This study was undertaken to determine free radical scavenging capacity and oxidative DNA damage protecting activity of methanol extract of red tea stem. The extract was subjected to assess their antioxidant potential using various in vitro systems such as DPPH•, ABTS•+ , super oxide and nitric oxide free radicals and it exhibited IC50 values of 68.88 ± 1.1, 12.08 ± 0.65, 404.38 ± 1.6, 93.6 ± 2.7, µg/mL respectively. Red tea extract also showed ferric reducing ability (FRAP) with 2606.85 mmol Fe (II)/g of extract. Furthermore, Methanol extract of red tea stem showed significant DNA damage protecting activity in concentration dependent manner against H2O2+UV induced photolysis on pUC19 plasmid DNA. Results of this study showed that the methanol extract of Red Tea stem has strong antioxidant potential along oxidative DNA damage protecting capacity that would be the significant sources of natural antioxidants, which might be helpful in preventing the progress of various oxidative stress generated diseases. Further study is necessary for isolation and characterization of the active antioxidants, which may serve as a potential source of natural antioxidant.

Inflammatory bowel disease (IBD) is a group of chronic disorders of unknown etiology characterized by inflammation of the gastrointestinal tract. Recent data showed that the development of IBD is associated with the interplay of genetic, bacterial, and environmental factors and dysregulation of the intestinal immune system. We investigated how the gut cells were repaired after injury in Drosophila melanogaster. In this study we made D. melanogaster intestine damage model by oral feeding with variety IBD inducer such as pathogenic bacteria Serratia marcescens, Dextran Sulfate Sodium (DSS) and bleomycin, because its function is very similar with human, even though D. melanogaster has relatively simple organism. We repeated oral feeding with variety IBD inducer and got the survival rate and 50% lethal dose (LD50). After feeding with IBD inducer, we investigated the change of the intestinal stem cells, innate immune-related gene expression, and apoptosis in D. melanogaster gut. We examined the Delta, stem cell marker, staining image in the gut after feeding with DSS and S. marcescens with LD50 concentration. The Delta positive cells greatly increased in gut cells damaged by DSS or S. marcescens. This result supports the idea that intestinal gut stem cells are increased after gut cell damage and play very important role in damaged cell repair. Expression level of antimicrobial peptides was dramatically up-regulation after gut damage. As a result of TUNEL (terminal deoxynucleotidyl transferase mediated X-dUTP nick end labeling) assay, we confirmed that cell death by apoptosis was very increased in DSS feeding flies. Accordingly, we suggest that D. melanogaster is a proper IBD model organism to study how intestine damage can be repaired.

Ostrinia furnacalis Guenee is the most important pest of Zea may L. Little is known about combining ability for stem damage to this insect. The objective of this study was to estimate of resistance to stem damage by the Oriental corn borer. The importance

Caulis Bambusae in Taenia is widely used in Korea and China due to its various pharmacological activity. The present study aims to investigate the effect of the methanol extract of Caulis Bambusae in Taenia (CB) from Phyllostachys nigra Munro var. henonis Stapf (Gramineae) on amyloid β protein (25-35) (Aβ (25-35)), a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. CB, over a concentration range of 10-50μg/μl, inhibited the Aβ (25-35) (10 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethyIthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. CB (50 μg/μl) inhibited glutamate release into medium induced by 10 μM Aβ, (25-35) which was measured by HPLC. Pretreatment of CB (50 μg/μl) inhibited 10μM Aβ (25-35)-induced elevation of cytosolic calcium concentration ([Ca2+]c), which was measured by a fluorescent dye, fluo-4 AM, and generation of reactive oxygen species. These results suggest that CB prevents Aβ (25-35)-induced neuronal ell damage in vitro.