Jae-Yong Kim

Antioxidative Effects of Peanut Sprout Extracts

For the long-term goal of using peanut sprouts as a functional food material, the total polyphenol content and the antioxidant activity of methanol extracts were examined with use of 9 day-old peanut sprouts and peanuts collected in Chungbuk, Gyeongbuk and Jeonbuk provinces of Korea, China and Vietnam. The polyphenol levels in the sprout extracts were higher than those of the peanut extracts. The phenolic content of the Gyeongbuk peanut sprout extract (20.4 mg/g) was the highest of the tested samples. After 9 days of germination the peanut sprout extracts had higher activities than those of the peanut extracts. In particular, the activity of Gyeongbuk peanut sprout extract was the highest (37.67% at a concentration of ), and its reducing power demonstrated a similar trend. The DPPH radical scavenging activities were measured for methanol extracts of cotyledon, root and stem of Gyeongbuk peanut sprouts; the highest (90.96% at a concentration of ) was the activity of cotyledon. ABTS radical scavenging and -carotene bleaching activities also were higher in the cotyledon extract than in those of the root or the stem. The resveratrol content was higher in the Gyeongbuk peanut sprout extract than in the Gyeongbuk peanut extract (and , respectively). These results suggest that peanut sprouts potentially could be used as a functional food material exhibiting antioxidant effects.

Induction of apoptosis in HT-29 colon cancer cells by crude saponin from Platycodi Radix.

This study examined the apoptotic effects of crude saponins acquired from the roots of Platycodon grandiflorum (SPR) in HT-29 human colon cancer cells. SPR decreased HT-29 cell proliferation in dose- and time-dependent manners by inducing apoptosis via DNA fragmentation and poly (ADP-ribose) polymerase (PARP) cleavage. The apoptosis induced by SPR was associated with the activation of initiator caspases-8 and -9, as well as the effector caspase-3. SPR stimulated Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9. SPR increased the expression of the pro-apoptotic protein, Bax, and decreased the expression of the anti-apoptotic protein, Bcl-2. SPR also increased the expression of the caspase-independent mitochondrial apoptosis factor, AIF, in HT-29 cells. These results indicate that SPR inhibits HT-29 cell proliferation by inducing apoptosis, which may be mediated via both caspase-dependent and -independent pathways.

α-Mangostin-induced apoptosis is mediated by estrogen receptor α in human breast cancer cells.

In this study, we evaluated the effects of α-mangostin on cell growth inhibition and induction of apoptosis in MCF-7 ERα-positive human breast cancer cells. Our results showed that α-mangostin inhibited MCF-7 cell proliferation whereas ERα-negative MDA-MB-231 cells were less sensitive to the agent. Additionally, α-mangostin effectively induced apoptosis as evidenced by the appearance of apoptotic nuclei observed with Hoechst 33258 staining and evaluation of sub-G1 DNA contents by flow cytometry. α-Mangostin also activated caspases-8, -9, and -7; increased the protein levels of Bax, p53, and cytosolic cytochrome c; and induced PARP cleavage while reducing Bid and Bcl-2 protein expression. In addition, apoptosis-inducing factor (AIF) was transported from mitochondria to the cytosol after α-mangostin treatment. α-mangostin also induced apoptosis in 17-β-estradiol (E2)-stimulated MCF-7 cells in parallel with the non-stimulated cells. Moreover, treatment with 10μM α-mangostin for 48h specifically decreased the expression of ERα and pS2, an estrogen-responsive gene, in MCF-7 cells. Furthermore, knockdown of ERα expression in MCF-7 cells with siRNA attenuated α-mangostin-induced cell growth inhibition and caspase-7 activation. These results suggest that ERα is required for α-mangostin-induced growth inhibition and apoptosis in human breast cancer cells. Therefore, α-mangostin may be used to prevent and treat of ER-positive breast cancer.

Supplementation of SK1 from Platycodi Radix Ameliorates Obesity and Glucose Intolerance in Mice Fed a High-Fat Diet

This study investigated the beneficial effects of SK1 on obesity and insulin resistance in C57BL/6 mice, which were fed a high-fat diet (37% calories from fat). SK1 is an edible saponin-rich compound from Platycodi radix. The mice were supplemented with two doses of SK1 (0.5% and 1.0%, wt/wt) for 9 weeks. The body weight, visceral fat mass, and adipocyte area were significantly decreased in the SK1 supplemented-groups in a dose-dependent manner compared to the high-fat group. The SK1 supplement significantly lowered plasma triglycerides, total cholesterol, and free fatty acid levels, whereas it significantly elevated the fecal excretion of lipids in the diet-induced obese mice. Supplementation of SK1 decreased the triglyceride and cholesterol levels and the accumulation of lipid droplets in the liver compared to the high-fat control group. High-fat diet induced glucose intolerance and insulin resistance with the elevation of blood glucose levels compared to the normal group; however, the SK1 supplement significantly improved postprandial glucose levels and insulin resistance index. After 9 weeks of being fed a high-fat diet, the mice presented with significantly increased activities of hepatic fatty acid synthase, fatty acid beta-oxidation, and glucokinase; however, both 0.5% and 1.0% SK1 supplementation normalized these activities. Notably, SK1 supplementation effectively diminished the ratio of fatty acid biosynthesis to fatty acid oxidation compared to the high-fat group. These results indicate that SK1 exhibits a potential anti-obesity effect and may prevent glucose intolerance by reducing body weight and fat accumulation, increasing fecal lipid excretions, and regulating hepatic lipid and glucose metabolism in high-fat fed mice.

Mechanisms of thiosulfinates from Allium tuberosum L.-induced apoptosis in HT-29 human colon cancer cells.

This study was performed to elucidate the apoptotic pathways by thiosulfinates, major biologically active components of Allium tuberosum L., in HT-29 human colon cancer cells. Thiosulfinates significantly induced cell death in dose- and time-dependent manners in HT-29 cells, which is associated with apoptosis. Thiosulfinates activated the initiator caspase-8, and -9, and the effector caspase-3. In the present study, thiosulfinates were found to stimulate Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9. Thiosulfinates down-regulated the expression of the anti-apoptotic protein Bcl-2, and up-regulated the expression of the pro-apoptotic protein Bax. We also found that thiosulfinates increased the expression of AIF, a caspase-independent mitochondrial apoptosis factor, and induced DNA fragmentation and chromatin condensation in HT-29 cells. These results indicate that thiosulfinates from A. tuberosum L. inhibited cell proliferation and activated both the caspase-dependent and caspase-independent apoptotic pathways in HT-29 cells.

Cultivated Orostachys japonicus Induces Apoptosis in Human Colon Cancer Cells

This study was performed to elucidate the anticancer activities and the mechanism of chloroform fractions from cultivated Orostachys japonicus (CFCOJ) in human colon cancer cells. CFCOJ markedly decreased viable cell numbers in both a dose-dependent and time-dependent manner within SW480 cells. Cell death induced by CFCOJ increased cell populations in the sub-G1 phase, as well as the formation of apoptotic bodies, nuclear condensation, and induced DNA fragmentation. CFCOJ-induced apoptosis was associated with the activation of initiator caspase-8 and -9, as well as the effector caspase-3. CFCOJ also stimulated Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9. CFCOJ increased the expression of the proapoptotic protein, Bax, and decreased the expression of the antiapoptotic protein, Bcl-2. These results indicate that CFCOJ exert anticancer effects on human colon cancer SW480 cells through a caspase-dependent apoptotic pathway.

Production of novel vinegar having antioxidant and anti-fatigue activities from Salicornia herbacea L.

BACKGROUND Salicornia herbacea L. is a halophyte that grows in salt marshes and contains significant amounts of salts and minerals. Because it is known as a folk medication to treat diseases, various processed products such as powder, globular type of powder, laver and extract have been developed. However, it is difficult to process as a drink because of its high salinity. In the present study, glasswort vinegar (GV) containing high amounts of organic acids and minerals was developed via two-step fermentation with unpolished rice substrates and investigated its antioxidant and anti-fatigue activities. RESULTS GV showed various free radical scavenging effects, reducing power, oxidized-LDL inhibition and superoxide dismutase-like activities. Compared with the control group (orally administered 7 g kg(-1) distilled water), the GV supplementation group showed increased running endurance and had higher glycogen accumulation in liver and muscles of rats exhausted by exercise. Furthermore, the GV-administered group demonstrated significantly elevated lactate and ATP metabolism, promoting enzyme activities such as muscle creatine kinase and lactate dehydrogenase, whereas serum fatigue biomarkers such as ammonia, lactate and inorganic acid were markedly decreased. CONCLUSION These results indicate that GV can be used as a functional food for the development of a dietary beverage to alleviate fatigue.

Lethariella zahlbruckneri Acetone Extract-Induced Apoptosis of MCF-7 Human Breast Cancer Cells Involves Caspase Cascade and Mitochondria- Mediated Death Signaling

Lethariella zahlbruckneri has been traditionally used in tea and medicines in China. This study aimed to evaluate the anti-cancer properties of L. zahlbruckneri acetone extract (AEL) and to explore its potential mechanisms on MCF- 7 human breast cancer cells. The polyphenol and flavonoid concentrations of were 14.4 mg gallic acid equivalent/g and 6.5 mg quercetin equivalent/g, respectively. AEL inhibited the growth of MCF-7 cells in a dose- and time dependent manner. AEL significantly induced apoptotic cell death, resulting in an increase in the sub-G1 apoptotic cell population, apoptotic DNA fragmentation, and a morphological change. Pretreatment with a caspase inhibitor modestly attenuated the AEL-induced increase in the sub-G1 cell population, implying that caspases play a partial role in AEL-induced apoptosis. Moreover, AEL-induced apoptosis was associated with changes of caspase activities, up-regulation of the apoptotic protein (Bax), and down-regulation of the anti-apoptotic protein (Bcl-2). AEL also induced apoptosis-inducing factor-release from mitochondria, indicating apoptosis stimulation through a caspaseindependent pathway. These results suggest that AEL exerts its anti-cancer effects on MCF-7 human breast cancer cells through mitochondrial caspase-dependent and caspase-independent apoptotic pathways.