Gi-Ok Kim

Compounds with Tyrosinase Inhibition, Elastase Inhibition and DPPH Radical Scavenging Activities from the Branches of Distylium racemosum Sieb. et Zucc

Twenty compounds were isolated from the ethanol extract of Distylium racemosum branches and their inhibitory activities on tyrosinase, elastase and free radicals evaluated. The isolated compounds were identified as dibenzofurans (1–4), abscisic acid (5), 6′‐O‐galloylsalidroside (6), catechin derivatives (7–11), gallic acid derivatives (12–14), tyrosol (15), flavonoids (16–18), lupeol (19) and 1,2,3,6‐tetragalloylglucose (20). For study of tyrosinase inhibition activities, when compared with arbutin (IC50 48.8 μg/mL), four compounds (8, 11, 13, 17) showed higher activities, with IC50 values of 4.8, 30.2, 40.5 and 37.7 μg/mL, respectively. For the elastase inhibition test, dibenzofuran 1 showed greater activity than the positive control, oleanolic acid (IC50 9.7 μg/mL), with an IC50 of 7.7 μg/mL. In the studies on DPPH radical scavenging activities, five compounds (11, 12, 13, 14, 15) showed higher activities than ascorbic acid (IC50 5.0 μg/mL), with IC50 values of 4.6, 3.9, 2.9, 3.8 and 4.7 μg/mL, respectively. Copyright

Neuroprotective effect of methyl lucidone against microglia-mediated neurotoxicity.

Excessive microglial activation-mediated neurotoxicity has been implicated in playing a crucial role in the pathogenesis of stroke and neurodegenerative diseases. Therefore, much attention has been paid to therapeutic strategies aimed at suppressing neurotoxic microglial activation. The microglial regulatory mechanism of methyl lucidone, a cyclopentenedione isolated from the stem bark of Lindera erythrocarpa Makino, was investigated in the present study. Methyl lucidone treatment (0.1-10 μM) significantly inhibited lipopolysaccharide (LPS, 100 ng/ml, 24 h)-stimulated nitric oxide (NO) production in a dose-dependent manner in both primary cortical microglia and BV-2 cell line. Moreover, it strongly inhibited LPS-stimulated secretion of pro-inflammatory cytokines, such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). Methyl lucidone treatment markedly induced down-regulation of LPS-induced nuclear translocation of nuclear factor κB (NF-κB) through preventing the degradation of the inhibitory protein IκBα. In addition, phosphorylation of Akt and mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase (ERK) and p38 kinases were also suppressed by methyl lucidone. The cell viabilities of HT-22 neurons were significantly attenuated by treatment of the conditioned media containing neurotoxic secretary molecules from LPS-stimulated microglia. However, methyl lucidone significantly blocked neuronal cell death induced by microglial conditioned media. These neuroprotective effects of methyl lucidone were also confirmed in a neuron-microglia co-culture system using EGFP-transfected B35 neuroblastoma cell line. Taken together, these results suggest that methyl lucidone may have a neuroprotective potential via inhibition of neurotoxic microglial activation implicated in neurodegeneration.

Hydroclathrus clathratus induces apoptosis in HL-60 leukaemia cells via caspase activation, upregulation of pro-apoptotic Bax/Bcl-2 ratio and ROS production

Hydroclathrus clathratus is a well-known endemic alga in Korea having antiviral effects. In this study, its ability to induce cytotoxicity and apoptosis in cultured HL-60 human promyelocytic leukaemia cells was investigated. Treatment of the human promyelocytic leukaemia cell line (HL-60), cells with various concentrations of H. clathratus ethyl acetate extract (HCE) resulted in growth inhibition and induction of apoptosis in a dose-dependent manner, as determined by the cell viability, chromatin condensation, DNA fragmentation and sub-G1 phase accumulation. The HCE-induced apoptotic cell-death was associated with caspase-3 and caspase-9 activation, and poly ADP-ribose polymerase (PARP) degradation in the HL-60 cells. This increase in the HCE-induced apoptosis was also associated with a reduction in the levels of Bcl-xL, a potent cell-death inhibitor, and an increase in the levels of the Bax protein, which heterodimerises with and thereby inhibits Bcl-2. Finally, the intracellular reactive oxygen species (ROS), especially hydrogen peroxide (H2O2) and superoxide anion (O2 − ), were found to be elevated after HCE treatment of these cells. In addition, antioxidant N-acetyl cysteine (NAC) pretreatment almost completely inhibited the HCE-induced apoptosis, suggesting that ROS are the key mediators of HCE-induced apoptosis. In conclusion, HCE induces apoptosis of human leukaemia cells through caspase activation, upregulation of the pro-apoptotic Bax/Bcl-2 ratio and ROS generation. Therefore, it may have anticancer properties valuable for application in food and drug products.

Lindera erythrocarpa Makino extract reduces obesity induced by high-fat diet in rats

Lindera erythrocarpa Makino (LE) is widely distributed on Jeju Island, where it has been used for various traditional therapies. Effects of a crude extract of LE were examined in rats with obesity induced by a high-fat diet (HFD). Anti-obesity effects were followed in rats receiving orally administered vehicle, 100mg/kg extract, or 250 mg/kg LE extract, for 56 days. LE extract (250 mg/kg) suppressed increases in body weight and epididymal fat, with amelioration of fatty changes in the liver. Additionally, serum levels of alanine aminotransferase, aspartate aminotransferase, and total cholesterol were significantly decreased compared with those of vehicle-treated groups (p