• The Journal of Korean Medicine
• /
• v.43 no.3
• /
• pp.1-15
• /
• 2022

Objectives: Myrrh have been used as a traditional remedy to treat infectious and inflammatory diseases. However, it is largely unknown whether myrrh ethanol extract could exhibit the inhibitory activities against particulate matter (PM)-induced skin injury on human keratinocytes, HaCaT cells. Therefore, this study was aimed to investigate the inhibitory activity of myrrh ethanol extract on PM-induced skin injury in HaCaT cells. Methods: To investigate the inhibitory effects of myrrh ethanol extract in HaCaT cells, the skin injury model of HaCaT cells was established under PM treatment. HaCaT keratinocyte cells were pre-treated with myrrh ethanol extract for 1 h, and then stimulated with PM. Then, the cells were harvested to measure the cell viability, reactive oxygen species (ROS), pro-inflammatory cytokines including interleukin (IL) 1-beta, IL-6, and tumor necrosis factor (TNF)-𝛼, hyaluronidase, collagen, MMPs. In addition, we examined the mitogen activated protein kinases (MAPKs) and inhibitory kappa B alpha (I𝜅-B𝛼) as inhibitory mechanisms of myrrh ethanol extract. Results: The treatment of myrrh ethanol extract inhibited the PM-induced cell death and ROS production in HaCaT cells. In addition, myrrh ethanol extract treatment inhibited the PM-induced elevation of IL-1beta, IL-6, and TNF-𝛼. Also, myrrh ethanol extract treatment inhibited the increase of hyaluronidase, MMP and decrease of collagen. Furthermore, myrrh ethanol extract treatment inhibited the activation of MAPKs and the degradation of I𝜅-B𝛼. Conclusions: Our result suggest that treatment of myrrh ethanol extract could inhibit the PM-induced skin injury via deactivation of MAPKs and nuclear factor (NF)-𝜅B in HaCaT cells. This study could suggest that myrrh ethanol extract could be a beneficial agent to prevent skin damage or inflammation.

• Bulletin of the Korean Chemical Society
• /
• v.6 no.5
• /
• pp.259-263
• /
• 1985

Rate Constants for the solvolysis of p-methylbenzyl chloride in various ethanol-water mixtures were studied at 30 and $40^{\circ}C$ under various pressures up to 1600 bar. The rates of reaction were increased with increasing temperature and pressure, and decreased with increasing solvent composition of ethanol mole fraction. From the rate constants, the values of the activation parameters (${\Delta}V^{\neq},{\Delta}{\beta}^{\neq},{\Delta}H^{\neq}\;and\;{\Delta}S^{\neq}$) were evaluated. The values of ${\Delta}V^{\neq}\;and\;{\Delta}{\beta}^{\neq}$ exhibit the extremum behavior at about 0.30 mole fraction of ethanol. This behavior is discussed in terms of solvent structure variation (electrostriction). From the relation between the reaction rate and the dielectric constant of solvent or the number of water molecule participated in the transition state, it could be postulated that the reaction proceeds through $S_N1$ mechanism.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.20 no.6
• /
• pp.1664-1671
• /
• 2006

Cisplatin is a anti-neoplastic agent which is commonly used for the treatment of solid tumor. Cisplatin activates multiple signal transduction pathways involved in the stress-induced apoptosis in a variety of cell types. Cytotoxicity of cisplatin was detected in rat mesangial cells and the value of $IC_{50}$ is about 20 ${\mu}M$. The treatment of cisplatin to rat mesangial cells showed the apoptotic bodies and DNA fragmentation. The activation of caspase-3, -8, and -9 and proteolytic cleavage of PARP were observed in the rat mesangial cells treated time-dependently with cisplatin. The activation of ERK, p38 and JNK was also observed in the apoptosis induced by cisplatin in rat mesangial cells. The ethanol extract of Bojungbangam-tang (EBJT), a new hergal prescription composed of nine crude drugs, inhibited cisplatin-induced apoptosis in rat mesangial cells. EBJT reduced sub-G1 peak (apoptotic peak) in cisplatin-treated rat mesangial cells. The cisplatin-induced ERK and JNK activation in rat mesangial cells were blocked by EBJT, but EBJT had no effect on p38 activation. Taken together, these results con suggest that EBJT prevents cisplatin-induced apoptotic cell death in rat mesangial cells through inhibition of ERK and JNK activation.

• The Journal of Korean Medicine
• /
• v.20 no.1 s.37
• /
• pp.113-121
• /
• 1999

This Study was carried out to investigate the protective effect of GalHwaHaJungTang(GHT) on the gastric lesions indused by ethanol in rats. Rats were pretreated with GHT extract 1.7ml/kg, 3.4ml/kg, 5ml/kg and then were given orally 1ml of absolute ethanol 30min later. The animals were killed 1hr after ethanol treatment In morphorogic change, ethanol induced prominent longitudinal hemorrhagic lesions in the stomach. But GHT-pretreatment showed a dose-depentent decrease in the mucosa lesions. GHT extract siginificantly reduced lipid peroxidation and also induced an increase of superoxide dismutase(SOD), catalase and gluthathion(GSH) levels, but showed no influence in the type conversion of xanthine oxidase. These results suggest that the proposed gastroprotective effect may involve activation of antioxidant effects, but independent of the xanthine oxidase system.

• Journal of Microbiology and Biotechnology
• /
• v.7 no.1
• /
• pp.62-67
• /
• 1997

To enhance the hyperproductive and low energy-consuming ethanol fermentation rate, the thermotolerant yeast S. cerevisiae RA-74-2 cells were immobilized. An efficient immobilization condition was proved to be $1.5{\%}$ (w/v) alginate solution, neutral pH and 20 h activation of beads. The fermentation characteristics and stability at various temperatures were examined as compared with free S. cerevisiae RA-74-2 cells. The immobilized cells had excellent fermentation rate at the range of pH 3-7 at 30-$42^{\circ}C$ in 15-$20{\%}$ glucose media. When the seed volume was adjusted to 0.12 (v/v) (6ml bead/50 ml medium), $11{\%}$ (w/v) ethanol was produced during the first 34 hand $12.15{\%}$ (w/v) ethanol [$95{\%}$ (w/v) of theoretical yield] during the first 60 h in $25{\%}$ glucose medium. In repetitive fermentation using a 2 litre fermentor, 5.79-$7.27{\%}$ (w/v) ethanol [76-$95{\%}$ (w/v) of theoretical yield] was produced during the 40-55 h in $15{\%}$ glucose media. These data suggested the fact that alginate beads of thermotolerant S. cerevisiae RA-74-2 cells would contribute to economic and hyperproductive ethanol fermentation at high temperature.

• Molecules and Cells
• /
• v.20 no.2
• /
• pp.189-195
• /
• 2005

Ethanol has long been implicated in triggering apoptotic neurodegeneration. We examined the effects of ethanol on the rat brain during synaptogenesis when a spurt in brain growth occurs. This period corresponds to the first 2 postnatal weeks in rats and is very sensitive to ethanol exposure. Ethanol was administered subcutaneously to 7-day- postnatal rat pups by a dosing regimen of 3 g/kg at 0 h and again at 2 h. Blood ethanol levels peaked ($677{\pm}16.4mg/dl$) at 4 h after the first ethanol administration. The cerebral cortexes of the ethanol-treated group showed several typical symptoms of apoptosis such as chromosome condensation and disintegration of cell bodies. Activated caspase-3 positive cells were found in the cortex within 2 h of the first injection, and reached a peak at 12 h. In addition, TUNEL staining revealed DNA fragmentation in the same regions. These results demonstrate that acute ethanol administration causes neuronal cell death via a caspase-3-dependent pathway within 24 h, suggesting that activation of caspase-3 is a marker of the developmental neurotoxicity of ethanol.

• The Korean Journal of Physiology and Pharmacology
• /
• v.16 no.3
• /
• pp.153-158
• /
• 2012

Cellular effects of ethanol in YD-15 tongue carcinoma cells were assessed by MTT assay, caspase activity assay, Western blotting and flow cytometry. Ethanol inhibited the growth and proliferation of YD-15 cells in a dose- and time-dependent manner in an MTT assay. The effects of ethanol on cell cycle control at low percent range of ethanol concentration (0 to 1.5%), the condition not inducing YD-15 cell death, was investigated after exposing cells to alcohol for a certain period of time. Western blotting on the expression of cell cycle inhibitors showed that p21 and p27 was up-regulated as ethanol concentration increases from 0 to 1.5% whilst the cell cycle regulators, cdk1, cdk2, and cdk4 as well as Cyclin A, Cyclin B1 and Cyclin E1, were gradually down-regulated. Flow cytometric analysis of cell cycle distribution revealed that YD-15 cells exposed to 1.5% ethanol for 24 h was mainly arrested at G2/M phase. However, ethanol induced apoptosis in YD-15 cells exposed to 2.5% or higher percent of ethanol. The cleaved PARP, a marker of caspase-3 mediated apoptosis, and the activation of caspase-3 and -7 were detected by caspase activity assay or Western blotting. Our results suggest that ethanol elicits inhibitory effect on the growth and proliferation of YD-15 tongue carcinoma cells by mediating cell cycle arrest at G2/M at low concentration range and ultimately induces apoptosis under the condition of high concentration.

• Proceedings of the Korean Society of Embryo Transfer Conference
• /
• 2002.11a
• /
• pp.115-115
• /
• 2002

To evaluate the correlations between the expression of cyclin B1 mRNA and protein after stimulation and oocyte activation and development of nuclear transferred mouse embryos, this study was performed. The oocyte activation was induced by 7% ethanol or 10$\mu\textrm{g}$/$m\ell$ Ca-ionophore without (single) or with (combined) 10$\mu\textrm{g}$/$m\ell$ cycloheximide (CH). Cyclin B1 mRNA and protein in mouse oocytes was evaluated by PCR and western blot. The activation and blastocyst development in both single (P<0.05) and combined (P<0.01) stimulation was higher than in non-activated group. The cyclin B1 mRNA and protein levels were significantly reduced in both single and combined stimulation groups (P<0.05), respectively. Cyclin B1 mRNA expression showed a negative correlation between activation and blastocyst development in both single and combined stimulation groups. And also the expression of cyclin B1 protein showed a negative correlation with between oocyte activation and blastocysts development in both single and combined stimulation groups. In conclusion, it may suggest that single and combined stimulation increases the oocyte activation and blastocyst development of nuclear transferred embryos, because it induces the degradation of cyclin B1 mRNA and protein after activation in enucleated mouse oocytes.

• Development and Reproduction
• /
• v.15 no.3
• /
• pp.205-213
• /
• 2011

Ethanol treatment during the brain growth spurt period has been known to induce the death of Purkinje cells. The underlying molecular mechanisms and the role of reactive oxygen species (ROS) in triggering ethanol-induced Purkinje cell death are, however, largely unresolved. We undertook TUNEL staining, western blotting assay and immunohistochemistry for the cleaved forms of caspase-3 and -9, with calbindin D28K double immunostaining to identify apoptotic Purkinje cells. The possibility of ROS-induced Purkinje cell death was immunohistochemically determined by using anti-8-hydroxy-2'deoxyguanosine (8-OHdG), a specific cellular marker for oxidative damage. The results show that Purkinje cell death of PD 5 rat cerebellum following ethanol administration is mediated by the activation of caspase-3 and -9. However, unexpectedly, TUNEL staining did not reveal any positive Purkinje cells while there were some TUNEL-positive cells in the internal and external granular layer. 8-OHdG was detected in the Purkinje cell layers at 8 h, peaked at 12-24 h, but not at 30 h post-ethanol treatment. No 8-0HdG immunoreactive cells were detected in the internal and external granular layer. The lobule specific 8-OHdG staining patterns following ethanol exposure are consistent with that of ethanol-induced Purkinje cell loss. Thus, we suggest that ethanol-induced Purkinje cell death may not occur by the classical apoptotic pathway and oxidative damage is involved in ethanol-induced Purkinje cell death in the developing cerebellum.

• Nutrition Research and Practice
• /
• v.4 no.1
• /
• pp.11-15
• /
• 2010

The purpose of the present study was to investigate the effect of ethanol extracts from red pepper seeds on the antioxidative defense system and oxidative stress in rats fed a high fat high cholesterol diet. Rats were divided into four experimental groups which were composed of high fat high cholesterol diet group (HF), high fat high cholesterol diet with 0.1% ethanol extracts from red pepper seeds supplemented group (HEA), high fat high cholesterol diet with 0.2% ethanol extracts from red pepper seeds supplemented group (HEB) and high fat high cholesterol diet with 0.5% ethanol extracts from red pepper seeds supplemented group (HEC). Supplementation of ethanol extracts from red pepper seeds groups (HEA, HEB and HEC) resulted in significantly increased activities of hepatic glutathione peroxidase and catalase. Hepatic superoxide radical contents in microsome and mitochondria were significantly reduced in the groups supplemented with red pepper seeds ethanol extracts. Hepatic hydrogen peroxide content in the mitochondria was reduced in ethanol extracts from red pepper seeds supplemented groups. TBARS values in the liver were reduced in red pepper seeds ethanol extracts supplemented groups. Especially, HEB and HEC groups were significantly decreased compared to the HF group. Hepatic carbonyl values were significantly reduced in mitochondria in these supplemented groups. These results suggest that red pepper seeds ethanol extracts may reduce oxidative damage, by activation of antioxidative defense system in rats fed high fat high cholesterol diets.