Amyloid-β protein (Aβ) is known to increase free radical production in neuronal cells, leading to cell death by oxidative stress. The purpose of this study was to evaluate the protective effects of PineXol® on Aβ25-35 induced neuronal cell death. Rat pheochromocytoma (PC-12) cells were pre-treated with 100 μg/mL of PineXol® for 2 h. The cells were exposed to single dose of 30 μM Aβ25-35 for 24 h. Cell death was assessed by a cell count kit-8 (CCK-8) assay, lactate and dehydrogenase (LDH) release assay. An Apoptotic process was analyzed by a protein expression of the Bcl-2 family using western blotting. Cell viability increased in PC-12 cells treated with both Aβ25-35 and PineXol®, compared to the control group. PineXol® induced a decrease of the Bcl-2 protein expression (p<0.05), while Bax and Sod1 increased (p<0.05), indicating attenuation of Aβ25-35 induced apoptosis. These results suggest that PineXol® may be a good candidate for the prevention of Alzheimer’s disease(AD).

The purpose of this study was to evaluate the protective effect of PineXol® on H2O2-induced cell death in SK-N-MC cells, and in early stage focal ischemia rodent model. SK-N-MC cells were pre-treated with 200 μM H2O2 or various concentrations of PineXol® (10, 30, and 50 pg/mL) for 24 h, and then exposed to H2O2 for 3 h. Cell death was assessed by the CCK-8 assay, reactive oxygen species (ROS) assay, and lactate and dehydrogenase (LDH) release assay. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) expressions were also analyzed by western blotting. Focal ischemia rodent model was used as the in vivo model, and different concentrations of PineXol® (1, 10, and 100 mg/kg) were administered. One week after administration, reduction of infarct volume was analyzed by TTC staining. Cell viability of H2O2-treated SK-N-MC cells significantly increased by pre-treatment of PineXol® (p<0.05). PineXol® pre-treatment also induced significant decrease of ROS and LDH expressions. However, PineXol® did not affect the infarct volume. These results suggest that PineXol® has significant neuroprotective effect in vitro, but statistical significance was not confirmed in the in vivo focal ischemia mo

Menopausal status and hormonal changes are important factors related to the prevalence of metabolic syndrome in women. Nutrient intake is also a risk factor for metabolic syndrome. Although, postmenopausal status and hormonal changes result in a 60% increased risk for metabolic syndrome, there has been no method to elucidate the effects of nutrient intake on metabolic syndrome following menopause. This study was conducted to evaluate the effects of nutrient intake by menopausal women on the prevalence of metabolic syndrome. All data were obtained from the Korean National Health and Nutrition Examination Survey 2007–2009. Menopausal women showed a 1.8-fold increase in the prevalence of metabolic syndrome. Metabolic syndrome group showed significantly lower values in calcium, iron, vitamin A, carotin, retinol and riboflavin intake than those of normal group in premenopausal women. In postmenopausal women, there are significant differences in crude fiber, calcium, iron, potassium, riboflavin and niacin. Indeed, different patterns of nutrient intake were observed by menopausal status and metabolic syndrome. As menopause cannot be controlled, a diet with adequate nutrient intake may be useful to control the rapid increase in the prevalence of metabolic syndrome due to menopause.

This study was conducted to evaluate the neuroprotective effects of Cheonggukjang extract in in-vitro and in-vivo models. T98G-human glioblastoma cells were pretreated with various concentrations (1~10 mg/mL) of Cheonggukjang extract for 24 h and then exposed to H2O2 (1 mM) for 3 h. The neuroprotective effects of Cheonggukjang extract were measured using a CCK-8 kit assay, total antioxidant capacity (TAC) assay, reactive oxygen species (ROS) assay, and lactate dehydrogenase (LDH) release assay. The early stage focal ischemia rodent model was used as the in-vivo neurotoxicity model. Various concentrations (10~200 mg) of Cheonggukjang extract were administered to the animal models for 1 week. Peripheral blood was analyzed for glutathione peroxidase (GPx) expression by ELISA, and infarct volume reduction was analyzed by TTC staining. Cheonggukjang extract significantly (p<0.05) increased cell viability in T98G cells against H2O2 as well as against the induced neurotoxicity. Indeed, treatment with the Cheonggukjang extract induced a decrease in ROS and LDH expression and increased TAC significantly (p<0.05). However, Cheonggukjang extract did not induce a decrease in infarct volume or an increase in GPx expression in the in-vivo model. Despite the limitation in neuroprotection, Cheonggukjang extract may be useful for treating ROS injury.