• Korean Journal of Ecology and Environment
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• v.37 no.3 s.108
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• pp.313-318
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• 2004

Di-2-ethylhexyl phthalate (DEHP) is a widely used plasticizer known to be a suspected xenoestrogen and a causative agent of oxidative damage to the RBC cell membrane ir vitro. We evaluated the toxic effects of a scarcely documented aquatic environmental pollutant, DEHP, on selected haematological endpoints in the bagrid catfish, Pseudobagrus fulvidraco. Bagrid catfish were exposed to DEHP (300, 1,000 mg DEHP kg body weight$^{-1}$) through thrice intraperitoneal injection and effects were assessed in blood of the exposed organisms. Haematological property, serum organic and inorganic chemistry were monitored in blood of Bagrid catfish. DEHP exposed-fish showed erythropenia; low hematocrit (Ht) and hemoglobin (Hb) content and red blood cell count showed a significantly higher than in that of the control group. The treatment group showed a significantly lower concentration of serum total protein, cholesterol and triglyceride compared with those in the control group. The value of calcium and osmolality were significantly decreased in the DEHP treatment group, compared with the control group.

• The Korean Journal of Food And Nutrition
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• v.30 no.4
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• pp.673-680
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• 2017

Fludarabine, a chain terminating anti-cancer drug, is a purine analogue that causes DNA strand breaks in normal cells. In this study, we determined if A. melanocarpa and Korean red ginseng extract mixture reduce cytotoxicity of fludarabine. Treatment of HaCaT cells with $10{\mu}M$ of fludarabine for 24 hours decreased cell viability and increased DNA strand breaks. Treatment of A. melanocarpa and Korean red ginseng extract mixture for 24 hours increased cell viability as compared with single extract treatment. The protective effect of these extracts on cell activity increased in a concentration-dependent manner. DNA strand breaks induced by fludarabine decreased as concentration of extract mixture increased. p-H2AX level, a marker of DNA strand breakage, decreased depending on the concentration of extract mixture. The effect of mixed extract of A. melanocarpa and Korean red ginseng on DNA damage is due to the anti-oxidative effect of A. melanocarpa and signal transmission through glucocorticoid receptor upon binding of saponin of Korean red ginseng.

• The Journal of Traditional Korean Medicine
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• v.15 no.1
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• pp.97-105
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• 2006

To study on antioxidant effects in the liver of 40-week-old mouse, the sample were orally pretreated 5mg/kg/day for 5 days with red ginseng saponin components(total saponin, protopanaxadiol saponin, protopanaxatriol saponin, ginsenoside-Rd, ginsenoside-Re, compound-K) for 5 days. The ability of saponin to protect the mouse liver from oxidative damage was examined by determining the activity of superoxide dismutase(SOD), glutathione peroxidase(GPx) and the contents of glutathione, the level of malondialdehyde, The only protopanaxadiol among the ginseng saponin fractions was significantly increased the hepatic SOD activity(p<0.01). The red ginseng saponin induced a slight increase of GPx activity, especially ginsenoside Rd, compound K and protopanaxatriol treatments significantly increased its activity. The content of glutathione was significantly increased by total saponin, protopanaxadiol and ginsenoside Rd(p<0.01), but the oxidized glutathione level was lowered in all the red ginseng saponin. Finally, the level of malondialdehyde was significantly decreased by ginsenoside Rd and protopanaxadiol. In conclusion, protopanaxadiol and ginsenoside Rd among the saponin fraction were especially increased in the activity of hepatic antioxidative enzyme and decreased the lipid peroxidation that was expressed in term of MDA formation. This comprehensive antioxidant effects of red ginseng saponin seems to be by a certain action of saponin other than a direct antioxidant action.

• Toxicological Research
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• v.35 no.3
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• pp.249-255
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• 2019

Cadmium is a strong toxic heavy metal which presents in paints and liquid wastes and causes oxidative stress in fish. On the other hand, lead is widely used for different purposes, e.g. lead pipes, it targets vital organs such as liver and kidney causing biochemical alterations. The present study evaluates the effects of 60 days exposure to Cd and Pb either single or combined together in African catfish. Sixty-four fishes were divided into 3 groups and exposed to $CdCl_2$ (7.02 mg/L) or $PbCl_2$ (69.3 mg/L) or a combination of them along with control group. Activities of acid phosphatase (ACP), lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) were estimated. Moreover, gill, liver and kidney were assayed for activities of superoxide dismutase (SOD), catalase (CAT) and levels of glutathione (GSH) and malondialdehyde (MDA). Individual exposure showed that both Cd and Pb significantly decreased LDH activity and SOD activity in the kidney. Pb significantly increased G-6-PDH activity and decreased GSH level in the gill. CAT activity in liver and kidney elevated significantly on Cd exposure while lead caused a significant depletion in the liver and significant elevation in the kidney. Both Cd and Pb significantly increased MDA levels in liver and kidney while Pb increased its level in gills. The combined exposure resulted in normalization of LDH, G-6-PDH activity, and CAT activity in liver and kidney as well as GSH level in both tissues and MDA in gill and kidney. The combination increased SOD activity and MDA level in liver and decreased SOD activity in kidney and GSH level in gills. In conclusion, the antioxidant system of African catfish was adversely affected by prolonged exposure to Cd and Pb. The combined exposure caused less damage than individual exposure and returned most parameters to those of controls.

• Journal of Preventive Veterinary Medicine
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• v.42 no.4
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• pp.133-142
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• 2018

This study investigated the characteristics of obesity induced by a high-fat diet (HD) over 13 weeks in Rhbdf2 gene knockout (KO) mice. Forty 7-week-old Rhbdf2 wild and KO mice were used and the mice were divided into 4 groups: Wild-ND (n=10, Rhbdf2 wild mice, normal diet (ND)), Wild-HD (n=10, Rhbdf2 wild mice, HD), KO-ND (n=10, Rhbdf2 KO mice, ND) and KO-HD (n=10, Rhbdf2 KO mice, HD). The relative epididymal fat weight in KO-HD was significantly increased compared with that in KO-ND (P<0.01). The relative liver and spleen weights in KO-HD were decreased compared with those in Wild-HD (p < 0.05) and KO-ND (p < 0.01). The mRNA expression of SOD1 in KO-ND was significantly reduced compared with that in Wild-ND (p < 0.05). In Wild-ND and HD, the mRNA expressions of $TNF-{\alpha}$ and IL-6 in epididymal fat were significantly increased compared with those in KO-ND and HD (p < 0.01). A significant increase of $TNF-{\alpha}$ and IL-6 mRNA expression was observed in KO-HD compared with KO-ND (p < 0.01). These results indicated that Rhbdf2 genes may regulate high fat diet-induced obesity damage by anti-inflammatory and anti-oxidative roles in fat tissue of mice.

• Biomedical Science Letters
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• v.27 no.3
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• pp.142-153
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• 2021

Liver fibrosis is a wound-healing response to chronic liver injury, which is caused by the continuous and excess deposition of extracellular matrix (ECM). The aim of this study is to investigate whether Uncaria rhynchophylla water extract (UR) can ameliorate thioacetamide (TAA)-induced liver fibrosis. The liver fibrosis model was induced on C57BL/6 mice by intraperitoneal injection with TAA three times a week for 8 weeks. UR (200 mg/kg) or silymarin (50 mg/kg) was administered orally daily for 8 weeks. Biochemical analyses including AST, ALT, MPO, and Ammonia levels were measured in serum. In the mice liver tissues, western blot and histological staining were analyzed. As a result, UR dramatically reduced the levels in serum AST, ALT, MPO, and Ammonia levels. UR treatment regulated NADPH oxidase factors expression, and antioxidant enzymes except for GPx-1/2 were significantly increased via Nrf2 activation. Furthermore, pro-inflammatory mediators, such as COX-2 and iNOS were markedly suppressed through the inhibition of NF-κB activation. Expressions of ECM-related protein including α-SMA and Collagen I were noticeably decreased. The additional histological evaluation confirmed that hepatocyte damage and collagenous fiber accumulation were attenuated. Taken together, these data suggest that UR possessed hepatoprotective effects in TAA-induced liver fibrosis via the NF-κB inactivation and Nrf2 activation. Therefore, UR may act as a potential therapeutic drug against liver fibrosis.

• Journal of Ginseng Research
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• v.45 no.1
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• pp.108-118
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• 2021

Background: Korean ginseng (Panax ginseng Meyer) contains a variety of ginsenosides that can be metabolized to a biologically active substance, compound K. Previous research showed that compound K could be enriched in the red ginseng extract (RGE) after hydrolysis by pectinase. The current study investigated whether the enzymatically hydrolyzed red ginseng extract (HRGE) containing a notable level of compound K has cognitive improving and neuroprotective effects. Methods: A scopolamine-induced hypomnesic mouse model was subjected to behavioral tasks, such as the Y-maze, passive avoidance, and the Morris water maze tests. After sacrificing the mice, the brains were collected, histologically examined (hematoxylin and eosin staining), and the expressions of antioxidant proteins analyzed by western blot. Results: Behavioral assessment indicated that the oral administration of HRGE at a dosage of 300 mg/kg body weight reversed scopolamine-induced learning and memory deficits. Histological examination demonstrated that the hippocampal damage observed in scopolamine-treated mouse brains was reduced by HRGE administration. In addition, HRGE administration increased the expression of nuclear-factor-E2-related factor 2 and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase and heme oxygenase-1 in hippocampal tissue homogenates. An in vitro assay using HT22 mouse hippocampal neuronal cells demonstrated that HRGE treatment attenuated glutamate-induced cytotoxicity by decreasing the intracellular levels of reactive oxygen species. Conclusion: These findings suggest that HRGE administration can effectively alleviate hippocampus-mediated cognitive impairment, possibly through cytoprotective mechanisms, preventing oxidative-stress-induced neuronal cell death via the upregulation of phase 2 antioxidant molecules.

• International Journal of Oral Biology
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• v.45 no.4
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• pp.179-189
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• 2020

Green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiation-induced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiation-induced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.

• Journal of Ginseng Research
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• v.46 no.2
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• pp.266-274
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• 2022

Colon cancer, the third most frequent occurred cancer, has high mortality and extremely poor prognosis. Ginsenoside, the active components of traditional Chinese herbal medicine Panax ginseng, exerts antitumor effect in various cancers, including colon cancer. However, the detailed molecular mechanism of Ginsenoside in the tumor suppression have not been fully elucidated. Here, we chose the representative ginsenoside Rg3 and reported for the first time that Rg3 induces mitophagy in human colon cancer cells, which is responsible for its anticancer effect. Rg3 treatment leads to mitochondria damage and the formation of mitophagosome; when autophagy is inhibited, the clearance of damaged mitochondria can be reversed. Next, our results showed that Rg3 treatment activates the PINK1-Parkin signaling pathway and recruits Parkin and ubiquitin proteins to mitochondria to induce mitophagy. GO analysis of Parkin targets showed that Parkin interacts with a large number of mitochondrial proteins and regulates the molecular function of mitochondria. The cellular energy metabolism enzyme GAPDH is validated as a novel substrate of Parkin, which is ubiquitinated by Parkin. Moreover, GAPDH participates in the Rg3-induced mitophagy and regulates the translocation of Parkin to mitochondria. Functionally, Rg3 exerts the inhibitory effect through regulating the nonglycolytic activity of GAPDH, which could be associated with the cellular oxidative stress. Thus, our results revealed GAPDH ubiquitination by Parkin as a crucial mechanism for mitophagy induction that contributes to the tumor-suppressive function of ginsenoside, which could be a novel treatment strategy for colon cancer.

• BMB Reports
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• v.55 no.8
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• pp.370-379
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• 2022

Human pregnancy is a delicate and complex process where multiorgan interactions between two independent systems, the mother, and her fetus, maintain pregnancy. Intercellular interactions that can define homeostasis at the various cellular level between the two systems allow uninterrupted fetal growth and development until delivery. Interactions are needed for tissue remodeling during pregnancy at both fetal and maternal tissue layers. One of the mechanisms that help tissue remodeling is via cellular transitions where epithelial cells undergo a cyclic transition from epithelial to mesenchymal (EMT) and back from mesenchymal to epithelial (MET). Two major pregnancy-associated tissue systems that use EMT, and MET are the fetal membrane (amniochorion) amnion epithelial layer and cervical epithelial cells and will be reviewed here. EMT is often associated with localized inflammation, and it is a well-balanced process to facilitate tissue remodeling. Cyclic transition processes are important because a terminal state or the static state of EMT can cause accumulation of proinflammatory mesenchymal cells in the matrix regions of these tissues and increase localized inflammation that can cause tissue damage. Interactions that determine homeostasis are often controlled by both endocrine and paracrine mediators. Pregnancy maintenance hormone progesterone and its receptors are critical for maintaining the balance between EMT and MET. Increased intrauterine oxidative stress at term can force a static (terminal) EMT and increase inflammation that are physiologic processes that destabilize homeostasis that maintain pregnancy to promote labor and delivery of the fetus. However, conditions that can produce an untimely increase in EMT and inflammation can be pathologic. These tissue damages are often associated with adverse pregnancy complications such as preterm prelabor rupture of the membranes (pPROM) and spontaneous preterm birth (PTB). Therefore, an understanding of the biomolecular processes that maintain cyclic EMT-MET is critical to reducing the risk of pPROM and PTB. Extracellular vesicles (exosomes of 40-160 nm) that can carry various cargo are involved in cellular transitions as paracrine mediators. Exosomes can carry a variety of biomolecules as cargo. Studies specifically using exosomes from cells undergone EMT can carry a pro-inflammatory cargo and in a paracrine fashion can modify the neighboring tissue environment to cause enhancement of uterine inflammation.