Enzymatic Modification of Rice Bran Polysaccharides by Enzymes from Grifola Frondosa: Natural Killer Cell Cytotoxicity and Antioxidant Activity.

Rice bran polysaccharides (RBPSs) are the major active constituents of rice bran (RB). In this study, we utilized intracellular enzymes from Grifola frondosa to modify RBPSs, which were extracted from RB using ultrasound. To enhance the effect on natural killer (NK) cell cytotoxicity of modified polysaccharides (mRBPSs) generated from RBPSs, an orthogonal test (L9 [3]4 ) was employed to optimize the modification conditions. Based on the results of a single-factor test, the enzyme to polysaccharide ratio, reaction temperature, reaction pH, and reaction time were the main factors affecting mRBPSs-enhanced NK-cell cytotoxicity. The best conditions were determined to be an enzyme to polysaccharide ratio of 1:5, a reaction temperature of 40 °C, a reaction pH of 4, and a reaction time of 4 hr. By optimizing the conditions, the NK-cell cytotoxicity induced by mRBPSs6 was the highest, increasing by 12.01% ± 0.08%. Gas chromatographic analysis revealed that mRBPSs6 consists of rhamnose, arabinose, xylose, mannose, glucose, and galactose at a molar ratio of 7:21:6:5:53:48, which was 8:13:8:5:44:44 before modification. High-performance liquid chromatography results indicated molecular weights for the RBPSs of approximately 106 Da, which decreased to 104 to 105 Da after modification. Antioxidant activity tests revealed high capacity of mRBPSs6 for scavenging 1,1-diphenyl-2-picrylhydrazyl radicals and hydroxyl free radicals at 1.0 mg/mL. PRACTICAL APPLICATION: Rice bran polysaccharides (RBPSs) contain compounds with many biological activities. However, these polysaccharides difficult to absorb due to high molecular weights and unexposed active sites, which are the main factors that limit their use in functional foods. The results of this study demonstrate that modification of RBPSs using intracellular enzymes from an edible fungus alters the molecular weights and monosaccharide composition of RBPSs. In addition, immune and antioxidant activities of RBPSs were increased. The findings provide a new and beneficial application for rice bran.

Rice bran polysaccharides and oligosaccharides modified by Grifola frondosa fermentation: Antioxidant activities and effects on the production of NO.

Rice bran polysaccharides (RBPSs) are valuable compounds with many biological activities. In this work, a fungus called Grifola frondosa, was selected to ferment defatted rice bran water extracts and modify the RBPSs, which were then isolated by ethanol precipitation and deproteinization. GC analysis of fermented products suggested they are composed of glucose, arabinose, galactose, mannose, and xylose at a molar ratio of 9:5:8:2:5, which was 32:4:6:2:5 before fermentation. HPLC analysis revealed that the molecular weight of unfermented RBPS was distributed mainly from 103 to 104Da, and it changed to 102 to 103Da after fermentation. Antioxidant activities and effects on the production of NO were analyzed and it indicated that the scavenging ratios of hydroxyl and DPPH radicals by the fermented products were significantly enhanced compared to the unfermented ones, and also the products fermented for 9days exhibited two-way adjusting effects on the production of NO in macrophages.

HIV associated neurodegeneration requires p53 in neurons and microglia.

HIV infection of the central nervous system leads to HIV-associated dementia (HAD) in a substantial subset of infected individuals. The pathogenesis of neuronal dysfunction in HAD is not well understood, but previous studies have demonstrated evidence for activation of apoptotic pathways. The tumor suppressor transcription factor p53 is an apical mediator of neuronal apoptosis following a variety of injurious stimuli. To determine whether p53 participates in HAD, we exposed cerebrocortical cultures from wild-type and p53 deficient mice to the neurotoxic HIV envelope protein gp120. Using neuron/microglia co-culture of mixed p53 genotype, we observed that both neurons and microglia require p53 for gp120 induced neuronal apoptosis. Additionally, accumulation of p53 protein in neurons was recently reported in post-mortem cortical tissue from a small group of HAD patients. Using a much larger cohort of HAD cases, we extend this finding and report that p53 protein also increases in non-neuronal cells, including microglia. Taken together these findings demonstrate a novel role for p53 in the microglial response to gp120. Additionally, these findings, in conjunction with a recent report that monocytes expressing HIV-Tat also secrete neurotoxins that promote p53 activation, suggest that distinct HIV proteins may converge on the p53 pathway to promote neurotoxicity.