• Journal of Life Science
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• v.21 no.12
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• pp.1752-1760
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• 2011

In this study, the effect of the Opuntiahumifusa extracts on proliferation, alkaline phosphatase (ALP) activity, collagen synthesis and ROS level of a cell was investigated using an osteoblast. Opuntiahumifusawas separated intoOpuntiahumifusapeel (OH-P), seed (OH-Se) and stem (OH-St).These were subjected to extraction by using hot water and ethanol. The proliferation of the MC3T3-E1 osteoblastic cells that were treated with OH-Se water extract were increased by approximately 120%. Regarding the effects of OH-Se on ALP activity, the $50{\mu}g/ml$ ethanol extract group showed the highest activity. The synthesis of collagen increased significantly in response to treatment with OH-Se water extract. The ROS scavenging effects of Opuntiahumifusawere investigated for involvement of oxidativedamage, cell culture and staining. Also, when OH-Se water extract $100{\mu}g/ml$ was added, the ROS level decreased by 54%. These results indicate that Opuntiahumifusa extracts have an anabolic effect on bone through the promotion of osteoblastic differentiation, suggesting that it could be used for the treatment of common metabolic bone diseases.

• Journal of Life Science
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• v.19 no.7
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• pp.839-844
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• 2009

This experiment was conducted to evaluate pollen viability of Nakdongbyeo, transgenic rice lines, an F$_1$ hybrid from a cross between Milyang weedy rice and ABC-promoter transgenic rice line containing basta-resistant (bar) gene and subsequent selfed progenies, F$_2$ and F$_3$. The reaction of pollen with 3-{4,5 dimethylthiazolyl-2}-2,5-diphenyl monotetrazolium bromide (MTT) as a staining chemical immediately after pollen shedding showed maximum pollen viability of 86% in Nakdongbeyo, 75% in ABC-promoter transgenic rice line, 62% in ubiquitin-promoter transgenic line, 68% in F$_1$, 79% in F$_2$ and 78% in F$_3$. Viability gradually declined during subsequent observations at 20-minute intervals. However, there was a drastic decline in pollen viability after 40 minutes of pollen shedding. The mean difference of pollen viability among rice lines and time was highly significant, indicating significantly different pollen viabilities at different time intervals. Maximum viability of 36.2% was observed in F$_3$ and minimum viability of 3.5% was found in F$_2$ at 90 min after pollen shedding. Results of this experiment on pollen viability and longevity elucidate potential risks of pollen-mediated flow of herbicide-resistant gene from transgenic rice lines and possible integration of it into the weedy rice population.

• Journal of Life Science
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• v.24 no.6
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• pp.595-602
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• 2014

Styela Clava tunic (SCT) has found some applications in many areas of medical treatment including as an anti-inflammatory compound, a wound healing film, in guided bone regeneration, and as a food additive. The protective effect of SCT aqueous extract (AE-SCT) on cell death induced by $H_2O_2$ treatment was investigated by measuring the changes in cell viability in HepG2 cells after AE-SCT treatment. High concentrations of antioxidant compounds including flavonoids (3.3 mg/g) and phenolics (32.3 mg/g) were detected in AE-SCT but no significant cytotoxicity was observed in HepG2 cells treated with AE-SCT. The viability of HepG2 cells was also not changed by treatment with different concentrations of AE-SCT after $H_2O_2$ treatment. However, cell viability was significantly increased in cells treated with three different concentrations of AE-SCT before $H_2O_2$ treatment. The greatest increase in cell viability was observed in the group treated with $50{\mu}g/ml$ AE-SCT, when compared with vehicle-treated group. FACS and DAPI staining analysis indicated that the decrease in number of dead cells was dependent on the concentration of AE-SCT. Alterations in the Bax/Bcl-2 ratio after $H_2O_2$ treatment were significantly restored by treatment with different concentrations of AE-SCT. These results indicate that AE-SCT, which contains high levels of antioxidants, may protect cells against death induced by $H_2O_2$ treatment.

• Tuberculosis and Respiratory Diseases
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• v.54 no.6
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• pp.610-620
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• 2003

Background : 3p deletion has been shown to be the most frequently occurring change in lung cancers, suggesting the presence of a tumor suppressor gene in this region. Recent attention has focused on a candidate 3p14.2 tumor suppressor gene, FHIT. Therefore, the association of the expression of FHIT, with apoptosis, cell proliferation cycle and the clinicopathological features, including survival, were investigated Materials and Methods : 83 patients with non-small cell lung cancer, who underwent curative operation, between Jan. 1996 and Aug. 2000, at the Wonkwang university hospital, were analyzed. The expression of the FHIT was identified by immunohistochemical staining, and rate of apoptosis and cell proliferation cycle by flow cytometry. Results : 43% (36/83) of patients exhibited no FHIT expression. The rates of FHIT loss were 52% (28/54), 22% (5/23), 50% (3/6); 30% (11/37), 48% (16/33), 69% (9/13); 54% (30/56) and 22% (6/27), in squamous cell cancers, adenocarcinomas, large cell cancers, TNM stages I, II and III, smokers and non-smokers, respectively. All the differences in FHIT loss rates, according to the histopathology, TNM stages and smoking habits, were statistically significant. The median survival time and 2-year survival rate of the FHIT(-) group were 24 months and 44%, and those of the FHIT(+) group were 25 months and 51% (p>0.05), respectively. The apoptotic rate of the FHIT(-) and FHIT(+) groups were 50.72 (${\pm}13.93$) and 59.38 (${\pm}14.33$)%, respectively (p=0.01). The S- and G1-phase fractions of the FHIT(-) and FHIT(+) groups were 13.93 (${\pm}7.35$) and $51.50({\pm}23.15$)% and 15.65(${\pm}6.59$) and 54.16 (${\pm}20.25$)%, respectively (p>0.05). Conclusion : The loss of FHIT expression was increased to a greater extent with advancing TNM stage, smoking habits and squamous cell cancer compared to the adenocarcinomas. However, no survival differences were found according to the expression of FHIT. The apoptotic rate of the FHIT(+) group was greater than in the FHIT(-) group, but differences in the S- and G1-phase fractions, according to the expression of the FHIT, were not found.

• Tuberculosis and Respiratory Diseases
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• v.54 no.5
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• pp.495-509
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• 2003

Background : Neutrophil-mediated inflammation is usually self-limiting, because neutrophils have a remarkably short life span. Prolonged neutrophil survival, which is caused by decreased spontaneous apoptosis, leads to persistent inflammation in sepsis. Because many inflammatory cytokines, which generate signals that delay apoptosis, are regulated by nuclear factor-${\kappa}B$ transcription factor, we hypothesized that nuclear factor-${\kappa}B$ might be related to the reduced neutrophil apoptosis observed in sepsis. Methods : Neutrophils of healthy volunteers and sepsis patients were freshly isolated from venous blood. Neutrophil apoptosis was assayed with two approaches : by counting apoptotic cells under a microscope and by flow cytometry using Annexin V. The activity of nuclear factor-${\kappa}B$ was assessed by immunofluorescent staining or electrophoretic mobility shift assay. Expression of X-linked inhibitor of apoptosis was measured by western blot assay. Results : We confirmed reduced spontaneous neutrophil apoptosis in patients with sepsis. The number of apoptotic neutrophils in patients with sepsis increased to the level of that in healthy controls after cycloheximide treatment, suggesting that decreased spontaneous neutrophil apoptosis is dependent on de novo protein synthesis. In patients with sepsis, basal neutrophil nuclear factor-${\kappa}B$ was activated compared to the level in healthy controls. Moreover, a blockade of nuclear factor-${\kappa}B$ activity reversed the decreased spontaneous neutrophil apoptosis in sepsis patients. Meanwhile, X-linked inhibition of apoptosis expression, which is regulated by nuclear factor-${\kappa}B$, decreased 24 hours after incubation in healthy persons, but persisted for 24 hours in patients with sepsis. Conclusion : These observations suggest that the reduced spontaneous neutrophil apoptosis observed in patients with sepsis may be related to the induction of survival protein by nuclear factor-${\kappa}B$.

• Journal of Gastric Cancer
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• v.6 no.4
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• pp.227-236
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• 2006

Purpose: Methylation of gene regulatory elements plays an important role in gene inactivation without genetic alteration. Gastric cancer is one of the tumors that exhibit a high frequency of CpG island hypermethylation. The purpose of this study was to investigate the occurrence of CpG island hypermethylation in gastric carcinoma in relation to H. pylori infection, CIMP and clincopathologic variables. Materials and Methods: We investigated the promoter methylation Status of six genes (hMLH1, p16, p14, COX-2, MGMT, E-cadherin) and CIMP in 36 gastric carcinoma tissues as well as in nontumor tissues. CIMP status was investigated by examining the methylation status of MINT 1, 2, 12, 25 and 31. The methylation status of the promoter was examined by methylation-specific PCR (MSP) and H. pylori infection was examined by histological diagnosis after staining with Warthin-Starry silver. Results: Among the 36 gastric carcinoma tissues, DNA hypermethylation was detected in the following frequencies: 14 (38.9%) for p14, 13 (36.1%) for p16, 8 (22.2%) for MGMT, 10 (27.8%) for COX-2, 21 (58.3%) for E-cadherin, and 6 (16.7%) for hMLH1. The frequencies for MINT1 and MINT25 hypermethylation were significantly higher in tumor tissues than in nontumor tissues. 16 (44.4%) of the 36 gastric carcinoma tissues were positive for the CIMP CIMP-H tumors were associated with older patients and larger tumor size than CIMP-L tumors. We found a significant association between the presence of the CIMP and hypermethylation of p16. Hypermethylation of p16 and MINT2 were significantly different when compared by age. MINT1 gene methylation was significantly associated with H. pylori infection (P=0.004). Conclusion: Our results suggest that aberrant hypermethylation of multiple tumor related genes (hMLH1, p16, p14, COX-2, MGMT, E-cadherin, MINT1, 2, 12, 25, 31) occurs frequently in gastric carcinoma tissues. The hypermethylation of MINT1 was significantly higher in the tumor tissues and was associated with H. pylori infection.

• Journal of Gastric Cancer
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• v.6 no.4
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• pp.250-256
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• 2006

Purpose: Recently, interest in peroxisome-proliferator-activated receptors (PPAR) has increased, although clinical studies of the effect of $PPAR-{\gamma}$ expression on gastric cancer have not been reported yet. In this study, we investigated the role of $PPAR-{\gamma}$ expression in gastric cancer patients. Materials and Methods: One hundred twenty-eight (128) samples of both gastric cancer and normal tissues were obtained from 128 patients who had undergone at a curative gastrectomy at Seoul Medical Center from Jan. 2001 to Dec. 2005. $PPAR-{\gamma}$ expression was determined by using immunohistochemical staining, and the results were analyzed. The statistical analysis was based on clinicopathological findings and the differences in survival rates. Results: The mean age of the patients was 6n, and the male : female ratio was 1.9 : 1. $PPAR-{\gamma}$ expression was significantly higher in cancer tissues than in normal tissue (81.3% vs. 57.0%, p<0.001). There was insignificant difference between well and moderately differentiated types and poorly differentiated types in terms of the expression of $PPAR-{\gamma}$ (87.0% vs. 74.6%, P=0.074). In the univariate analysis the survival rate was significantly increased when $PPAR-{\gamma}$ was expressed in normal tissue (P=0.003). In the multivariate analysis, only the UICC TNM staging had significance related to the survival rate. Conclusion: The rate of $PPAR-{\gamma}$ expression was higher in cancer tissue than it was in normal tissue from gastric cancer patients. In the univariate analysis, $PPAR-{\gamma}$ expression in normal tissue had significance with respect to survival, but the multivariate analysis showed no such significance. Thus, we should further evaluate more cases to determine whether or not such a significance exists.

• Journal of Gastric Cancer
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• v.8 no.4
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• pp.176-181
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• 2008

Purpose: The adipocyte-derived cytokine leptin plays a major role in the control of stable body weight by suppressing food intake and increasing energy metabolism. Leptin regulates the cell proliferation of various epithelial cells and it may be involved in the promotion of cancer. Leptin and its receptor are highly expressed in gastric adenocarcinoma, but the association between the serum leptin level and the tissue expression of leptin is uncertain. We evaluated the serum leptin level and the expressions of leptin and leptin receptor in gastric cancer, and we explore the possible mechanism and role of leptin in the carcinogenesis of gastric cancer. Materials and Methods: 72 carcinomas that were curatively resected at our hospital from October 2005 to March 2007 were included in this study. By immunoassay and immunohistochemical staining, we evaluated the serum leptin level and the expressions of leptin and its receptor, and we analyzed their relationship together with the clinicopathological variables. Results: The serum leptin level was increased as the patient's BMI increased and it was decreased in H. pylori infected patients. The expression of leptin was increased as the TNM stage increased (P=0.014), and the expression of leptin receptor in the intestinal type gastric adenocarcinoma was higher than that in the diffuse type gastric adenocarcinoma (71.4% vs 28.6%, respectively, P=0.033). Conclusion: There was no significant correlation between the serum leptin level and expression of leptin in gastric cancer patients. The expression of leptin was associated with the TNM stage, but its role in the pathogenesis of gastric cancer has to be elucidated.

• Journal of Gastric Cancer
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• v.8 no.4
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• pp.182-188
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• 2008

Purpose: Transcriptional factors of CREB (cAMP response element binding protein) are involved in regulating the gene expression in response to a variety of signaling pathways. The proteins produced by the CREB genes play key roles in many physiological processes, including memory and long-term potentiation. The retinoic acid receptor (RAR) axis mediates epithelial cell differentiation and proliferation in many tissues. This study examined the expressions of RAR and CREB and their relationship with the clinicopathologic factors and their significance. Materials and Methods: The levels of the RAR and CREB expressions were measured in 150 gastric adenocarcinomas by performing immunohistochemical staining. Results: 1. An RAR protein expression was found in 63.3% of the adenocarcinomas (95/150) and a CREB expression was found in 60.7% (91/150) of the adenocarcinomas. 2. An RAR protein expression was found in 72.2% (78/108) of the intestinal type adenocarcinomas and in 40.5% (17/42) of the diffuse type adenocarcinomas (P<0.05). Based on the depth of invasion, an RAR protein expression was found in 58.3% (14/24) of the T1 adenocarcinomas, in 61.9% (13/21) of the T2 adenocarcinomas, in 63.5% (61/96) of the T3 adenocarcinomas, in 77.8% (7/9) of the T4 adenocarcinomas and in 74.7% (62/83) of the adenocarcinomas with lymph node metastasis and in 49.2% (33/67) of the adenocarcinomas without lymph node metastasis (P<0.01). 3. A CREB expression was found in 69.4% (75/108) of the intestinal type and in 38.1% (16/42) of the diffuse type (P>0.05). Based on the depth of invasion, a CREB expression was found in 50% (12/24) of the T1 adenocarcinomas, in 52.4% (11/21) of the T2 adenocarcinomas, in 64.6% (62/96) of the T3 adenocarcinomas, in 66.6% (6/9) of the T4 adenocarcinomas, in 71.1% (59/83) of the adenocarcinomas with lymph node metastasis and in 47.8% (32/67) of the adenocarcinomas without lymph node metastasis (P<0.01). 4. The RAR protein and CREB expressions coincided in 71.4% of the gastric adenocarcinomas and a significant correlation between them was found (P<0.05). Conclusion: We found a significant relationship between the expression of RAR and CREB and the histology and lymph node metastasis of gastric cancer. Further studies are needed to confirm their biologic meaning in gastric carcinogenesis.

• Korean Journal of Food Science and Technology
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• v.29 no.6
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• pp.1255-1263
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• 1997

This study was performed to investigate the effects of green tea on fat metabolism of rats and prevention to cardiovascular disease in drinking green tea. Male Spague-Dawley rats were divided into seven groups consisting of the control, lard and cholestrol, aqueous green tea at the level of 1% and 3%. After 4 weeks of feeding serum lipid levels were measured for experimental rats, and analyzed the total cholesterol (TC), HDL-cholesterol (HDL-C), triglyceride (TG), phospholipid (PL). And total lipid (TL) to Folch method, lipid deposition to oil red O staining on liver tissue. The results are as follows: Total cholesterol (TC) decreased by administration of 1% aqueous green tea group and increased addition to lard and cholesterol (LC) group as compared to each groups (p<0.05). HDL-cholestrol in serum increased by administration of la aqueous green tea group (1G) and decreased to the control group, 1% aqueous green tea (L-1G) added lard group (p<0.05). Triglyceride (TG) decreased by administration of 3% aqueous green tea groups (L-3G, LC-3G) and increased by lard and cholesterol group (LC) (p<0.01). Phospholipid(PL) decreased by administration of 3% aqueous green tea added lard and cholesterol group (LC-3G) and increased by control group, lard and cholestrol group (LC) (p<0.05). Total lipid of liver decreased by administration of aqueous green tea at the level of 1% group and increased by LC group (p<0.01). The fat deposition of liver was increased in fat diet groups and decrease in the drink green tea of some but did not showed significant differences from concentration of the green tea.