AbstractThis present study was designed to evaluate the immunomodulatory activity of Konjac glucomannan (KGM) on immunosuppressed mice induced by cyclophosphamide (CTX) treatment. The mice immunodeficiency model was established by CTX. KGM was used to modulate the activities of immunosuppressive mice. It was proved that KGM could promote the proliferation of lymphocyte, thymus, and spleen indices, and alleviate the atrophy of immune organs and weight loss. Besides, in mice serum, the levels of cytokines including TNF‐α, IgG, IL‐2, and the contents of hemolysin were also increased after treatment with KGM. Furtherly, in nonspecific immunity, KGM could enhance natural killer (NK) cell lethality and pinocytic activity of mouse peritoneal macrophages. Therefore, all of these results revealed that KGM could improve the reduced immunity of CTX‐induced mice via modulation innate immunity and adaptive immunity.

Polysaccharides are a group of compounds composed of multiple monosaccharides of the same or different structures combined by glycosidic bonds, and are widely found in animals and plants and in the cell walls of microorganisms. Polysaccharides possess the advantages of high safety and low toxicity. Recent studies revealed that polysaccharides have a wide range of biological activities including immunoregulation, anti-tumor, antiviral, antioxidant activities, and blood glucose-and lipid- lowering effects. The effects of polysaccharides in improving insulin sensitivity and regulating glucose and lipid metabolism have drawn much attention from researchers. Many polysaccharides can reduce blood glucose and blood lipid by repairing pancreatic islet cells, improving insulin resistance, regulating intestinal flora, enhancing antioxidant capacity, and regulating the activities of key enzymes in glucose and lipid metabolism. This reviews examines the role and mechanism of polysaccharides in regulating glucose and lipid metabolism. The mechanisms of polysaccharide in regulating glucose metabolism include repairing islet cells and increasing insulin content, increasing insulin sensitivity and improving insulin resistance, regulating the activity of key enzymes in glucose metabolism, increasing synthesis of liver glycogen, and regulating intestinal flora. Polysaccharides can also regulate glucose metabolism by improving immune regulation and antagonizing glucagon. Polysaccharide also regulate lipid metabolism by regulating lipid absorption, expression of the related genes such as PPAR-α, enzyme activities in lipid metabolism, improving antioxidant capacity, and modulating intestinal flora and signaling pathways.

Hyperglycemia-induced apoptosis and oxidative stress injury are thought to play important roles in the pathogenesis of diabetic nephropathy (DN). Attenuating high glucose (HG)-induced renal tubular epithelial cell injury has become a potential approach to ameliorate DN. In recent years, burdock fructooligosaccharide (BFO), a water-soluble inulin-type fructooligosaccharide extracted from burdock root, has been shown to have a wide range of pharmacological activities, including antiviral, anti-inflammatory, and hypolipidemic activities. However, the role and mechanism of BFO in rat renal tubular epithelial cells (NRK-52E cells) have rarely been investigated. The present study investigated the protective effect of BFO on HG-induced damage in NRK-52E cells. BFO could protect NRK-52E cells against the reduced cell viability and significantly increased apoptosis rate induced by HG. These anti-oxidative stress effects of BFO were related to the significant inhibition of the production of reactive oxygen species, stabilization of mitochondrial membrane potential, and increased antioxidant (superoxide dismutase and catalase) activities. Furthermore, BFO increased the expression of Nrf2, HO-1, and Bcl-2 and decreased the expression of Bax. In conclusion, these findings suggest that BFO protects NRK-52E cells against HG-induced damage by inhibiting apoptosis and oxidative stress through the Nrf2/HO-1 signaling pathway.

Gel mixtures play an important role in food processing. We investigated the interactions among three polysaccharides, konjac glucomannan (KGM), κ-carrageenan (κCG), and modified corn starch (MCS), by applying central composite design of response surface methodology to model and optimize the weighted value (WV) for water holding capacity (WHC), hardness (H), and springiness (S) of gelation. Using statistical analysis, we determined the optimum gel mixture formulation as 6 g κCG, 8 g KGM, and 9 g MCS, with a maximum WV of 0.945. The order of influence of the three polysaccharides on the gel properties of the mixture was κCG > MCS > KGM. Scanning electron microscopy revealed that KGM and κCG formed a spiral structure with the gaps filled with MCS; the three polysaccharides formed a closely networked structure. Our results demonstrated that optimizing gel mixture using response surface methodology is effective, particularly, where high-quality gel mixture is required.

Diabetic nephropathy (DN) is the second most common complication of diabetes mellitus after cardiovascular complications. Endoplasmic reticulum (ER) stress is known to be associated with DN. Resveratrol (RSV) exhibits anti-oxidative, anti-inflammatory and cytoprotective effects. Therefore, the aims of the present study were to investigate the role of RSV in the inhibition of high concentration glucose (HG)-induced apoptosis in renal tubular cells, as well as to examine the protective effects of RSV against diabetes-mediated renal damage via inhibition of ER stress in DN. RSV was orally administered to diabetic db/db mice once a day for 12 consecutive weeks. Compared with untreated db/db mice, treating db/db mice with RSV significantly decreased urine albumin excretion and the urine albumin to creatinine ratio, and attenuated renal histopathological injury. Furthermore, RSV treatment resulted in decreased expression levels of glucose-regulated protein of 78 kDa and C/EBP-homologous protein (two ER stress markers) and caspase12 in murine kidneys. RSV administration also inhibited the apoptosis of NRK-52E cells and activation of the ER stress signal transduction pathway induced by HG treatment in vitro. Collectively, the present results indicated that RSV protected renal tubular cells against HG-induced apoptosis in DN by suppressing ER stress.