Influence of Adding Chinese Yam (Dioscorea opposita Thunb.) Flour on Dough Rheology, Gluten Structure, Baking Performance, and Antioxidant Properties of Bread.

Impacts of wheat flour substituted with various levels of Chinese yam (Dioscorea opposita Thunb.) flour (from 0% to 25%) on the dough rheological characteristics, gluten structure, baking performance, and antioxidant properties of bread were investigated. The water absorption increased significantly (p < 0.05), while development time and stability decreased remarkably (p < 0.05) as the proportion of yam flour increased. SEM results indicated that the addition of yam flour destroyed the gluten network structure in the dough. Fourier Transform Infrared Spectroscopy (FTIR) spectra showed that addition of yam flour decreased the content of α-helix and ß-sheet in gluten. With the increase in the proportion of yam flour, the specific volume and overall acceptability decreased (p < 0.05) whereas the total phenolics content (TPC), polysaccharides content, total flavonoids content (TFC), allantoin content, The 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging capability, fractal dimension, and hardness increased (p < 0.05). Overall, breads made of wheat flour replacement with no more than 15% Guihuai number 2 yam flour were of a high quality and had more antioxidant properties. These showed that Guihuai number 2 had broad application prospects in baked products.

Protection of capsaicin against hypoxia-reoxygenation-induced apoptosis of rat hippocampal neurons.

The aim of this study was to investigate the effect of capsaicin on hypoxia-reoxygenation (H/R)-induced apoptosis in primary rat hippocampal neurons. Three hours of hypoxia (1% O2) and subsequent reoxygenation for 24 h significantly increased the apoptotic death of hippocampal neurons, as evidenced by increases in both TUNEL-positive cell number and caspase-3 activity. Pretreatment with capsaicin (3-30 micromol/L) or the caspase-3-specific inhibitor acetyl-DEVD-CHO (100 micromol/L) markedly attenuated H/R-induced apoptosis in hippocampal neurons. Capsaicin also markedly induced the phosphorylation of Akt. The phosphoinositide 3-kinase (PI3K) inhibitor LY294002 (10 micromol/L) prevented any capsaicin-induced survival effect in hippocampal neurons. Intracellular levels of reactive oxygen species (ROS), which were greatly increased after H/R, were significantly inhibited by capsaicin, pyrrolidine dithiocarbamate (PDTC) (50 micromol/L), and LY294002. Taken together, these data suggest that capsaicin protects against H/R-induced apoptosis of hippocampal neurons via the PI3K/Akt-mediated signaling pathway, which is related to the inhibition of oxidative stress and caspase-3 activation.

Brief small intestinal ischemia lessens renal ischemia-reperfusion injury in rats.

Ischemic preconditioning (IPC) not only reduces local tissue injury caused by subsequent ischemia-reperfusion (IR) but may also have a beneficial effect on IR injury of tissues remote from those undergoing preconditioning. In this study, we investigated the effect of small intestinal IPC on renal IR injury in rats. Renal IR injury was induced by a 45-min renal artery occlusion and reperfusion for 2 or 24 h in rats with a previous contralateral nephrectomy, and ischemic preconditioning was induced by 3 cycles of 8-min ischemia and 5-min reperfusion of the small intestine. We then measured the concentrations of plasma creatinine (Cr) and blood urine nitrogen (BUN) and the level of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and catalase (CAT) in the renal cortex. Renal histopathology also was evaluated. Pretreatment with intestinal ischemic preconditioning significantly alleviated renal IR injury, as shown by decreases in the levels of Cr, BUN, and MDA, decreased renal morphologic change, and improved preservation of SOD and CAT activities. These results suggest that remote ischemic preconditioning of the small intestine protects against renal IR injury by inhibition of lipid peroxidation and preservation of antioxidant enzyme activities.