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1.
Article | WPRIM (Western Pacific) | ID: wpr-836209

ABSTRACT

Purpose@#The rice germ fraction is a better source of protein, lipid, and fiber than the rice endosperm. Furthermore, the rice germ is rich in bioactive phytochemicals such as γ-aminobutyric acid, tocopherols, tocotrienols, phytic acid, and so on. In this study, the phytosterol content and antioxidant activity of Keunnunjami germ (KG) or normal rice germ supplement were investigated in healthy adult rats. @*Methods@#In vitro, quantitative assessment of phytosterols, including β-sitosterol, campesterol, cycloartenol, and stigmasterol, was performed. Comparative antioxidant activities of 2 rice germs were measured based on DPPH radical scavenging activity, reducing power, and ABTS radical scavenging capacity. In vivo, male Spraque-Dawley rats (30-weeks-old) were randomly assigned a diet of normal control (NC, AIN-93M diet), AIN-93M diet supplemented with normal rice germ 3% (NG3), or AIN-93M diet supplemented with KG 3% (KG3) and fed for 8 weeks. @*Results@#KG contained significantly higher campesterol and stigmasterol contents and antioxidant activity than normal rice germ. The KG3 group exhibited significantly lower body weight gain as well as inguinal and total white adipose tissue weights. There were no significant differences in plasma glucose, insulin, C-peptide, or homeostasis model assessment of insulin resistance level among the 3 groups. The plasma tumor necrosis factor-α concentration was significantly lower while leptin, advanced oxidation protein products, and interleukin-6 showed downward trends in the KG3 group. In addition, the superoxide dismutase level of the KG3 group was significantly higher compared to the NC and NG3 groups. @*Conclusion@#This study indicates that KG can be considered as a valuable source of phytosterol components. Lastly, KG has strong antioxidant properties and may have potential to ameliorate elevation of proinflammatory cytokine production with age.

2.
Article in English | WPRIM (Western Pacific) | ID: wpr-717729

ABSTRACT

BACKGROUND/OBJECTIVES: Oxidative stress is a major cause of cancer. This study investigated the effects of the ethanol extracts from germinated and non-germinated Keunnunjami rice, a blackish-purple pigmented cultivar with giant embryo, on selected human cancer cell lines and on the antioxidant defense system of mice fed with a high-fat diet. MATERIALS/METHODS: High fat-fed mice were orally administered with either distilled water (HF) or extracts (0.25%, w/w) from brown (B), germinated brown (GB), Keunnunjami (K), and germinated Keunnunjami (GK) rice. RESULTS: In comparison with the brown rice extract, Keunnunjami extract showed higher anticancer effect against cervical and gastric cell lines but lower anticancer activity on liver and colon cancer cells. Mice from the HF group showed significantly higher lipid peroxidation and lower antioxidant enzyme activities than the control group. However, the oxidative stress induced by high-fat diet markedly decreased in B, GB, K, and GK groups as compared with the HF group. CONCLUSIONS: Germination may be an effective method for improving the anticancer and antioxidative properties of Keunnunjami rice and extracts from germinated Keunnunjami rice may serve as a therapeutic agent against cervical and gastric cancers and oxidative damage.


Subject(s)
Animals , Humans , Mice , Cell Line , Colonic Neoplasms , Diet, High-Fat , Embryonic Structures , Ethanol , Germination , Lipid Peroxidation , Liver , Methods , Nutritional and Metabolic Diseases , Oxidative Stress , Stomach Neoplasms , Water
3.
Article in Korean | WPRIM (Western Pacific) | ID: wpr-153192

ABSTRACT

PURPOSE: The purposes of this study were to evaluate symptom experience and quality of life (QOL) and to identify the predictors of QOL among breast cancer survivors. METHODS: A cross-sectional study was conducted on 200 disease-free breast cancer survivors at two hospitals between December 2007 and July 2008. Functional Assessment of Cancer Therapy Scale-B, Memorial Symptom Assessment Scale-short Form and The Linear Analogue Self Assessment Scale were used to assess symptom experience and QOL in these patients. Data were analyzed using the Pearson correlation, t-test, ANOVA, and stepwise multiple regression with SPSS/WIN 12.0. RESULTS: The mean score of QOL for breast cancer survivors was 95.81 (+/-18.02). The highest scores among physical and psychological symptoms were sexual interest and anxiety. Year since treatment completion was significantly associated with QOL in sociodemographic variables. Physical and psychological symptoms have a significant negative association with QOL. The results of the regression analyses showed that physical and psychological symptoms were statistically significant in predicting patients' QOL. CONCLUSION: Symptom experience and QOL are essential variables that should be acknowledged when delivering health care to breast cancer survivors. More attention to the reduction and management of psychological distress could improve QOL among breast cancer survivors.


Subject(s)
Adult , Female , Humans , Middle Aged , Adaptation, Psychological , Anxiety , Breast Neoplasms/psychology , Cross-Sectional Studies , Data Interpretation, Statistical , Disease-Free Survival , Emotions , Health Status , Quality of Life , Surveys and Questionnaires , Survivors/psychology
4.
Article in English | WPRIM (Western Pacific) | ID: wpr-727514

ABSTRACT

53BP1 is an important genome stability regulator, which protects cells against double-strand breaks. Following DNA damage, 53BP1 is rapidly recruited to sites of DNA breakage, along with other DNA damage response proteins, including gamma-H2AX, MDC1, and BRCA1. The recruitment of 53BP1 requires a tandem Tudor fold which associates with methylated histones H3 and H4. It has already been determined that the majority of DNA damage response proteins are phosphorylated by ATM and/or ATR after DNA damage, and then recruited to the break sites. 53BP1 is also phosphorylated at several sites, like other proteins after DNA damage, but this phosphorylation is not critically relevant to recruitment or repair processes. In this study, we evaluated the functions of phosphor-53BP1 and the role of the BRCT domain of 53BP1 in DNA repair. From our data, we were able to detect differences in the phosphorylation patterns in Ser25 and Ser1778 of 53BP1 after neocarzinostatin-induced DNA damage. Furthermore, the foci formation patterns in both phosphorylation sites of 53BP1 also evidenced sizeable differences following DNA damage. From our results, we concluded that each phosphoryaltion site of 53BP1 performs different roles, and Ser1778 is more important than Ser25 in the process of DNA repair.


Subject(s)
DNA , DNA Damage , DNA Repair , Genomic Instability , Histones , Phosphorylation , Proteins
5.
Article in English | WPRIM (Western Pacific) | ID: wpr-727513

ABSTRACT

We previously reported that glial cell line-derived neurotropic factor (GDNF) receptor alpha1 (GFR alpha1) is a direct target of apurinic/apyrimidinic endonuclease 1 (Ape1/Ref-1). In the present study, we further analyzed the physiological roles of Ape1/Ref-1-induced GFRalpha1 expression in Neuro2a mouse neuroblastoma cells. Ape1/Ref-1 expression caused the clustering of GFR alpha1 immunoreactivity in lipid rafts in response to GDNF. We also found that Ret, a downstream target of GFRalpha1, was functionally activated by GDNF in Ape1/Ref-1-expressing cells. Moreover, GDNF promoted the proliferation of Ape1/Ref-1-expressing Neuro2a cells. Furthermore, GFR alpha1-specific RNA experiments demonstrated that the downregulation of GFR alpha1 by siRNA in Ape1/Ref-1-expressing cells impaired the ability of GDNF to phosphorylate Akt and PLC gamma-1 and to stimulate cellular proliferation. These results show an association between Ape1/Ref-1 and GDNF/GFR alpha signaling, and suggest a potential molecular mechanism for the involvement of Ape1/Ref-1 in neuronal proliferation.


Subject(s)
Animals , Mice , Cell Proliferation , Down-Regulation , Glial Cell Line-Derived Neurotrophic Factor , Neuroblastoma , Neuroglia , Neurons , RNA , RNA, Small Interfering , Signal Transduction
6.
Article in English | WPRIM (Western Pacific) | ID: wpr-727349

ABSTRACT

The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC (20~180 microgram/ml) perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high K+ (56 mM), DMPP (100 micrometer) and McN-A-343 (100 micrometer). PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC (60 microgram/ml), the CA secretory responses to veratridine (a selective Na+ channel activator (10 micrometer), Bay-K-8644 (a L-type dihydropyridine Ca2+ channel activator, 10 micrometer), and cyclopiazonic acid (a cytoplasmic Ca2+ -ATPase inhibitor, 10 micrometer) were significantly reduced, respectively. In the simultaneous presence of PCRC (60 microgram/ml) and L-NAME (an inhibitor of NO synthase, 30 micrometer), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high K+, DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC (60 microgram/ml) was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of Ca2+ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.


Subject(s)
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride , 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester , Adrenal Medulla , Calcium , Catecholamines , Chromaffin Cells , Cytoplasm , Dihydropyridines , Dimethylphenylpiperazinium Iodide , Indoles , NG-Nitroarginine Methyl Ester , Nitric Oxide , Nitric Oxide Synthase , Polyphenols , Rats, Inbred SHR , Receptors, Cholinergic , Sodium , Veins , Veratridine , Wine
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