Polysaccharides are usually composed of more than ten monosaccharide units, which are connected by linear or branched glycosidic bonds. The immunomodulatory effect of natural polysaccharides is one of the most important bioactive function. In this review, molecular weight, monosaccharide (including galactose, mannose, rhamnogalacturonan-I arabinogalactan and uronic acid), functional groups (namely sulfate, selenium, and acetyl groups), types of glycoside bond connection (including β-1,3-D-glucosyl, α-1,4-D-glucosyl, β-1,4-D-glucosyl, α-1,6-D-glucosyl, β-1,4-D-mannosyl, and β-1,4-D-Xylopyranosyl), conformation and the branching degrees are systematically identified as their contribution to the immunostimulatory activity of polysaccharides. At present, studies on the structure-activity relationships of polysaccharides are limited due to their low purity and high heterogeneity. However, it is an important step in providing useful guidance for dietary supplements with polysaccharides. The chemical structures and the process of immune responses induced are necessary to be discussed. Polysaccharides may bind with the cell surface receptors to modulate immune responses. This review mainly discusses the structure-activity relationship of dietary polysaccharides.

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Several flavonoids have been recognized as nutraceuticals, and myricetin is a good example. Myricetin is commonly found in plants and their antimicrobial and antioxidant activities is well demonstrated. One of its beneficial biological effects is the neuroprotective activity, showing preclinical activities on Alzheimer, Parkinson, and Huntington diseases, and even in amyotrophic lateral sclerosis. Also, myricetin has revealed other biological activities, among them as antidiabetic, anticancer, immunomodulatory, cardiovascular, analgesic and antihypertensive. However, few clinical trials have been performed using myricetin as nutraceutical. Thus, this review provides new insights on myricetin preclinical pharmacological activities, and role in selected clinical trials.

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Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer's disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health.

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Background Dihydromyricetin (DMY) is an important plant flavonoid, which has received great attention due to its health-benefiting activities, including antioxidant, antimicrobial, anti-inflammatory, anticancer, antidiabetic and neuroprotective activities. DMY capsules have been sold in US as a nutraceutical supplement to prevent alcoholic hangovers. The major disadvantage associated with DMY is its chemical instability and poor bioavailability caused by the combined effects of its low solubility and poor membrane permeability. This limits its practical use in the food and pharmaceutical fields. Scope and approach The present paper gives an overview of the current methods for the identification and quantification of DMY. Furthermore, recent findings regarding the main biological properties and chemical stability of DMY, the metabolism of DMY as well as different approaches to increase DMY bioavailability in both aqueous and lipid phases are discussed. Key findings and conclusions Current trends on identification and quantification of DMY have been focused on spectral and chromatographic techniques. Many factors such as heat, pH, metal ions, could affect the chemical stability of DMY. Despite the diverse biological effects of DMY, DMY faces with the problem of poor bioavailability. Utilization of different delivery systems including solid dispersion, nanocapsule, microemuslion, cyclodextrin inclusion complexes, co-crystallization, phospholipid complexes, and chemical or enzymatic acylation has the potential to improve both the solubility and bioavailability. DMY digested in laboratory animals undergoes reduction, dehydroxylation, methylation, glucuronidation, and sulfation. Novel DMY delivery systems and basic pharmacokinetic studies of encapsulated DMY on higher animals and humans might be required in the future.

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Alcohol use disorders (AUDs) constitute the most common form of substance abuse. The development of AUDs involves repeated alcohol use leading to tolerance, alcohol withdrawal syndrome, and physical and psychological dependence, with loss of ability to control excessive drinking. Currently there is no effective therapeutic agent for AUDs without major side effects. Dihydromyricetin (DHM; 1 mg/kg, i.p. injection), a flavonoid component of herbal medicines, counteracted acute alcohol (EtOH) intoxication, and also withdrawal signs in rats including tolerance, increased anxiety, and seizure susceptibility; DHM greatly reduced EtOH consumption in an intermittent voluntary EtOH intake paradigm in rats. GABA(A) receptors (GABA(A)Rs) are major targets of acute and chronic EtOH actions on the brain. At the cellular levels, DHM (1 μM) antagonized both acute EtOH-induced potentiation of GABA(A)Rs and EtOH exposure/withdrawal-induced GABA(A)R plasticity, including alterations in responsiveness of extrasynaptic and postsynaptic GABA(A)Rs to acute EtOH and, most importantly, increases in GABA(A)R α4 subunit expression in hippocampus and cultured neurons. DHM anti-alcohol effects on both behavior and CNS neurons were antagonized by flumazenil (10 mg/kg in vivo; 10 μM in vitro), the benzodiazepine (BZ) antagonist. DHM competitively inhibited BZ-site [(3)H]flunitrazepam binding (IC(50), 4.36 μM), suggesting DHM interaction with EtOH involves the BZ sites on GABA(A)Rs. In summary, we determined DHM anti-alcoholic effects on animal models and determined a major molecular target and cellular mechanism of DHM for counteracting alcohol intoxication and dependence. We demonstrated pharmacological properties of DHM consistent with those expected to underlie successful medical treatment of AUDs; therefore DHM is a therapeutic candidate.

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