• Journal of Radiation Protection and Research
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• v.15 no.2
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• pp.27-39
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• 1990

Appreciable radiation exposures certainly were occurred in the reactor burn-up, the nuelear fall-out and the surroundings of nuclear installations with radioactive effluents. Therefore, radioactive nuclides is not only potentially hazardous to workers of nuclear power plants and related industrials, but also the wokers who handle radioactive nuclides in biochemical research and nuclear medicine diagnostics. And in the case of occurring the nuclear accidents, the early medical treatment of radiation injury should be necessary but little is established medical procedures to decontaminate the victims of internal contamination of radioactive nuclides in korea. Accordingly, to achieve the basic data for protective roles and medical treatment of radiation injury, the present studies were carrid out to evaluate the decontamination of uranium by the chemical drugs. The results observed were summarized as follows: 1. The combined treatmet group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection were increased significantly in the change of body weight than uranyl nitrate-only group (P<0.005). 2. All the experimental groups were increased the fluid intake and urine volume on the uranyl nitrate-induced acute renal failure. but the combined treatment group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection have the higher increment of fluid intake and urine volume (P<0.05). 3. When sodium bicarbonate and saline was treated with uranyl nitrate injection simultaneously. and dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was significantly reduced in BUN concentration (P<0.01). 4. When dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was reduced more significantly on the increment of serum creatinine concentration than that observed in uranyl nitrate-only group(P<0.01). but when the combined treatment of sodium bicarbonate and saline with uranyl nitrate simultaneously, there was still. albeit much less marked. decrease in serum creatinine concentration. 5. The sodium bicarbonate and saline was treated with uranyl nitrate simultaneously and dithiothreitol was administered at 30 minutes after uranyl nitrate were excreted markedly higher urine creatinine concentration than the uranyl nitrate-only group. 6. Uranyl nitrate has been used in experimental animals to produce hydropic degeneration and swelling of proximal tubules, disappearance of microvilli and brush border or necrosis in the kidney and centrilobular necrosis, congestion, and telangiectasia of the liver. When the sodium bicarbonate and saline was treated with uranyl nitrate simultaneously, and dithiothreitol was administered. 30 minutes after uranyl nitrate, there was more marked the protective effect than uranyl nitrate-only group. Finally, if the sodium bicarbonate and saline may administered as quickly as possible each time that some risk for internal contamination, with uranium, and dithiothreitol is administered 30 minutes after uranium contamination, there ameliorates the course of uranyl nitrate-induced acute renal failure.and this effect is assocciated with prevention of uranium (heavy metal)-induced alterations in BUN, serum creatinine, urine creatinine, fluid intake, urine volume and body weight.

• The Korea Journal of Herbology
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• v.38 no.1
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• pp.11-19
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• 2023

Objectives : Neuroinflammation is a common pathological mechanism of neurodegenerative diseases, and the development of therapeutic agents is urgently needed. Red ginseng has been known to be good for the immune stimulation in Eastern Asia. Although the immuno-stimulatory activity of red ginseng are already known, the neuro-protective effects of cultivated red ginseng with fermented complex mushroom-cereal mycelium (RGFM) have not been conducted. Thus, in this study, we tried to investigate the anti-neuroinflammatory effect of RGFM water extract on lipopolysaccharide (LPS) stimulated BV2 cells. Methods : BV2 cells were pretreated with RGFM 1 h prior to LPS exposure. To determine the neuro-protective effects of RGFM water extract, we measured the expression of inflammatory mediators including inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and nitric oxide (NO) and pro-inflammatory cytokines such as interleukin (IL)-1𝛽, IL-6 and tumor necrosis factor (TNF)-𝛼 in LPS-stimulated BV2 cells. In addition, to find out the regulatory mechanism of RGFM water extract, we assessed the protein levels of mitogen-activated protein kinases (MAPKs) and inhibitory 𝜅B𝛼 (I𝜅B𝛼) by western blotting. Results : In our study, treatment of RGFM reduced the mRNA expression of iNOS and COX-2 and suppressed NO production in LPS-stimulated BV2 cells. Additionally, the secretion of IL-1𝛽 and TNF-𝛼 but not IL-6 was significantly inhibited by RGFM. Furthermore, RGFM water extract inhibited the phosphorylation of c-Jun N-terminal kinase (JNK). Conclusions : Taken together, these findings suggest that RGFM water extract has a protective effect on neuroinflammation through inhibition of JNK.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.159-164
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• 2005

Effects of antioxidants on the established nephropathy were investigated. The experimental nephropathy was induced in rats by intravenous injection of adriamycin (2 mg/kg). Six weeks later, when proteinuria was apparent, the rats were supplemented with N-acetylcysteine (NAC, 1 g/kg/day) in drinking water for additional 6 weeks. Glomerulosclerosis score and tubulointerstitial injury index were determined by light microscopy. Expression of transforming growth factor (TGF) ${\beta}1$ and laminin ${\beta}1$ was determined in the renal cortex by reverse transcription-polymerase chain reaction, Western blotting, immunohistochemistry, and immunogold electron microscopy. The adriamycin-induced proteinuria as well as the glomerulosclerosis and tubulointerstitial injury was ameliorated by the treatment with NAC. Adriamycin increased the expression of TGF ${\beta}1$ mRNA and protein, which was ameliorated by NAC. Although the expression of laminin ${\beta}1$ mRNA was increased, adriamycin did not significantly alter that of its protein. These results indicate that antioxidants ameliorate the established nephropathy in association with normalization of overexpressed TGF ${\beta}1$.

• Childhood Kidney Diseases
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• v.3 no.1
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• pp.64-71
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• 1999

Purpose : The protective effects of dietary protein on the progression of renal failure were studied in subtotally nephrectomized rats. Methods : Treatment groups were as follows; 5/6 nephrectomy and a normal protein ($18.5\%$) diet (NP); 5/6 nephrectomy and a low protein ($6\%$) diet (LP): 5/6 nephrectomy, a normal protein diet and converting enzyme inhibitor, enalapril (NPE): 5/6 nephrectomy, a low protein diet and enalapril (LPE). Both diets were isocaloric and had the same phosphorus content. Proteinuria, remnant kidney weight, mesangial matrix expansion score and glomerular volume were assessed at 4, 12 and 16 weeks after renal ablation. Results : LP and NP developed progressive hypertension. Eight weeks after surgery, LPE and NPE controlled hypertension. LP, LPE, and NPE had significantly less proteinuria than NP at 16 weeks (P<0.05). Kidney weight in LP were markedly less enlarged than NP (P<0.05). There was no difference in kidney weight between LPE and NPE. At 12 and 16 weeks the mesangial matrix expansion score was significantly less in LP, LPE, and NPE compared to NP (P<0.05). At 12 and 16 weeks mean glomerular volume was significantly less in LP compared to NP (P<0.05). At 12 and 16 weeks mean glomerular volume in LPE was significantly less compared to NPE. Conclusion : Dietary protein restriction afforded considerable protection from renal injury in the rat remnant kidney model. During the enalapril treatment, there was no additional protective effect of dietary protein restriction against the development of renal lesions.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.8
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• pp.303-312
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• 2019

Oxidative stress in kidneys can precede the development of chronic renal injury. We investigated the antioxidative effect of membrane-free stem cell extract (MFSCE) from adipose tissue in LLC-$PK_1$ renal proximal tubule cells. Treatment of LLC-$PK_1$ cells with MFSCE showed the up-regulation of heme-oxygenase-1, thioredoxin reductase 1, and NADPH quinine oxidoreductase-1 protein expressions, which are proteins related with antioxidative activities. When oxidative stress was induced by 3-morpholinosydnonimine (SIN-1), cell viability was decreased, indicating that LLC-$PK_1$ cells were damaged by SIN-1. However, MFSCE significantly elevated cell viability from 58.84% to 64.43% at the concentration of $2.5{\mu}g/mL$ in oxidative stress-induced LLC-$PK_1$ cells. Furthermore, MFSCE ameliorated inflammation and apoptosis in SIN-1-treated LLC-$PK_1$ cells by modulating protein expressions. Inducible nitric oxide synthase and cyclooxygenase-2 protein expressions were down-regulated when LLC-$PK_1$ cells were treated with MFSCE. Apoptosis-related proteins, including B-cell lymphoma-2-associated X protein/B-cell lymphoma-2 ratio, cleaved caspase-3, and cleaved-poly (ADP-ribose) polymerase, were also down-regulated. It indicated that MFSCE protected apoptosis against oxidative stress in LLC-$PK_1$ cells. Taken together, these results suggested that MFSCE had a protective effect against SIN-1-induced oxidative stress in LLC-$PK_1$ cells. Therefore, MFSCE could be a promising therapeutic agent for oxidative stress-induced renal injury.

• Korean Journal of Medicinal Crop Science
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• v.24 no.2
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• pp.115-120
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• 2016

Background: This study examined the hypoglycemic and kidney protective effect of black ginseng in streptozotocin-induced diabetic mice. Methods and Results: Diabetes was induced by treating mice with streptozotocin (STZ) for four weeks. In vivo studies were performed in order to investigate the hypoglycemic effect of the black ginseng prosapogenin (GBG05-FF) extract. The body weight and blood glucose level were measured. Moreover, after the mice were sacrificed, the kidneys were isolated and histological changes were observed with hematoxylin and eosin staining. Blood urea nitrogen and creatinine levels were also measured. The results showed that administration of black ginseng increased body weight. Compared to blood glucose levels in STZ mice, blood glucose levels were reduced by 48% in STZ mice supplemented with 300 mg/kg of black ginseng, and by 69% in STZ mice supplemented with 900 mg/kg. Furthermore, histopathological examination of STZ mouse kidneys revealed, changes in the kidneys, epithelial cell damages, inflammatory cell infiltration and glomerulus hypertrophy. However, a significant reduction of glomerular water droplets (indicative of glomerulus hypertrophy) was observed in the kidneys of STZ mice supplemented with black ginseng extract. Conclusions: These results suggest that black prosapogenin (GBG05-FF) ginseng extract has a significant hypoglycemic effect and can be used as an anti-diabetic substance and renal protective agents as part of dietary supplements or novel drugs.

• Korean Journal of Medicinal Crop Science
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• v.25 no.5
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• pp.322-327
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• 2017

Background: Cynaroside is a flavone, a flavonoid-like compound, known by different names (luteoloside and cinaroside). It is commonly found in Lonicera japonica Thunb., Chrysanthemum moriflium, and Angelica keiskei. The process of cell death has been classified as necrosis and apoptosis. Necrosis refers to unregulated cell death induced by a chemotherapeutic agent. Doxorubicin is an anthracycline anti-cancer drug used to treat acute leukemia, cancer, and lymphoma. However, it induces nephrotoxicity including tubular damage. Therefore, we investigated the protective effect of cynaroside against doxorubicin-induced necrosis in HK-2 cells. Methods and Results: To confirm the beneficial effect of cynaroside on doxorubicin-induced necrosis, HK-2 cells, a human proximal tubule epithelial cell line were treated with $10{\mu}M$ doxorubicin and $80{\mu}M$ cynaroside. Doxorubicin treatment resulted in increased DNA fragmentation, caspase-3 activity and mitochondria hyperactivation during cell necrosis. However, pretreatment with $80{\mu}M$ cynaroside attenuated DNA fragmentation, caspase-3 activity and mitochondria hyperactivation induced by $10{\mu}M$ doxorubicin in HK-2 cells. Conclusions: These results indicated that pretreatment with cynaroside ameliorated doxorubicin-induced necrosis in HK-2 cells. Therefore, cynaroside be used as a therapeutic agent for improving doxorubicin-induced nephrotoxicity. However, further studies are required to evaluated the toxicity of cynaroside treatment in animals and to determine its protective effect against doxorubicin-induced nephrotoxicity in an animal model.

• Journal of the Korean Society of Food Culture
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• v.18 no.3
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• pp.202-210
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• 2003

The purpose of this study was to investigate the effects of dietary purple sweet potato(Ipomoea batatas) powder on serum lipid levels and antioxidative enzymes in normal and pretective effect on hepatotoxicity rats induced by carbon tetrachlolide. Four groups of rats (3-week-old inbred Sprague-Dawley male rats) were normal rats fed control diet(C), induced hepatotoxicity rats fed control diet(EC), normal rats fed purple sweet potato diet(P), and induced hepatotoxicity rats fed purple potato sweet diet(EP). Rats were induced by single injection of 50% carbon tetrachlolide(0.1 mL/100 g B.W., i.p.). The rats were fed ad libitum each of the experimental diet for 5 weeks. After 5 weeks the rats were sacrificed and activities of antioxidant enzymes and lipid peroxidation products were determined in their liver homogenates. But serum concentrations of lipid was not significant in all groups. Serum alanine aminotransferase(ALT/GPT) and aspartate aminotransferase(AST/GOT) of the EC and EP groups were heigher than the C and P groups. The hepatic glucose 6-phosphatase(G6Pase) activity of the group fed purple potato diet(P) was lower than the other groups(p<0.05). However, The glutathione peroxidase(GPx) activities was not statistically different between the groups. Renal glutathione S-transferase(GST) activity of the EC and EP groups were lower than the C and P groups(p<0.05). In conclusion, these results suggest that purple sweet potato is believed to be possible protective effect on hepatotoxicity rats induced by carbon tetrachlolide.

• Journal of Ginseng Research
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• v.40 no.2
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• pp.135-140
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• 2016

Background: Nephrotoxicity is a common side effect of medications. Panax ginseng is one of the best-known herbal medicines, and its individual constituents enhance renal function. Identification of its efficacy and mechanisms of action against drug-induced nephrotoxicity, as well as the specific constituents mediating this effect, have recently emerged as an interesting research area focusing on the kidney protective efficacy of P. ginseng. Methods: The present study investigated the kidney protective effect of fermented black ginseng (FBG) and its active component ginsenoside 20(S)-Rg3 against cisplatin (chemotherapy drug)-induced damage in pig kidney (LLC-PK1) cells. It focused on assessing the role of mitogen-activated protein kinases as important mechanistic elements in kidney protection. Results: The reduced cell viability induced by cisplatin was significantly recovered with FBG extract and ginsenoside 20(S)-Rg3 dose-dependently. The cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), p53, and cleaved caspase-3 were decreased after cotreatment with FBG extract or ginsenoside 20(S)-Rg3. The elevated percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment was significantly abrogated by cotreatment with FBG and the ginsenoside 20(S)-Rg3. Conclusion: FBG and its major ginsenoside 20(S)-Rg3, ameliorated cisplatin-induced nephrotoxicity in LLC-PK1 cells by blocking the JNKep53ecaspase-3 signaling cascade.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.220-226
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• 2014

BACKGROUND/OBJECTIVES: Arsenic, which causes human carcinogenicity, is ubiquitous in the environment. This study was designed to evaluate modulation of arsenic induced cancer by resveratrol, a phytoalexin found in vegetal dietary sources that has antioxidant and chemopreventive properties, in arsenic trioxide ($As_2O_3$)-induced Male Wistar rats. MATERIALS/METHODS: Adult rats received 3 mg/kg $As_2O_3$ (intravenous injection, iv.) on alternate days for 4 days. Resveratrol (8 mg/kg) was administered (iv.) 1 h before $As_2O_3$ treatment. The plasma and homogenization enzymes associated with oxidative stress of rat kidneys were measured, the kidneys were examined histologically and trace element contents were assessed. RESULTS: Rats treated with $As_2O_3$ had significantly higher oxidative stress and kidney arsenic accumulation; however, pretreatment with resveratrol reversed these changes. In addition, prior to treatment with resveratrol resulted in lower blood urea nitrogen, creatinine and insignificant renal tubular epithelial cell necrosis. Furthermore, the presence of resveratrol preserved the selenium content ($0.805{\pm}0.059{\mu}g/g$) of kidneys in rats treated with $As_2O_3$. However, resveratrol had no effect on zinc level in the kidney relative to $As_2O_3$-treated groups. CONCLUSIONS: Our data show that supplementation with resveratrol alleviated nephrotoxicity by improving antioxidant capacity and arsenic efflux. These findings suggest that resveratrol has the potential to protect against kidney damage in populations exposed to arsenic.