Momordica grosvenori is a valuable edible plant with medicinal purposes, and it is widely used in medicated diets and traditional Chinese medicine in Asia. Mogroside V (MV), the main bioactive component from M. grosvenori, is commonly used as a natural sweetener. M. grosvenori extracts have been reported to exert potent anti-inflammatory property, however the underlying molecular mechanism still remains unknown. In the present study, the biological effect of MV in inflammation was investigated in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The ELISA and western blot analysis results showed that MV significantly inhibited LPS-induced prostaglandin E2 (PGE2) production and cyclooxygenase-2 (COX-2) expression. MV markedly decreased the phosphorylation of IκB-α, increased IκB-α, and reduced nuclear p-65 and C/EBPδ. Furthermore, MV attenuated LPS-induced phosphorylation of MAPKs and AKT1, and only the phosphorylation status of AKT1 was found to be consistent with the expression trend of COX-2. Moreover, MV reduced ROS level and restored overexpressed HO-1 and AP-1 to basal level, which can be markedly reversed by AKT1 inhibitor LY294002. These results revealed that AKT1 plays a key role in LPS-induced COX-2 expression, and acts as a mediator to keep the redox balance in LPS-stimulated RAW264.7 cells. MV exerts anti-inflammatory property by blocking AKT1-mediated NF-κB and C/EBPδ activation, ROS generation and AP-1/ HO-1 expression. Therefore, the present study indicated that MV has a significant chemopreventive effect on the inflammatory lesions and suggested that AKT1 is a potential specific target of MV for relieving inflammation.

Gardenia jasminoides Ellis is abundant in crocin and has a longstanding historical usage both as a dietary and natural ethnic medicine. Enhanced studies have increasingly revealed the intricate interplay between glycolipid metabolism and gut microbiota, wherein their imbalance is regarded as a pivotal indicator of metabolic disorders. Currently, the precise molecular mechanism of the crude extract of crocin from Gardenia jasminoides Ellis (GC) targeting gut microbiota to regulate glycolipid metabolism disorder is still unclear. Firstly, we explored the effect of GC on digestive enzymes (α-amylase and α-glucosidase) in vitro. Secondly, we investigated the effect of GC on the physical and chemical parameters of high-fat diet (HFD) rats, such as body weight change, fasting blood glucose and lipid levels, and liver oxidative stress and injury. Then, 16S rDNA sequencing was used to analyze the effects of GC on the composition and structure of gut microbiota. Finally, the impact of GC on the TLR4/Myd88/NF-κB signaling pathway in the intestine was assessed by Western Blotting. In the present study, GC was found to exhibit a hypoglycemic effect in vitro, by inhibition of digestive enzymes. In animal experiments, we observed that GC significantly reduced fasting blood glucose, TC, and TG levels while increasing HDL-C levels. Additionally, GC demonstrated hepatoprotective properties by enhancing liver antioxidative capacity through the upregulation of SOD, CAT, and GSH-Px, while reducing ROS. 16S rDNA sequencing results showed that GC had a significant effect on the gut microbiota of HFD rats, mainly by reducing the ratio of Firmicutes/Bateroidota, and significantly affected the genera related to glycolipid metabolism, such as Akkermansia, Ligilactobacillus, Lactobacillus, Bacteroides, Prevotellaceae, etc. The Western Blotting results demonstrated that GC effectively downregulated the protein expressions of TLR4, Myd88, and NF-κB in the intestine of HFD rats, indicating that GC could target the TLR4/Myd88/NF-κB pathway to interfere with glycolipid metabolism disorder. Correlation analysis revealed that GC could target the Akkermansia-TLR4/Myd88/NF-κB pathway axis which attenuates glycolipid metabolism disorder. Therefore, this study establishes the foundation for GC as a novel therapeutic agent for glycolipid metabolism disorder chemoprevention, and it introduces a novel methodology for harnessing the potential of natural botanical extracts in the prevention and treatment of metabolic syndrome.

Lotus seed is well known as traditional food and medicine, but its skin is usually discarded. Recent studies have shown that lotus seed skin contains a high concentration of proanthocyanidins that have multi-functions, such as antioxidation, anti-inflammation, and anti-cancer effects. In the present study, we aimed to isolate and purify the proanthocyanidins from lotus seed skin by acetone extraction and rotary evaporation, identify their chemical structures by HPLC-MS-MS and NMR, and further investigate the antioxidant properties of the extract purified by macroporous resin (PMR) from lotus seed skin both in vitro and in vivo. The results showed that PMR mainly contained oligomeric proanthocyanidins, especially dimeric procyanidin B1 (PB1), procyanidin B2 and procyanidin B4. Although it had limited ability to directly scavenge radicals in vitro, PMR could significantly enhance the expressions of antioxidant proteins via activation of nuclear factor-E2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway in HepG2 cells. Molecular data revealed that PB1, a major component in PMR, stabilized Nrf2 by inhibiting the ubiquitination of Nrf2, which led to subsequent activation of the Nrf2-ARE pathway, including the enhancements of Nrf2 nuclear translocation, Nrf2-ARE binding and ARE transcriptional activity. Moreover, the in vivo results in high fat diet-induced mice further verified the powerful antioxidant property of PMR. These results revealed that lotus seed skin is a promising resource for functional food development.

A previous study using healthy “Valencia” orange fruit found that juicing extraction methods dramatically changed the orange juice (OJ) flavor and phytochemical profiles. The present study was conducted to confirm whether the same changes occur when Huanglongbing (HLB)-affected oranges were used. HLB has extensively spread to most OJ processing regions around the world, substantially deteriorating fruit and juice flavor quality and altering the phytochemical profiles. In this study, the effect of two major juice extractor types, a shear force extractor (SFE) and a reamer extractor (RE), on the juice quality and physiochemical profile was assessed using HLB-affected orange fruit. Juice extracted via SFE resulted in a lower yield with lower peel oil and higher pellet (peel tissue particles) content compared to juice obtained via RE. The SFE juice also had higher levels of hesperidin and other flavonoid glycosides, mainly due to plentiful peel tissue particles. The SFE juice was also abundant in carotenoids due to a large amount of flavedo particles in the juice. On the other hand, polymethoxylated flavones occurred at higher concentrations in the RE juice, and this may be due to the higher peel oil content in this juice. The SFE juice was rich in flavonoid glycosides and carotenoids, which are associated with potential antioxidant properties; however, the extra portion of the phytonutrients mostly existed in the pellets and possibly had low bioavailability. The results obtained from the HLB-affected oranges are in agreement with the previous observations of healthy oranges.

High glucose levels can lead to the apoptosis of islet β cells, while autophagy can provide cytoprotection and promote autophagic cell death. Vitamin B12, a water-soluble B vitamin, has been shown to regulate insulin secretion and increase insulin sensitivity. However, the precise mechanism of action remains unclear. In this study, we investigated the influence of vitamin B12 on high glucose-induced apoptosis and autophagy in RIN-m5F cells to elucidate how vitamin B12 modulates insulin release. Our results demonstrate that exposure to 45 mM glucose led to a significant increase in the apoptosis rate of RIN-m5F cells. The treatment with vitamin B12 reduced the apoptosis rate and increased the number of autophagosomes. Moreover, vitamin B12 increased the ratio of microtubule-associated protein 1 light chain 3 beta to microtubule-associated protein 1 light chain 3 alpha (LC3-II/LC3-I), while decreasing the amount of sequestosome 1 (p62) and inhibiting the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K) under both normal- and high-glucose conditions. The additional experiments revealed that vitamin B12 inhibited high glucose-induced apoptosis. Notably, this protective effect was attenuated when the autophagy inhibitor 3-methyladenine was introduced. Our findings suggest that vitamin B12 protects islet β cells against apoptosis induced by high glucose levels, possibly by inducing autophagy.