• The Journal of Internal Korean Medicine
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• v.26 no.2
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• pp.379-389
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• 2005

Objectives: It is well known that aging and aging-related diseases are linked to the increased level of oxidative stress caused by reactive oxygen species(ROS) and reactive nitrogen species(RNS). Nonprotein-SH decreases during aging, while substances such as ROS, nitric oxide(NO), peroxynitrite($ONOO^-$), myeloperoxidase(MPO), and dityrosine show a significant increase. This study investigated the effect of Ichungwhan on the aging process by examining its effect on the generation of the above-mentioned substances. Methods: Four comparison groups of SD rats were used. They were 6 month-old rats, 24 month-old rats, and 24 month-old rats fed with food containing 0.1% and 0.3% of Ichungwhan extract. The amount of NO, $ONOO^-$, and ROS in the rats' kidneys were examined using a fluorescence microplate reader. The reagents used for this purpose include: dihydrorhodamine 123 (DHR 123), 2',7' -dichlorodihydrofluorescein, diacetate(DCFDA), and 4,5-diaminofluorescein(DAF-2). A spectrophotometer was used to investigate the reactivity of nonprotein-SH and myeioperoxidase(MPO), using reagents such as trichloroacetic acid(TCA) and tetramethylbenzidine(TMB). The amounts of MPO protein and dityrosine were measued by western blot. Results: The observed effects of Ichungwhan on rats were as follows: increase of nonprotein-SH; effective decrease of RNS level by suppression of the generation system of $ONOO^-$ and NO; decrease of ROS level; decrease of the MPO reactivity and the subsequent reduction of amount of MPO protein; retardation of dityrosine formation. It can be hypothesized, therefore, that Ichungwhan affects both the earlier and later phases of the molecular inflammatory process, and retards the aging process. Conclusions: Empirical evidence in this study supports a role for Ichungwhan in generation mechanisms of aging process-linked substances ROS, NO, $ONOO^-$, nonprotein-SH, MPO and dityrosine. Affects contrary to the aging process observed in rats beg further empiricism to investigate potential application of Ichungwhan as a medication for age-related diseases in humans.

• Journal of Life Science
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• v.25 no.11
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• pp.1235-1243
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• 2015

Hwangheuk-san (HHS) is a Korean multi-herb formula comprising four medicinal herbs. HHS, which was recorded in “Dongeuibogam,” has been used to treat patients with inflammation syndromes and digestive tract cancer for hundreds of years. However, little is known about its anti-tumor efficacy. The present study investigated the pro-apoptotic effect and mode of action of HHS against AGS human gastric carcinoma cells. HHS inhibited the cell growth of AGS cells in a dose-dependent manner, which was associated with the induction of apoptotic cell death, as evidenced by the formation of apoptotic bodies, chromatin condensation, and an accumulation of cells in the sub-G1 phase. HHS-induced apoptotic cell death was associated with the up-regulation of pro-apoptotic Bax protein expression, down-regulation of antiapoptotic Bcl-2 protein, and the release of cytochrome c from mitochondria to the cytosol. The treatment of AGS cells with HHS significantly elevated the generation of reactive oxygen species (ROS). Additionally, apoptosis-inducing concentrations of HHS induced the activation of both caspase-9 and -8, initiator caspases of the mitochondrial-mediated intrinsic and death receptor-mediated extrinsic pathways, respectively, and caspase-3, accompanied by proteolytic degradation of poly (ADP-ribose)-polymerase. However, ROS scavenger and pan-caspases inhibitor significantly blocked HHS-induced growth inhibition and apoptosis. Taken together, these findings suggest that HHS induces apoptosis through ROS- and caspase-dependent mechanisms and that HHS may be a potential chemotherapeutic agent for the control of human gastric cancer.

• The Journal of Korean Medicine
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• v.26 no.2 s.62
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• pp.63-76
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• 2005

Objectives: Reactive oxygen species (ROS) have been implicated in the pathogenesis of a wide range of acute and longterm neurodegenerative diseases. This study was undertaken to examine whether Sunghyangchungisan(SHCS), a well-known prescription in Korean traditional medicine, might have beneficial effects on ROS-induced brain cell injury. Methods: Human neuroglioma cell line A172 and H2O2 were employed as an experimental model cell and oxidant. Results: SHCS effectively protected the cells against both the necrotic and apoptotic cell death induced by H2O2. The effect of SHCS was dose-dependent at concentrations ranging from 0.2 to 5mg/ml. SHCS significantly prevented depletion of cellular ATP and activation of poly (ADP-ribose) polymerase induced by H2O2. It also helped mitochondria to preserve its functional integrity estimated by MTT reduction ability. Furthermore, SHCS significantly prevented H202-induced release of cytochrome c into cytosol. Determination of intracellular ROS showed that SHCS might exert its role as a powerful scavenger of intracellular ROS. Conclusions: The present study provides clear evidence for the beneficial effect of SHCS on ROS-induced neuroglial cell injury. The action of SHCS as an ROS-scavenger might underlie the mechanism.

• KSBB Journal
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• v.18 no.3
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• pp.170-173
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• 2003

This study was studies biophoton characteristics of Madin-Darby canine kidney cells under the influence of CsA and each cell type (mock, wt, R55A) by employing a Photomultipliertube. $\textrm{H}_2\textrm{O}_2$ was used for producing reactive oxygen species (ROS) in this measurement. ROS is also generated during oxidative metabolism in living organism. Images from a fluorescence show an increase of photon intensity emitted from the sample on the influence of CsA and each cell type (mock, wt, R55A). It is believed chemiluminescence (CL) occurred by ROS is responsible for the biophoton emission. hence PMT measurement might be considered as a useful tool for studying biochemical characteristics in relation to ROS.

• Toxicological Research
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• v.21 no.2
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• pp.129-134
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• 2005

Styrene is a commercially important chemical used mainly in the production of plastics. A toxic effect exerted by styrene exposure may cause infertility, congenital anomalies or death in offspring. Treatment with styrene for 0, 50, 100, and 500 mg/kg for 5 days in Sprague-Dawley rats significantly decreased sperm motilities and sperm counts while sperm abnormalities were significantly increased. To determine the relationship between changes in sperm motilities and roles of reactive oxygen species (ROS), we determined the effect of styrene on ROS production and mRNA expression of antioxidant enzymes in rats. ROS production was enhanced by styrene treatment in a dose-dependent manner. The mRNA expression of catalase and superoxide dismutase (SOD) 2 was strongly suppressed by styrene treatment although SOD1 or glutathione peroxidase (GPX) 4 expressions were not significantly changed. Taken together, these results indicate that styrene may cause toxic effect in rat sperm cells by enhancing oxidative stresses.

• Biomolecules & Therapeutics
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• v.21 no.5
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• pp.358-363
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• 2013

In the present study, we investigated the effect of intracellular glutathione (GSH) depletion in heart-derived H9c2 cells and its mechanism. L-buthionine-S,R-sulfoximine (BSO) induced the depletion of cellular GSH, and BSO-induced reactive oxygen species (ROS) production was inhibited by glutathione monoethyl ester (GME). Additionally, GME inhibited BSO-induced caspase-3 activation, annexin V-positive cells, and annexin V-negative/propidium iodide (PI)-positive cells. Treatment with rottlerin completely blocked BSO-induced cell death and ROS generation. BSO-induced GSH depletion caused a translocation of PKC-${\delta}$ from the cytosol to the membrane fraction, which was inhibited by treatment with GME. From these results, it is suggested that BSO-induced depletion of cellular GSH causes an activation of PKC-${\delta}$ and, subsequently, generation of ROS, thereby inducing H9c2 cell death.

• IMMUNE NETWORK
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• v.14 no.5
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• pp.241-248
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• 2014

It is debatable whether AMP-activated protein kinase (AMPK) activation is involved in anti-apoptotic or pro-apoptotic signaling. AICAR treatment increases AMPK-${\alpha}1$ phosphorylation, decreases intracellular reactive oxygen species (ROS) levels, and significantly increases Annexin V-positive cells, DNA laddering, and caspase activity in human myeloid cell. AMPK activation is therefore implicated in apoptosis. However, AMPK-${\alpha}1$-knockdown THP-1 cells are more sensitive to apoptosis than control THP-1 cells are, suggesting that the apoptosis is AMPK-independent. Low doses of AICAR induce cell proliferation, whereas high doses of AICAR suppress cell proliferation. Moreover, these effects are significantly correlated with the downregulation of intracellular ROS, strongly suggesting that AICAR-induced apoptosis is critically associated with the inhibition of NADPH oxidase by AICAR. Collectively, our results demonstrate that in AICAR-induced apoptosis, intracellular ROS levels are far more relevant than AMPK activation.

• Proceedings of the Korean Society of Fisheries Technology Conference
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• 2001.10a
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• pp.206-207
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• 2001

Cochlodinium polykrikoides is one of the most harmful red tide dinoflagellates and is highly toxic to fish. Red tides due to this dinoflagellate have been reported in Korea, Japan, and other countries, and frequently cause severe damage to fish farming. Recently study has suggested that C. polykrikoides generates reactive oxygen species (ROS) such as superoxide anion ($O_{2-}$) and hydrogen peroxide ($H_2O_2$), and the ROS-mediated ichthyotoxicity has been proposed. (omitted)

• Interdisciplinary Bio Central
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• v.3 no.4
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• pp.16.1-16.8
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• 2011

Defects in mitochondrial DNA (mtDNA) cause many human diseases and are critical factors that contribute to aging. The mechanisms of maternally-inherited mtDNA mutations are well studied. However, the role of acquired mutations during the aging process is still poorly understood. The most plausible mechanism is that increased reactive oxygen species (ROS) may affect the opening of mitochondrial voltage dependent anion channel (VDAC) and thus results in damage to mtDNA. This review focuses on recent trends in mtDNA research and the mutations that appear to be associated with increased ROS.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.134.1-134.1
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• 2003

In regard to $A\beta$ toxicity and AD, reactive oxygen species (ROS) are produced by macrophage families in response to $A\beta$ stimulation. In addition to this, neurotrophins (NTs) regulate the neuronal function as well as cell survival and the growth of various types of neurons in both the peripheral nervous system (PNS) and central nervous system (CNS). As high expressions of the ROS and NTs are a routine findings in neuronal cell damage, we wanted to investigate whether Rg3 can inhibit the production of ROS and NTs primary cell cultures. (omitted)