Epigallocatechin gallate (EGCG) alleviates the inflammatory response and recovers oral microbiota in acetic acid-induced oral inflammation mice.

The oral microbiota, the second largest microbiome in the human body, plays an integral role in maintaining both the local oral and systemic health of the host. Oral microecological imbalances have been identified as a potential risk factor for numerous oral and systemic diseases. As a representative component of tea, epigallocatechin gallate (EGCG) has demonstrated inhibitory effects on most pathogens in single-microbial models. In this study, the regulatory effect of EGCG on more complex oral microbial systems was further explored through a mouse model of acetic acid-induced oral inflammation. Acetic acid induces histological damage in the cheek pouch, tongue, and throat, such as broken mucosa, submucosal edema, and muscular disorders. These detrimental effects were ameliorated significantly following EGCG treatment. Additionally, EGCG reduced the levels of the inflammatory cytokines interleukin-6 and tumor necrosis factor-α to alleviate the inflammation of the tongue, cheek pouch, and throat. According to the 16S rDNA gene sequencing data, EGCG treatment contributed to increased diversity of the oral microbiota and the reversal of oral microecological disorder. This study demonstrates the regulatory effect of EGCG on dysregulated oral microbiota, providing a potential option for the prevention and treatment of oral-microbiota-associated diseases.

Green tea extracts alleviate acetic acid-induced oral inflammation and reconstruct oral microbial balance in mice.

Oral cavity contains the second largest microbial community in the human body. Due to the highly vascularized feature of mouth, oral microbes could directly access the bloodstream and affect the host healthy systemically. The imbalance of oral microbiota is closely related to various oral and systemic diseases. Green tea extracts (GTE) mainly contain tea polyphenols, alkaloids, amino acid, flavones, and so on, which equipped with excellent anti-inflammatory activities. Previous studies have demonstrated the beneficial effects of GTE on oral health. However, most researches used in vitro models or focused on limited microorganisms. In this study, the regulatory effect of GTE on oral microbiome and the alleviative effect on oral inflammation in vivo were evaluated. The results showed that GTE could efficiently alleviate the inflammations of the tongue, cheek pouch, as well as throat. GTE effectively inhibited the activation of NF-κB through the upregulation of the anti-inflammatory cytokine interleukin (IL)-10, consequently leading to reduced expression of pro-inflammatory cytokines IL-6 and tumor necrosis factor-α. The indexes of spleen and thymus were also elevated by GTE in stomatitis mice. Moreover, GTE promoted the growth of probiotics Lactobacillus and Bacillus, inhibited the reproduction of pathogens Achromobacter, reversing the microbiota disorders in oral cavity. This study not only presents a novel approach for enhancing oral microecology but also facilitates the wider adoption of tea consumption.

Structural characterization and immunomodulatory activity of a polysaccharide from finger citron extracted by continuous phase-transition extraction.

FCP-2-1, a water-soluble polysaccharide rich in galacturonic acid was isolated by continuous phase-transition extraction and purified with DEAE-52 cellulose and Sephadex G-100 column chromatography from finger citron with essential oil and flavonoids removed. The structural characterization and immunomodulatory activity of FCP-2-1 were further investigated in this work. FCP-2-1 with a Mw and Mn of 1.503 × 104 g/mol and 1.125 × 104 g/mol, respectively, was predominantly composed of galacturonic acid, galactose, and arabinose in a molar ratio of 0.685: 0.032: 0.283. The main linkage types of FCP-2-1 were proved to be →5)-α-L-Araf-(1→ and →4)-α-D-GalpA-(1→ based on methylation and NMR analysis. Moreover, FCP-2-1 was demonstrated to have significant immunomodulatory effects on macrophages in vitro by improving the cell viability, and enhancing phagocytic activity and secretion of NO and cytokines (IL-1ß, IL-6, IL-10 and TNF-α), indicating that FCP-2-1 could be used as a natural agent in immunoregulation functional foods.

The potential mechanisms of bergamot-derived dietary fiber alleviating high-fat diet-induced hyperlipidemia and obesity in rats.

This study is aimed to investigate the health-associated benefits of bergamot-dietary fibers (DFs) with a special emphasis on weight loss and lipid-lowering effects, as well as the potential mechanisms involved. The feeding experiment of Sprague-Dawley (SD) rats for 6 weeks showed that DFs had dose-dependent regulatory effects against metabolic syndrome and they controlled obesity by slowing down the rate of weight growth, and reduced body mass index (BMI) and Lee's index without affecting appetite. Furthermore, DFs inhibited increment in TG, TC, LDL-C levels and AI index caused by a high-fat diet, and improved the pathological abnormality of the liver. Western blot results showed that DFs significantly up-regulated the protein expression levels of LXRα and CYP7A1, and down-regulated the levels of SREBP-1c, FAS, ACC and SREBP-2 in the liver. QRT-PCR results showed that DFs up-regulated PGC-1α, PRDM16, UCP-1, and PPARγ in brown adipose tissue. These results suggest that DFs played an effective role in reducing weight and lipids levels by promoting the decomposition and transport of lipids in liver, increasing the energy consumption of brown adipose tissue. DFs intervention reduced the difference in the intestinal microflora between rats fed with a normal diet and those fed with a high-fat diet. Soluble dietary fiber (SDF) and total dietary fiber (TDF) showed better weight loss and hypolipidemic potential compared to insoluble dietary fiber (IDF) at the same dose. In conclusion, bergamot-derived DFs demonstrated the potential to lower blood cholesterol and body weight and could be used to develop novel functional foods for the prevention or treatment of obesity and hyperlipidemia.