The Potential Role of Vitamin E and the Mechanism in the Prevention and Treatment of Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD) includes ulcerative colitis and Crohn's disease, and it is a multifactorial disease of the intestinal mucosa. Oxidative stress damage and inflammation are major risk factors for IBD. Vitamin E has powerful antioxidant and anti-inflammatory effects. Our previous work and other investigations have shown that vitamin E has a positive effect on the prevention and treatment of IBD. In this paper, the source and structure of vitamin E and the potential mechanism of vitamin E's role in IBD were summarized, and we also analyzed the status of vitamin E deficiency in patients with IBD and the effect of vitamin E supplementation on IBD. The potential mechanisms by which vitamin E plays a role in the prevention and treatment of IBD include improvement of oxidative damage, enhancement of immunity, maintenance of intestinal barrier integrity, and suppression of inflammatory cytokines, modulating the gut microbiota and other relevant factors. The review will improve our understanding of the complex mechanism by which vitamin E inhibits IBD, and it also provides references for doctors in clinical practice and researchers in this field.

Functional Perspective of Leeks: Active Components, Health Benefits and Action Mechanisms.

Leek (Allium fistulosum L.), a common and widely used food ingredient, is a traditional medicine used in Asia to treat a variety of diseases. Leeks contain a variety of bioactive substances, including sulfur compounds, dietary fiber, steroid compounds and flavonoid compounds. Many studies have shown that these active ingredients produce the following effects: promotion of blood circulation, lowering of cholesterol, relief of fatigue, anti-inflammation, anti-bacteria, regulation of cell metabolism, anti-cancer, anti-oxidation, and the lowering of fat and blood sugar levels. In this paper, the main bioactive components and biological functions of leeks were systemically reviewed, and the action mechanisms of bioactive components were discussed. As a common food, the health benefits of leeks are not well known, and there is no systematic summary of leek investigations. In light of this, it is valuable to review the recent progress and provide reference to investigators in the field, which will promote future applications and investigations of leeks.

A Comprehensive Review of Health-Benefiting Components in Rapeseed Oil.

Rapeseed oil is the third most consumed culinary oil in the world. It is well-known for its high content of unsaturated fatty acids, especially polyunsaturated fatty acids, which make it of great nutritional value. There is increasing evidence that a diet rich in unsaturated fatty acids offers health benefits. Although the consumption of rapeseed oil cuts across many areas around the world, the nutritional elements of rapeseed oil and the exact efficacy of the nutrients remain unclear. In this review, we systematically summarized the latest studies on functional rapeseed components to ascertain which component of canola oil contributes to its function. Apart from unsaturated fatty acids, there are nine functional components in rapeseed oil that contribute to its anti-microbial, anti-inflammatory, anti-obesity, anti-diabetic, anti-cancer, neuroprotective, and cardioprotective, among others. These nine functional components are vitamin E, flavonoids, squalene, carotenoids, glucoraphanin, indole-3-Carbinol, sterols, phospholipids, and ferulic acid, which themselves or their derivatives have health-benefiting properties. This review sheds light on the health-benefiting effects of rapeseed oil in the hope of further development of functional foods from rapeseed.

Oryzanol Ameliorates DSS-Stimulated Gut Barrier Damage via Targeting the Gut Microbiota Accompanied by the TLR4/NF-κB/NLRP3 Cascade Response In Vivo.

Inflammatory bowel disease (IBD) is a global chronic disease with a long duration and repeated relapse. Currently, there is still a lack of effective approaches to prevent IBD. Food-derived oryzanol (ORY) possesses extensive biological activities, such as ameliorating bowel diseases, antioxidation, and antiobesity. However, the mechanism of ORY in preventing colitis remains unclear. The present research aims to explore the potential mechanism of ORY in dextran sulfate sodium (DSS)-stimulated colitis in a rat model. The results showed that the symptoms of colitis were significantly improved with the administration of ORY. Mechanismly, the expression levels of Zonula occludens-1 (ZO-1), Claudin-1, Occludin, MUC2, and TFF3 were elevated through ORY treatment, suggesting that oral ORY relieved the degree of gut barrier damage of colitis rats. Meanwhile, 16S sequencing results found that ORY supplementation increased the abundances of Alloprevotella, Roseburia, Treponema, Muribaculaceae, and Ruminococcus, which are associated with the synthesis of short-chain fatty acids (SCFAs). Moreover, GC-MS results confirmed that ORY supplementation reversed the DSS-induced reduction of acetic acid, butyric acid, and total acid. Further research indicated that ORY intervention downregulated the TLR4/NF-κB/NLRP3 pathway, which is closely linked to the expression of proinflammatory cytokines and colon injury. Taken together, ORY ameliorates DSS-stimulated gut barrier damage and inflammatory responses via the gut microbiota-TLR4/NF-κB/NLRP3 signaling axis.

Laminarin ameliorates alcohol-induced liver damage and its molecular mechanism in mice.

Alcoholic liver disease (ALD) has become a health issue globally. Laminarin, a low molecular weight marine-derived ß-glucan, has been identified with multiple biological activities. In this study, the ameliorative effect on ALD of laminarin isolated from brown algae was investigated. Phenotypic, pathological alterations and biochemical characteristics indicated that laminarin administration (100 mg/kg/day) significantly alleviated liver injury and improved liver function in the alcohol-induced mice. Gene chip results indicated that laminarin treatment caused 52 up-regulated and 13 down-regulated genes in the hepatic tissues of alcohol-induced damage mice, and most of these genes are associated with regulation of oxidative stress (such as CYP450/glutathione-dependent antioxidation), Wnt signaling pathway, retinol metabolism, and cAMP pathway based on GO and KEGG analysis. PPI network analysis indicated that the downstream target genes lied in the hub of the net. Our experiments also confirmed the changed expressions of some target genes. Taken together, these results suggest that laminarin can ameliorate alcohol-induced damage in mice and its molecular mechanism lies in modulating anti-oxidation pathway, WNT pathway, and cAMP pathway, which regulate the expressions of downstream target genes and alleviate alcohol-induced damage. Our study provides new clue to prevent alcohol-induced damage and will be benefit to develop functional foods. PRACTICAL APPLICATIONS: This study verified the positive effect on alcoholic liver disease (ALD) of laminarin, a water-soluble brown algae-derived ß-glucan, linked by ß-(1,3) glycosidic bonds with ß-(1,6) branches. Laminarin significantly alleviated liver injury and improved liver function of ALD mice. Moreover, transcriptomics and bioinformatics analysis further revealed the gene expression patterns, hub targets, and signalings including CYP450/glutathione, Wnt, retinol metabolism, cAMP pathways regulated by laminarin. This research is the first evidence for hepatoprotective effect of laminarin against ALD and its molecular mechanism, which will be advantage to develop functional foods or adjuvant therapy of ALD.

Targeting lncRNA/Wnt axis by flavonoids: A promising therapeutic approach for colorectal cancer.

Despite the dramatic advances in our understanding of the etiology of colorectal cancer (CRC) in recent decades, effective therapeutic strategies are still urgently needed. Oncogenic mutations in the Wnt/ß-Catenin pathway are hallmarks of CRC. Moreover, long non-coding RNAs (lncRNAs) as molecular managers are involved in the initiation, progression, and metastasis of CRC. Therefore, it is important to further explore the interaction between lncRNAs and Wnt/ß-Catenin signaling pathway for targeted therapy of CRC. Natural phytochemicals have not toxicity and can target carcinogenesis-related pathways. Growing evidences suggest that flavonoids are inversely associated with CRC risk. These bioactive compounds could target carcinogenesis pathways of CRC and reduced the side effects of anti-cancer drugs. The review systematically summarized the progress of flavonoids targeting lncRNA/Wnt axis in the investigations of CRC, which will provide a promising therapeutic approach for CRC and develop nutrition-oriented preventive strategies for CRC based on epigenetic mechanisms. In the field, more epidemiological and clinical trials are required in the future to verify feasibility of targeting lncRNA/Wnt axis by flavonoids in the therapy and prevention of CRC.

Dietary flavonoids prevent diabetes through epigenetic regulation: advance and challenge.

The pathophysiology of diabetes has been studied extensively in various countries, but effective prevention and treatment methods are still insufficient. In recent years, epigenetics has received increasing attention from researchers in exploring the etiology and treatment of diabetes. DNA methylation, histone modifications, and non-coding RNAs play critical roles in the occurrence, maintenance, and progression of diabetes and its complications. Therefore, preventing or reversing the epigenetic alterations that occur during the development of diabetes may reduce the individual and societal burden of the disease. Dietary flavonoids serve as natural epigenetic modulators for the discovery of biomarkers for diabetes prevention and the development of alternative therapies. However, there is limited knowledge about the potential beneficial effects of flavonoids on the epigenetics of diabetes. In this review, the multidimensional epigenetic effects of different flavonoid subtypes in diabetes were summarized. Furthermore, it was discussed that parental flavonoid diets might reduce diabetes incidence in offspring, which represent a promising opportunity to prevent diabetes in the future. Future work will depend on exploring anti-diabetic effects of different flavonoids with different epigenetic regulation mechanisms and clinical trials. Highlights• "Epigenetic therapy" could reduce the burden of diabetic patients• "Epigenetic diet" ameliorates diabetes• Targeting epigenetic regulations by dietary flavonoids in the diabetes prevention• Dietary flavonoids prevent diabetes via transgenerational epigenetic inheritance.

Oryzanol Attenuates High Fat and Cholesterol Diet-Induced Hyperlipidemia by Regulating the Gut Microbiome and Amino Acid Metabolism.

Hyperlipidemia is intricately associated with the dysregulation of gut microbiota and host metabolomes. This study explored the antihyperlipidemic function of oryzanol and investigated whether the function of oryzanol affected the gut microbiome and its related metabolites. Hamsters were fed a standard diet (Control) and a high fat and cholesterol (HFCD) diet with or without oryzanol, separately. Our results showed that oryzanol significantly decreased HFCD-induced fat accumulation, serum total cholesterol, low-density lipoprotein cholesterol (LDL-c), LDL-c/HDL-c ratio, triglyceride, and liver steatohepatitis, attenuated HFCD-induced gut microbiota alterations, and altered amino acid concentrations in feces and the liver. We investigated the role of the gut microbiota in the observed beneficial effects; the protective effects of oryzanol were partly diminished by suppressing the gut bacteria of hamsters after using antibiotics. A fecal microbiota transplantation experiment was carried out by transplanting the feces from HFCD group hamsters or hamsters given oryzanol supplementation (as a donor hamster). Our results showed that administering the fecal liquid from oryzanol-treated hamsters attenuated HFCD-induced hyperlipidemia, significantly decreased the abundance of norank_f__Erysipelotrichaceae, norank_f__Eubacteriaceae, and norank_f__Oscillospiraceae and the concentration of tyrosine. These outcomes are significantly positively correlated with serum lipid concentration. This study illustrated that gut microbiota is the target of oryzanol in the antihyperlipidemic effect.

Oryzanol alleviates high fat and cholesterol diet-induced hypercholesterolemia associated with the modulation of the gut microbiota in hamsters.

A high fat and cholesterol diet (HFCD) can modulate the gut microbiota, which is closely related with hypercholesterolemia. This study aimed to explore the anti-hypercholesterolemia effect of oryzanol, and investigate whether the function of oryzanol is associated with the gut microbiota and related metabolites. 16S rRNA and ultrahigh-performance liquid chromatography-quadrupole time-of-flight mass spectrometry were applied for the gut microbiota and untargeted metabolomics, respectively. The results showed that HFCD significantly upregulated body fat accumulation and serum lipids, including triglyceride, total cholesterol, low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol (HDL-c), and ratio of LDL-c/HDL-c, which induced hypercholesterolemia. Oryzanol supplementation decreased body fat accumulation and serum lipids, especially the LDL-c concentration and LDL-c/HDL-c ratio. In addition, the abundances of Desulfovibrio, Colidextribacter, norank_f__Oscillospiraceae, unclassified_f__Erysipelotrichaceae, unclassified_f__Oscillospiraceae, norank_f__Peptococcaceae, Oscillibacter, Bilophila and Harryflintia were increased and the abundance of norank_f__Muribaculaceae was decreased in HFCD-induced hyperlipidemia hamsters. Metabolites were changed after HFCD treatment and 9 differential metabolites belonged to bile acids and 8 differential metabolites belonged to amino acids. Those genera and metabolites were significantly associated with serum lipids. HFCD also disrupted the intestinal barrier. Oryzanol supplementation reversed the changes of the gut microbiota and metabolites, and intestinal barrier injury was also partly relieved. This suggests that oryzanol supplementation modulating the gut microbiota contributes to its anti-hyperlipidemia function, especially anti-hypercholesterolemia.

Phenolics Profile and Protective Effect on Injuried HUVEC Cells of Epicarp Extracts from Kadsura coccinea.

This study evaluated the phenolics profile and the antioxidative properties of K. coccinea fruits epicarp. A total of 13 phenolic compounds (six phenolic acids, four anthocyanins, two flavonols, and one flavone) were identified by ultra performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spetrometry(UPLC-QTOF-MS/MS). Two anthocyanins, cyanidin-3-xylosylrutinoside and cyanidin-3-rutinoside, comprise 30.89~74.76% and 13.90~46.17% of the total amount of anthocyanins in K. Coccinea. Cytoprotective effect results evidenced that pretreatment of Human umbilical vein endothelial cells(HUVECs) with Kadsura. coccinea fruits' epicarp phenolic extracts at the concentrations of 50-200 µg/mL improved the cell viability after exposure to H2O2 significantly, and inhibited malonaldehyde(MDA) and reactive oxygen species(ROS) overproduction, as well as enhancing the content of superoxide dismutase (SOD) and glutathione Reductase (GR. This study proved that K. coccinea is a natural resource of phenolics rich with potential antioxidant ability, which may be valuable for developing nutraceuticals and dietary supplements.

Bioactive Peptide F2d Isolated from Rice Residue Exerts Antioxidant Effects via Nrf2 Signaling Pathway.

Studies have shown that the peroxidation caused by oxygen free radicals is an important reason of vascular endothelial dysfunction and multiple diseases. In this study, active peptides (F2ds) were isolated from the fermentation product of rice dregs and its antioxidant effects were approved. Human umbilical vein endothelial cells (HUVECs) stimulated by H2O2 were used to evaluate the antioxidation effect and its molecular mechanism in the oxidative stress model. F2d protected H2O2-induced damage in HUVECs in a dosage-dependent manner. F2d can reduce the expression of Keap1, promote the expression of Nrf2, and activate the downstream target HO-1, NQO1, etc. It means F2d can modulate the Nrf2 signaling pathway. Using Nrf2 inhibitor ML385 to block the Nrf2 activation, the protective function of F2d is partially lost in the damage model. Our results indicated that F2d isolated from rice exerts antioxidant effects via the Nrf2 signaling pathway in H2O2-induced damage, and the work will benefit to develop functional foods.

Understanding the aggregation structure, digestive and rheological properties of corn, potato, and pea starches modified by ultrasonic frequency.

Corn starch (CS), potato starch (PtS), and pea starch (PS) were modified by ultrasonic frequency (codes as UFCS, UFPtS and UFPS), and changes in aggregation structure, digestibility and rheology were investigated. For UFCS, the apparent amylose content and gelatinization enthalpy (∆H) decreased, while the R1047/1022 values and relative crystallinity (RC) increased under lower ultrasonic frequencies (20 kHz and 25 kHz). For UFPtS, the apparent amylose content, R1047/1022 values and RC increased, while the ∆H decreased under a higher ultrasonic frequency (28 kHz). For UFPS, the apparent amylose content, R1047/1022 values, RC, ∆H decreased at 20 kHz, 25 kHz and 28 kHz. Cracks were observed on the surface of UFCS, UFPtS and UFPS. These aggregation structure changes increased the resistant starch content to 31.11% (20 kHz) and 26.45% (25 kHz) for UFCS and to 39.68% (28 kHz) for UFPtS, but decreased the resistant starch content to 18.46% (28 kHz) for UFPS. Consistency coefficient, storage modulus, and loss modulus of UFCS, UFPtS and UFPS increased, while the flow behavior index and damping factor decreased. Results indicated that CS, PtS and PS had diverse digestion and rheology behaviors after ultrasonic frequency modification, which fulfilled different demands in starch-based products.

Dietary Supplementation of Octacosanol Improves Exercise-Induced Fatigue and Its Molecular Mechanism.

Several publications report that octacosanol (OCT) has different biological functions. This study was designed to evaluate the antifatigue effect and molecular mechanism of octacosanol (200 mg/(kg day)) in forced exercise-induced fatigue models of trained male C57BL/6 mice. Results showed that octacosanol ameliorated the mice's autonomic activities, forelimb grip strength, and swimming endurance, and the levels of liver glycogen (LG), muscle glycogen (MG), blood lactic acid (BLA), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were also regulated. Gene analysis results showed that treatment with OCT upregulated 29 genes, while 38 genes were downregulated in gastrocnemius tissue. Gene ontology (GO) analyses indicated that these genes enriched functions in relation to myofibril, contractile fiber, and calcium-dependent adenosinetriphosphatase (ATPase) activity. Octacosanol supplementation significantly adjusted the messenger RNA (mRNA) and protein expression levels related to fatigue performance. Octacosanol has an observably mitigating effect in exercise-induced fatigue models, and its molecular mechanism may be related to the regulation of tripartite motif-containing 63 (Trim63), periaxin (Prx), calcium voltage-gated channel subunit α1 H (Cacna1h), and myosin-binding protein C (Mybpc3) expression.

Changes in structural, digestive, and rheological properties of corn, potato, and pea starches as influenced by different ultrasonic treatments.

Ultrasound was widely used in starch modification, whereas there was no review focusing on the effects of different ultrasonic treatments on A-, B- and C-type starches. In this study, the effects of ultrasonic power (UP, 100-600 W) and ultrasonic time (UT, 5-35 min) on structural, digestibility and rheology of corn starch (CS), potato starch (PtS), and pea starch (PS) were investigated. As a result, UP and UT decreased the apparent amylose content of CS and PS, while increased the apparent amylose content of PtS. UP and UT enhanced R1047/1022 values of CS, whereas those of PtS and PS were decreased. Moreover, UP and UT decreased the gelatinization enthalpy of CS, PtS and PS. In vitro digestion revealed that UP and UT decreased the resistant starch content of PtS and PS, but increased the resistant starch content of CS. Rheological tests indicated that UP and UT decreased the flow behavior index of CS, PtS and PS pastes, and caused an increase in storage modulus and loss modulus. Results revealed that ultrasonic treatment represented a promising technology to obtain CS, PtS and PS with tailored digestibility and rheology, which allowed the texture and glycemic response of starch-based products to be adjusted.

Structural changes of A-, B- and C-type starches of corn, potato and pea as influenced by sonication temperature and their relationships with digestibility.

The effect of sonication temperature on the structures and digestion behaviour of corn starch (CS, A-type), potato starch (PtS, B-type), and pea starch (PS, C-type) was investigated. For CS, sonication temperature resulted in a rough surface, decreased apparent amylose content, gelatinization enthalpy and gelatinization degree, increased short-range orders, long-range orders, retrogradation degree and resistant starch content. For PtS, sonication temperature led to a coarser surface with scratches, increased apparent amylose content and gelatinization degree, decreased short-range orders, long-range orders, gelatinization enthalpy, retrogradation degree, and resistant starch content. For PS, sonication temperature showed partial disintegration on surface, increased gelatinization degree, decreased apparent amylose content, short-range orders, long-range orders, gelatinization enthalpy, retrogradation degree and resistant starch content. This study suggested that starch digestion features could be controlled by the crystalline pattern of starch used and the extent of sonication temperature, and thus were of value for rational control of starch digestion features.

Glutamate and aspartate alleviate testicular/epididymal oxidative stress by supporting antioxidant enzymes and immune defense systems in boars.

Several potential oxidative agents have damaging effects on mammalian reproductive systems. This study was conducted to investigate the effects of glutamate (Glu) and aspartate (Asp) supplementation on antioxidant enzymes and immune defense systems in the outer scrotum of boars injected with H2O2. A total of 24 healthy boars were randomly divided into 4 treatment groups: control (basal diet, saline-treated), H2O2 (basal diet, H2O2-challenged outer scrotum (1 mL kg-1 BW)), Glu (basal diet +2% Glu, H2O2-challenged), and Asp (basal diet+2% Asp, H2O2-challenged). Our results showed that both Glu and Asp supplementation improved testicular morphology and decreased the genital index in the H2O2-treated boars. Glu and Asp administration increased the antioxidant enzyme activities and affected the testicular inflammatory cytokine secretion but had no effect on sex hormone levels. Furthermore, the mRNA expression of CAT, CuZnSOD, and GPx4 was altered in the testes and epididymis of boars treated with Asp and Glu. Glu and Asp supplementation also modulated the expression of TGF-ß1, IL-10, TNF-α, IL-6 and IL-1ß in the testis and epididymis. These results indicate that dietary Glu and Asp supplementation might enhance antioxidant capacity and regulate the secretion and expression of inflammatory cytokines to protect the testes and epididymis of boars against oxidative stress.

Prevention of Oxidative Stress by α-Ketoglutarate via Activation of CAR Signaling and Modulation of the Expression of Key Antioxidant-Associated Targets in Vivo and in Vitro.

α-Ketoglutarate (AKG) can act as an antioxidant both in vitro and in vivo. However, the mechanisms of the protective effects of AKG are still not well understood. We evaluated the effects of AKG supplementation on the regulation of the constitutive-androstane-receptor (CAR) pathway in porcine intestinal cells and piglets exposed to H2O2. Our data showed that AKG treatment significantly increased not only the intra- and extracellular levels of AKG (26.9 ± 1.31 µmol/g protein, 1064.4 ± 39.80 µmol/L medium) but also those of Asp (29.3 ± 0.21 µmol/g, 4.20 ± 0.11 µmol/L), Gln (24.82 ± 1.50 µmol/g, 1087.80 ± 16.10 µmol/L), and Glu (91.90 ± 3.6 µmol/g, 19.76 ± 1.00 µmol/L). There was approximately a 4-fold increase in α-ketoglutarate dehydrogenase mRNA levels in enterocytes and a simultaneous reduction in ROS levels ( P < 0.05). Moreover, AKG treatment increased the activities of the antioxidant enzymes and the efficiency of cellular respiration ( P < 0.05). AKG also regulated the mRNA levels of the target genes involved in antioxidant responses and xenobiotic detoxification in enterocytes. Increases in the protein levels of SOD1, SOD2, CAR, RXRα, and UCP2 and marked reductions in the expression levels of Nrf2 and Keap1 proteins ( P < 0.05) were observed after AKG administration in the H2O2-induced piglets. Our results indicated that AKG may protect against oxidative stress by activating CAR signaling and modulating the expression of key antioxidant-related targets, which improves cellular respiration and antioxidant capacity. The in vivo and in vitro effects of AKG suggest that it may prove to be useful in the reduction of oxidative stress in animal and human trials and subsequent prevention of gastrointestinal pathologies.

Anti-hyperlipidemic effect of rice bran polysaccharide and its potential mechanism in high-fat diet mice.

Hyperlipidemia occurs very often in modern society along with a high calorie intake and is regarded as one of the greatest risk factors for the prevalence of cardiac vascular disease (CVD). In this study, we investigated the anti-hyperlipidemic effect of the rice bran polysaccharides (RBP) and its mechanism in a high fat diet animal model. 60 ICR mice were randomly divided into 3 groups, which included Control, HFD (high fat diet) and HFD + RBP, and each group included 20 mice. The control group was fed with a standard diet while the other two groups were fed with HFD. In addition, the HFD + RBP group was fed with 500 mg kg-1 of rice bran polysaccharides by intragastric administration while the other two groups were intragastrically administered with water. The results showed that RBP treatment for 10 weeks obviously decreased the body weight, liver weight and adipose tissues of mice; and it decreased the levels of total cholesterol (TC), triglycerides (TG) and low density lipoprotein-cholesterol (LDL-c) in the plasma. H&E staining of the liver tissues showed that RBP treatment decreased the size of fat droplets compared with the HFD group. Microarray analysis revealed that RBP treatment results in 80 genes being up-regulated while 72 genes were down-regulated in the tissues of liver. IPA software analysis suggested that NF-κB may play a vital role in the lipid-lowering effect of RBP. Real-time quantitative PCR confirmed that the mRNA levels of PPAR-α, PPAR-γ, PPAR-δ, SREBP-1C, FASN, ACC, SIRT and CD36, which are related to lipid metabolism, were significantly regulated by RBP supplementation compared to HFD. The western blot analysis further confirmed these altered expressions after RBP treatment. Taken together, these results suggest that the oral administration of RBP exerts lipid-lowering in high fat diet mice via regulating the lipid metabolism-related gene expression.

Effects of Non-Starch Polysaccharides on Inflammatory Bowel Disease.

The incidence of inflammatory bowel disease (IBD) has increased considerably over the past few decades. In the present review, we discuss several disadvantages existing in the treatment of IBD and current understandings of the structures, sources, and natures of various kinds of non-starch polysaccharides (NSPs). Available evidences for the use of different sources of NSPs in IBD treatment both in vitro and in vivo are analyzed, including glucan from oat bran, mushroom, seaweed, pectin, gum, prebiotics, etc. Their potential mechanisms, especially their related molecular mechanism of protective action in the treatment and prevention of IBD, are also summarized, covering the anti-inflammation, immune-stimulating, and gut microbiota-modulating activities, as well as short-chain fatty acids (SCFAs) production, anti-oxidative stress accompanied with inflammation, the promotion of gastric epithelial cell proliferation and tissue healing, and the reduction of the absorption of toxins of NSPs, thus ameliorating the symptoms and reducing the reoccurrence rate of IBD. In summary, NSPs exhibit the potential to be promising agents for an adjuvant therapy and for the prevention of IBD. Further investigating of the crosstalk between immune cells, epithelial cells, and gut microorganisms in addition to evaluating the effects of different kinds and different molecular weights of NSPs will lead to well-designed clinical intervention trials and eventually improve the treatment and prevention of IBD.

Octacosanol Attenuates Inflammation in Both RAW264.7 Macrophages and a Mouse Model of Colitis.

Octacosanol has multiple biological functions. In this study, the anti-inflammatory effect and molecular mechanism of octacosanol were evaluated by using dextran sulfate sodium (DSS)-induced ulcerative colitis model in mice and lipopolysaccharide (LPS)-stimulated mouse macrophage RAW264.7 cells. The colitis mouse model was induced by 3.0% DSS in 8-week ICR mice and octacosanol orally administered with 100 mg/kg/day. The results showed that octacosanol significantly improved the health status of mice and reduced DSS-induced pathological damage in the colonic tissues. Octacosanol obviously inhibited the mRNA and protein expression levels of pro-inflammatory factors of colonic tissues. In vitro, octacosanol administration significantly reduced the expression of mRNA or protein of pro-inflammatory cytokines and the phosphorylation of c-Jun N-terminal kinase and p38, and it also partly prevented LPS-induced translocations of NF-κB and AP-1. Octacosanol has anti-inflammatory effect, and its molecular mechanism may be involved in downregulating the expression of inflammatory factors and blocking of MAPK/NF-κB/AP-1 signaling pathway.