Inhibitory effect of pine extract on alpha-glucosidase activity and postprandial hyperglycemia.

OBJECTIVE: This study investigated the inhibitory effect of pine bark extract (PBE) and needle extract on carbohydrate-hydrolyzing enzymes and the hypoglycemic effect in diabetic mice (Lep(ob) [ob/ob]). METHODS: Pine bark and needle were dried and then placed in ethanol, and the extracts were assayed for the measurement of inhibition mode of PBE against alpha-amylase (EC 3.2.1.1) and alpha-glucosidase (EC 3.2.1.20). We also investigated the effect of long-term treatment with extracts on levels of postprandial blood glucose, body weight, food efficiency ratio, and gene expression of glucose transporter-4 in quadriceps muscle in diabetic mice (Lep(ob) [ob/ob]). RESULTS: The PBE showed competitive inhibition against salivary alpha-amylase and the combination of non-competitive and uncompetitive inhibition against yeast alpha-glucosidase. In animal experiments, PBE effectively suppressed the increase of postprandial blood glucose level by delaying absorption of diet, and body weights of the group that received PBE were significantly lower than that in the group administered 0.5% carboxylmethyl cellulose (control) 21 d after administration. CONCLUSIONS: PBE can be used to suppress postprandial hyperglycemia of diabetic patients. It also can be applied for control of obesity by decreasing the food efficiency ratio, especially carbohydrates.

Neuroprotective effects of grape seed extract on neuronal injury by inhibiting DNA damage in the gerbil hippocampus after transient forebrain ischemia.

Grape seed extract (GSE) possess cardioprotective abilities by functioning as in vivo antioxidants and by virtue of their ability to directly scavenge ROS including hydroxyl and peroxyl radicals. In the present study, we investigated the neuroprotective effects of grape seed extract (GSE) in the gerbil hippocampus after 5 min transient forebrain ischemia. Neuronal cell density in GSE-treated ischemic animals was significantly increased as compared with vehicle-treated ischemic animals 4 days after ischemic insult. In the GSE-treated groups, about 60% of pyramidal cells of the sham-operated group were stained with cresyl violet 4 days after ischemic insult. In this study, we found that GSE had neuroprotective effects on neuronal injury by inhibiting DNA damage in the CA1 region after ischemia. In vehicle-treated groups, 8-hydroxy-2'-deoxyguanosine (8-OHdG) immunoreactivity was significantly changed time-dependently, whereas the immunoreactivity in the GSE-treated group was similar to the sham-operated group. In addition, we confirmed that astrocytes and microglia did not show significant activation in the CA1 region 4 days after ischemia-reperfusion, because many CA1 pyramidal cells were not damaged. Therefore, these results suggest that GSE can protect ischemic neuronal damage by inhibiting DNA damage after transient forebrain ischemia.