• Biomedical Science Letters
• /
• v.9 no.4
• /
• pp.189-193
• /
• 2003

This study was undertaken to investigate the effect of baicalein, a major flavone component of Scutellaria balicalensis Georgi, on oxidant-induced cell injury in renal epithelial cells. Opossum kidney cells, an established proximal tubular epithelial cells, were used as a cell model of renal epithelial cells and t-butylhydroperoxide (tBHP) as an oxidant drug model. Cell viability was measured by MTT assay and lipid peroxidation was estimated by measuring the content of malondialdehyde, a product of lipid peroxidation. Exposure of cells to tBHP caused cell death and its effect was dose-dependent over concentration range of 0.1~1.0 mM. When cells were exposed to tBHP in the presence of various concentrations (0.1~10 $\mu$M) of baicalein, tBHP-induced cell death was prevented with a manner dependent of baicalein concentration. tBHP induced A TP depletion, which was significantly prevented by baicalein. Similarly, tBHP-induced DNA damage was prevented by baicalein. tBHP produced a marked increase in lipid peroxidation and its effect was completely inhibited by baicalein. These results indue ate that tBHP induces cell injury through a lipid peroxidation-dependent mechanism in renal epithelial cells, and baicalein prevented oxidant-induced cell injury via antioxidant action inhibiting lipid peroxidation. In addition, these results suggest that baicalein may be a candidate for development of drugs which are effective in preventing and treating renal diseases.

• Korean Journal of Environmental Biology
• /
• v.28 no.4
• /
• pp.196-201
• /
• 2010

The phenethyl ester of caffeic acid (CAPE), an active component of honeybee propolis extract, is shown to inhibit cancer growth previously. However, studies on human ovarian cancer are largely obscure. This study evaluated the effects of CAPE as a potential anti-proliferative and pro-apoptotic agent in the human ovarian cancer line, OVCAR-3. CAPE treated OVCAR-3 cells showed inhibition of cell viability and proliferation in a dose-dependent manner by WST-1 assay, LDH assay and bromodeoxyuridine (BrdU) incorporation assay. Furthermore, CAPE-mediated OVCAR-3 cell growth inhibition was associated with apoptotic changes as evident by cell cycle arrest and accumulation of cells in the apoptotic phase and DNA fragmentation. Taken together, CAPE inhibits cell proliferation via DNA synthesis reduction and induces apoptotic cell death via DNA damage, thus elucidating a novel, plausible mechanism of CAPE anti-tumorigenic property in OVCAR-3 cells.

• Korean Journal of Microbiology
• /
• v.29 no.2
• /
• pp.136-142
• /
• 1991

The selection of ethanol-tolerant strains was applied to enrichment culture of YPD broth medium containing various concentrations of ethanol. Isolates were identified to be Saccharomyces cerevisiae, the others as S. dairensis, S. exiguus, S. telluris, Saccharomycodes ludwigii, Schwanniomyces occidentalis var. occidentalis and Zygosaccharomyces florentinus. Among isolates S. cerevisiae YO-1 was screened as having the highest ethanol tolerance and produced 18% (v/v) ethanol after 4 days fermentation. The change of fatty-acyl residues represents that a progressive decrease in fatty-acyl unsaturation and a proportional increase in saturation in phospholipids of yeast cells during fermentation affected the yeast viability. Supplementation ethanol to the cultures led to an increase of unsaturated fatty-acyl residues, especially $C_{16}$ or $C_{18}$ residues, along with a decrease in the proportion of saturated residues in cellular phospholipids. Increasing the amount of soy flour led to an increase in the maximum number of viable yeast cells and ethanol production. It was possible in 4 days to reach 21% (v/v) ethanol by adding 4% soy flour as source of unsaturated fatty-acyl residues to the fermentation medium. Soy flour not only increased yeast population but also enhanced the physiological properties of yeast cells to be ethanol tolerant in the anaerobic culture.

• Nutrition Research and Practice
• /
• v.5 no.3
• /
• pp.214-218
• /
• 2011

Diets based on carbohydrates increase rapidly the blood glucose level due to the fast conversion of carbohydrates to glucose. High glucose diets have been known to induce many lifestyle diseases. Here, we demonstrated that high glucose diet shortened the lifespan of Caenorhabditis elegans through apoptosis induction. Control adult groups without glucose diet lived for 30 days, whereas animals fed 10 mg/L of D-glucose lived only for 20 days. The reduction of lifespan by glucose diet showed a dose-dependent profile in the concentration range of glucose from 1 to 20 mg/L. Aging effect of high glucose diet was examined by measurement of response time for locomotion after stimulating movement of the animals by touching. Glucose diet decreased the locomotion capacity of the animals during mid-adulthood. High glucose diets also induced ectopic apoptosis in the body of C. elegans, which is a potent mechanism that can explain the shortened lifespan and aging. Apoptotic cell corpses stained with SYTO 12 were found in the worms fed 10 mg/L of glucose. Mutation of core apoptotic regulatory genes, CED-3 and CED-4, inhibited the reduction of viability induced by high glucose diet, which indicates that these regulators were required for glucose-induced apoptosis or lifespan shortening. Thus, we conclude that high glucose diets have potential for inducing ectopic apoptosis in the body, resulting in a shortened lifespan accompanied with loss of locomotion capacity.

• The Journal of Internal Korean Medicine
• /
• v.26 no.2
• /
• pp.409-419
• /
• 2005

The water extract of Boyanghwanoh-tang has been used for treatment of ischemic vascular disease in oriental medicine. However, little is known about the mechanism by which the water extract of Boyanghwanoh-tang rescues cells from these damages. Therefore, this study was designed to evaluate the protective effects of Boyanghwanoh-tang on zinc-mediated cytotoxicity in H9c2 cardiomyoblast cells. This study demonstrates that, after treatment of H9c2 cells with zinc, there was a decrease in cell viability in a dose dependent manner, and there was a chromatin condensation. Zinc induced the change of cell morphology. In addition, zinc induced mitochondrial dysfunction. Zinc-induced H9c2 cell death was remarkably prevented by the pretreatment of Boyanghwanoh-tang consistently with increase of the peroxoredoxin 1, 2, 3, 5, and 6 expression. Taken together, the results suggest that zinc induced severe cell death in H9c2 cardiomyoblast cells, and that protective effects of Boyanghwanoh-tang against oxidative injuries are achieved through regulation of peroxiredoin expression.

• The Journal of Internal Korean Medicine
• /
• v.26 no.2
• /
• pp.420-430
• /
• 2005

The water extract of Omijatang(OMJT) has been traditionally used for treatment of abscess and heart palpitation in oriental medicine, However, little is known about the mechanism by which the water extract of OMJT rescues cells from these damages. This study was designed to investigate the protective mechanisms of OMJT in H9c2 cardiomyoblasts on oxidative stress-induced cytotoxicity including $H_2O_2,\;ZnCl_2$, hypoxia, and reoxygenation. Oxidative stress markedly decreased the viability of H9c2 cells. This was characterized with apparent apoptotic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, OMJT significantly reduced $H_2O_2$-induced cell death and apoptotic characteristics as well as $ZnCl_2$, hypoxialreoxygenation. Taken together, this study suggests that the water extract of OMJT has the protective effects against oxidative injuries.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.6
• /
• pp.565-570
• /
• 1999

Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver injury. Due to the detergent-like effect of the hydrophobic bile acids, hepatocellular injury has been attributed to direct membrane damage. However histological findings of cholestatic liver diseases suggest apoptosis can be a mechanism of cell death during cholestatic liver diseases instead of necrosis. To determine the pattern of hepatocellular toxicity induced by bile acid, we incubated primary cultured rat hepatocytes with a hydrophobic bile acid, Glycochenodeoxycholate (GCDC), up to 5 hours. After 5 hours incubation with $400\;{\mu}M$ GCDC, lactate dehydrogenase released significantly. Cell viability, quantitated in propidium iodide stained cells concomitant with fluoresceindiacetate was decreased time- and dose-dependently. Most nuclei with condensed chromatin and shrunk cytoplasm were heavily labelled time- and dose-dependently by a positive TUNEL reaction. These findings suggest that both apoptosis and necrosis are involved in hepatocytes injury caused by GCDC.

• The Journal of Pediatrics of Korean Medicine
• /
• v.23 no.1
• /
• pp.159-171
• /
• 2009

Objectives This study was evaluated the effects of CSE the regulatory mechanism of NO and cytokines in the LPS-stimulated Raw 264.7 cells. Methods The Coicis Semen MeOH extract dissolved in EMEM for 1 hour prior to the addition of LPS(1${mu}g/ml$). The cell viability was measured by MTT assay, and Nitric Oxide production was monitored by measuring the nitrite content in culture medium. The levels of cytokine and PGE2 were analyzed by sandwich immunoassays. Results CSE inhibited the production of NO (0.03 and 0.1 mg/ml), $TNF-{\alpha}$ (0.03 and 0.1 mg/ml), $IL-1{\beta}$ (0.03 and 0.1 mg/ml), IL-6 (0.03, 0.1 mg/ml) and PGE2(0.03 and 0.1 mg/ml) in Raw 264.7 cells activated with LPS(lipopolysaccharide). Conclusion According to the results above, Coicis Semen can produce anti-inflammatory effect, which may play a role in adjunctive therapy in Gram-negative bacterial infections.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.22
• /
• pp.9853-9857
• /
• 2014

Background: The morbidity and mortality rate of liver cancer continues to rise in China and advanced cases respond poorly to chemotherapy. Ribosomal protein L24 has been reported to be a potential therapeutic target whose depletion or acetylation inhibits polysome assembly and cell growth of cancer. Materials and Methods: Total RNA of cultured amycin-resistant and susceptible HepG2 cells was isolated, and real time quantitative RT-PCR were used to indicate differences between amycin-resistant and susceptible strains of HepG2 cells. Viability assays were used to determine amycin resistance in RPL24 transfected and control vector and null-transfected HepG2 cell lines. Results: The ribosomal protein L24 transcription level was 7.7 times higher in the drug-resistant HepG2 cells as compared to susceptible cells on quantitative RT-PCR analysis. This was associated with enhanced drug resistance as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions: The ribosomal protein L24 gene may have effects on drug resistance mechanisms in hepatocellular carcinoma HepG2 cells.

• Nutrition Research and Practice
• /
• v.14 no.5
• /
• pp.453-462
• /
• 2020

BACKGROUND/OBJECTIVES: Platycodon grandiflorum (PG), an oriental herbal medicine, has been known to improve liver function, and has both anti-inflammatory and antimicrobial properties. However, little is known about the immune-enhancing effects of PG and its mechanism. In this study, we aimed to investigate whether fermented PG extract (FPGE), which has increased platycodin D content, activates the immune response in a murine macrophage cell line, RAW 264.7. MATERIALS/METHODS: Cell viability was determined by Cell Counting Kit-8 assay and the nitric oxide (NO) levels were measured using Griess reagent. Cytokine messenger RNA levels of were monitored by quantitative reverse transcription polymerase chain reaction. To investigate the molecular mechanisms underlying immunomodulatory actions of FPGE in RAW 264.7 cells, we have conducted luciferase reporter gene assay and western blotting. RESULTS: We found that FPGE treatment induced macrophage cell proliferation in a dose-dependent manner. FPGE also modulated the expression of NO and pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. The activation and phosphorylation levels of nuclear factor kappa B (NF-κB) were increased by FPGE treatment. Moreover, 5-aminoimidazole-4-carboxamide ribonucleotide, an activator of AMP-activated kinase (AMPK), significantly reduced both lipopolysaccharides- and FPGE-induced NF-κB reporter gene activity. CONCLUSIONS: Taken together, our findings suggest that FPGE may be a novel immune-enhancing agent acting via AMPK-NF-κB signaling pathway.