Yifei Kang

Preventive effects of Goji berry on dextran-sulfate-sodium-induced colitis in mice

Goji berry (Lycium barbarum) exerts immune modulation and suppresses inflammation in vitro and in vivo. We hypothesized that Goji berry had beneficial effects on dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice through suppressing inflammation. Six-week-old male C57BL/6 mice were supplemented with a standard AIN-93G diet with or without 1% (w/w) Goji berry for 4 weeks. Then, colitis was induced by supplementing 3% DSS in drinking water for 7 days, followed by 7 days of remission period to mimic ulcerative colitis symptoms. Goji berry supplementation ameliorated DSS-induced body weight loss, diminished diarrhea and gross bleeding, and resulted in a significantly decreased disease activity index, as well as DSS-associated colon shortening. Moreover, 30% mortality rate caused by DSS-induced colitis was avoided because of Goji berry supplementation. Histologically, Goji berry ameliorated colonic edema, mucosal damage and neutrophil infiltration into colonic intestinal tissue in response to DSS challenge, which was associated with decreased expression of chemokine (C-X-C motif) ligand 1 and monocyte chemoattractant protein-1, as well as inflammatory mediators interleukin-6 and cyclooxygenase-2. In conclusion, Goji supplementation confers protective effects against DSS-induced colitis, which is associated with decreased neutrophil infiltration and suppressed inflammation. Thus, dietary Goji is likely beneficial to inflammatory bowel disease patients as a complementary therapeutic strategy.

Dietary red raspberries attenuate dextran sulfate sodium-induced acute colitis

Persistent intestinal inflammation severely impairs intestinal integrity resulting in inflammatory bowel disease. Red raspberries (RB) are a rich source of bioactive compounds; their beneficial effect on the colitis protection was evaluated in the current study using a dextran sulfate sodium (DSS)-induced acute colitis mouse model. Six-week-old mice were fed a standard rodent research diet supplemented with RB (0 or 5% w/w, n=20 each group) for 6 weeks. At the 4th week of dietary treatment, approximately half of mice in each dietary group (n=12 each group) were subjected to 2.5% DSS induction for 6 days, followed by 6 days of recovery, to induce colitis. RB supplementation decreased body weight loss (P≤.01), disease activity index (P≤.01), and colon shortening (P≤.05) in DSS-treated mice. In addition, RB supplementation protected the colonic structure (P≤.01), associated with suppressed NF-κB signaling and reduced expression of inflammatory interleukin (IL)-1β, IL-6, IL-17, cyclooxegenase-2, and tumor necrosis factor-α in DSS-treated mice. RB supplementation reduced neutrophil infiltration, monocyte chemoattractant protein-1 mRNA expression, and xanthine oxidase content, but enhanced catalase content in DSS-treated mice. Consistently, RB supplementation reduced pore forming tight junction protein claudin-2, increased barrier strengthening claudin-3, zonula occluden-1 protein content and mucin (MUC)-2 mRNA level, and activated AMP-activated protein kinase (AMPK) in DSS-treated mice. In conclusion, dietary RB protected against inflammation and colitis symptoms induced by DSS, providing a promising dietary approach for the management of colitis.

Maternal high‐fat diet consumption enhances offspring susceptibility to DSS‐induced colitis in mice

Maternal high‐fat diet (HFD) may alter the offspring intestinal immune system, thereby enhancing susceptibility toward inflammatory bowel disease. The objective of the current study was to investigate the impact of maternal HFD on offspring intestinal health using a mouse model of dextran sulfate sodium (DSS)‐induced colitis.

Red raspberries suppress NLRP3 inflammasome and attenuate metabolic abnormalities in diet-induced obese mice

The NLR family pyrin domain containing 3 (NLRP3) inflammasome plays a critical role in insulin resistance and the pathogenesis of type 2 diabetes. Red raspberry (RB) contains high amounts of dietary fibers and polyphenolic compounds, which are known for their anti-oxidative and anti-inflammatory effects. This study evaluated the preventive effects of RB supplementation on the NLRP3 inflammasome activation and associated metabolic abnormalities induced by high fat diet (HFD). Wild-type male mice (six weeks old) were randomized into 4 groups receiving a control or typical western HFD supplemented with or without 5% freeze-dried RB for 12 weeks, when mice were sacrificed for tissue collection. HFD feeding substantially increased body weight, which was alleviated by RB supplementation towards the end of the feeding trial. Dietary RB restored the baseline blood glucose level, ameliorating glucose intolerance and insulin resistance, which were aggravated by HFD. Additionally, HFD reduced O2 expenditure and CO2 production, which were ameliorated by RB consumption. The liver is the key site for energy metabolism and a key peripheral tissue responsive to insulin. RB supplementation reduced hepatic lipid accumulation in HFD mice. In agreement, RB consumption suppressed hepatic NLRP3 inflammasome activation and reduced interleukin (IL)-1β and IL-18 production in HFD mice, accompanied with normalized mitochondriogenesis. These results suggest that RB consumption improves insulin resistance and metabolic dysfunction in diet-induced obesity, which is concomitant with suppression of NLRP3 inflammasome elicited by HFD. Thus, dietary RB intake is a promising strategy for ameliorating diet-induced metabolic abnormalities.

Raspberry Supplementation Improves Insulin Signaling and Promotes Brown-Like Adipocyte Development in White Adipose Tissue of Obese Mice

SCOPE Excessive lipid accumulation in white adipose tissue (WAT) leads to chronic inflammation and metabolic dysfunction. Raspberry (RB) contains high amount of polyphenols and dietary fibers. The objective of the study is to evaluate the effects of RB supplementation on WAT morphology, inflammation, and insulin signaling in high fat diet (HFD)-induced obese mice, and further explore the underlying mechanisms. METHODS AND RESULTS C57BL/6J mice are fed with a control diet or a HFD supplemented with 0 or 5% freeze dried RB for 12 weeks. RB supplementation decreases WAT hypertrophy induced by HFD and suppresses pro-inflammatory cytokines expression and macrophage infiltration in WAT. Meanwhile, RB addition improves insulin sensitivity of HFD-mice. Additionally, RB supplementation drives the browning of WAT (beige adipogenesis), which is associated with elevated PGC-1α and FNDC5/irisin contents. Consistently, the content of beige adipocyte markers including UCP1, PRDM16, Cytochrome C, Cidea, and Elvol3 is enhanced in HFD-mice, which are correlated with increased AMPK phosphorylation and Sirt1 protein contents. CONCLUSION Dietary RB attenuated adipocyte hypertrophy and inflammation of WAT in HFD-mice and improves insulin sensitivity and beige adipogenesis, which is associated with increased FNDC5/irisin content and activation of AMPK/Sirt1 pathway. RB supplementation provides a promising strategy to prevent diet-induced obesity.

Goji Berry Modulates Gut Microbiota and Alleviates Colitis in IL‐10‐Deficient Mice

SCOPE This study examines the beneficial effects of Goji berry against spontaneous colitis and its prebiotic role in IL-10-deficient mice. METHODS IL-10-deficient mice are assigned to a standard rodent diet (control) or a control diet supplemented with Goji (1% of dry feed weight) for 10 weeks, at which point colonic tissues and fecal contents are collected. RESULTS Goji supplementation decreases colonic pathobiological scores and mRNA expression of Il17a and Tgfb1, while it enhances Muc1 expression and fecal IgA content. Illumina MiSeq sequencing reveals that Goji supplementation increases Actinobacteria phylum, resulting in a bloom of Bifidobacteria in gut microbiota. Additionally, dietary Goji promotes butyrate-producing bacteria including Lachnospiraceae-Ruminococcaceae family and Roseburia spp. under Clostridium cluster XIVa. Furthermore, butyrate-producers Clostridium leptum and its dominant constituent Fecalibacterium prazusnitzii are markedly increased in the Goji group. Moreover, the gene-encoding butyryl-coenzyme A CoA transferase, a key enzyme responsible for butyrate synthesis in butyrate-producing bacteria, is increased sixfold in the fecal samples of Goji group associated with increased fecal butyrate content. CONCLUSION Data collectively show that dietary Goji results in the blooming of Bifidobacteria and butyrate-producing bacteria. These bacteria may cross-feed each other, conferring preventative effects against colitis in IL-10-deficient mice.