extract (2 g L⁻¹) compared to that in the control group. Moreover, the generation of total volatile basic nitrogenous compounds (TVB-N), ATP degradation products (K-value) and thiobarbituric acid-reactive substances (TBARS) were significantly reduced compared to that in the control group. CONCLUSION: Our results demonstrated that the shelf life of large yellow croaker can be extended when supplemented with bayberry leaf extract, which might have implications for natural preservatives.

Myricitrin inhibits acrylamide-mediated cytotoxicity in human Caco-2 cells by preventing oxidative stress.

Oxidative stress was thought to be associated with acrylamide cytotoxicity, but the link between oxidative stress and acrylamide cytotoxicity in the gastrointestinal tract, the primary organ in contact with dietary acrylamide, is still unclear. This study was conducted to evaluate the antioxidant activity of natural dietary compound myricitrin and its protective role against acrylamide cytotoxicity. We found that myricitrin can effectively scavenge multiple free radicals (including DPPH free radical, hydroxyl radical, and ABTS free radical) in a concentration-dependent manner. Our results further indicated that the presence of myricitrin (2.5-10 µg/mL) was found to significantly inhibit acrylamide-induced cytotoxicity in human gastrointestinal Caco-2 cells. Moreover, acrylamide-induced cytotoxicity is closely related to oxidative stress in Caco-2 cells. Interestingly, myricitrin was able to suppress acrylamide toxicity by inhibiting ROS generation. Taken together, these results demonstrate that myricitrin had a profound antioxidant effect and can protect against acrylamide-mediated cytotoxicity.