• Journal of Korean Medicine for Obesity Research
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• v.15 no.2
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• pp.153-161
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• 2015

Gamrosu is a modified fasting therapy beverage (431 kcal/d). A retrospective observational study was conducted to investigate the detoxification feasibility of Gamrosu. Three cases were reviewed which participants have finished the fasting with Garmrosu for 10 consecutive days. Detoxification profiles of Gamrosu were reviewed at pre- and post-fasting sessions. Post-Gamrosu session, -6.3% of average weight, -6.5% of average body fat mass and -6.6% of average muscle mass were reduced with the nutrition indices being improved. The inflammation indices showed the significant diminished profiles. Liver/kidney functions and the standard of electrolytes were maintained within normal range in stable manners, however, marginal elevation of total bilirubin and mild ketoacidosis were observed. The indices of oxidative stress decreased and those of antioxidative activity increased. The fatigue scale scores indicated lower scores except insomnia symptom. Taken together, detoxification profiles of Gamrosu were sufficiently feasible and the observed findings should be considered for further clinical studies.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.15 no.1
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• pp.127-139
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• 2002

This study was carried out to prove the therapeutic effects of BNJB on the catract. The objects of this study were CXSD mice that spontaneously eye rupture occurred from three weeks after birth and eventually generate cataract within 12 weeks. We applied eyewash made from BNJB to eyes of CXSD mice twice in a day till all the eyes of the negative control showed up the symptoms of a cataract and recorded the increasing patterns of cataractous eyes. To explained the therapeutic effects of the BNJB, We carried out the ex vivo experiment which cultivating eyeballs were offered oxidative stress condition by $0.03{\%}$ $H_2O_2$ during three days. Total co-enzyme was extracted from the cultured eyeballs and used to measure activities of catalase, superoxide dismutase, glutathion S-transferase and content of GSH. The results were obtained as follows: 1. When we treated the catalin to CXSD mouse as a positive control, it represented the delaying effect for cataract generation for 2-3 days compare with negative control. But it seems that it doesn't appropriate as a therapeutic, or delaying agent. 2. In the experimental BNJB group, Cataract formation rate was dramatically reduced by BNJB. This rate was much lower than positive group and means our new formulation for the therapy of cataract has a good potential. 3. In the analysis of individual medicines of BNJB, Mok-Jeok-Cho, Hwang-Lyun and Ha-Go-Cho didn't have a major effect of BNJB. 4. The cataract formation rate was repressed by Bing-Pyun and Jin- Joo-Boon about $40{\%}$ and $50{\%}$, respectively. We can presume that the anti-cataract effect of BNJB was caused by these two medicines. 5. When we surveyed the anti-oxidant activities of BNJB, enzyme activities of GSH, SOD, and Catalase increased about $10{\%},\30{\%}$, and 2.5 folds, respectively.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.32 no.4 s.59
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• pp.263-267
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• 2006

Antioxidative and anti-inflammatory activities of Petasites japonicus extract were evaluated. P. japonicus extract showed 70.1% inhibition on peroxidation of linoleic acid. In the experiment using the cell permeable dye, 2',7'- dichlorofluorescein diacetate (DCFDA) as an indicator of reactive oxygen species (ROS) generation, intracellular oxidative stress in UVB-irradiated keratinocytes was shown to be decreased by P. japonicus extract. Also, UVB-induced production of interleukin-$1{\alpha}$ and prostaglandin $E_2$ in human HaCaT keratinocytes was reduced in a dose-dependent manner by treatment with P. japonicus extract. All these results suggest that P. japonicus extract can be effectively used for prevention of UV-induced adverse skin reactions such as radical production and inflammation.

• Archives of Pharmacal Research
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• v.28 no.3
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• pp.311-318
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• 2005

Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC­PK1 cells were treated with H$_2$O$_2$ in the absence of serum to induce cell death. Subsequent to exposure to H$_2$O$_2$, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H202-treated control cells, it was observed that 0.5 $\mu$M of desipramine and 25 $\mu$M of NAC exhibited about 90 and $95\%$ of cytoprotection, respectively, against H$_2$O$_2$-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and $3\%$ respectively, when compared to $71\%$ in H$_2$O$_2$-exposed cells. Cellular glutathione level in 500 $\mu$M H202-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H$_2$O$_2$-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H$_2$O$_2$-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

• Archives of Pharmacal Research
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• v.27 no.5
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• pp.531-538
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• 2004

Ginsan, a polysaccharide isolated from Panax ginseng, has been shown to be a potent immunomodulator, producing a variety of cytokines such as TNF-a, IL-1$\beta$, IL-2, IL-6, IL-12, IFN-${\gamma}$ and GM-CSF, and stimulating lymphoid cells to proliferate. In the present study, we analyzed some immune functions 1$^{st}$-5$^{th}$ days after ginsan i.p. injection, including the level of non-protein thiols (NPSH) as antioxidants, heme oxygenase (HO) activity as a marker of oxidative stress, zoxazolamine-induced paralysis time and level of hepatic cytochrome P-450 (CYP450) as indices of drug metabolism system, and activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and albumin level as indicators of hepatotoxicity. Ginsan in the dose of 100 mg/kg caused marked elevation (1.7-2 fold) of HO activity, decrease of total CYP450 level (by 20-34%), and prolongation of zoxazolamine-induced paralysis time (by 65-70%), and showed some differences between male and female mice. Ginsan treatment did not seem to cause hepatic injury, since serum AST, ALT, and ALP activities and levels of total bilirubin and albumin were not changed.d.

• YAKHAK HOEJI
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• v.41 no.1
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• pp.86-93
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• 1997

Even though both N-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine have been widely used to establish the experimental model for dopaminergic neuronal ce ll death. mechanisms underlying this phenomenon have not been firmly explored. To investigate how these dopaminergic neurotoxins induce neuronal cell death, murine dopaminergic neuronal cell line, MN9D cells were treated with various concentration of either 6-hydroxydopamine or active form of MPTP, N methyl-4-phenylpyridinium (MPP$^+$). Treatment of cells with 5-100 uM 6-hydroxydopamine resulted in apoptotic cell death whereas cell death induced by 5~50 uM MPP$^+$ was not demonstrated typical apoptotic characteristics such as cell shrinkage, apoptotic body and nuclear condensation. Cell death induced by 6-hydroxydopamine was partially blocked in the presence of antioxidants including soluble form of vitamin E or desferrioxamine suggesting that generation of oxidative stress may be associated with 6-hydroxydopamine-induced cell death in MN9D cells. In contrast, MPP$^+$-induced cell death was not blocked by treatment with any of antioxidants tested. As previously demonstrated that MPP$^+$ caused metabolic alterations such as glucose metabolism, removal of glucose from the medium partially inhibited MPP$^+$-induced cell death suggesting excessive cycles of glycolysis may be associated with MPP$^+$-induced cell death. Taken together, these studies demonstrate that two types of dopaminergic neurotoxins recruit distinct neuronal cell death pathways.

• YAKHAK HOEJI
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• v.55 no.2
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• pp.121-126
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• 2011

Sipjundaebo-tang was a well-known restorative traditional herbal prescription that used to treat anemia, anorexia, fatigue and inflammation. In this study, we examined the bioconversion of compounds in the Sipjundaebo-tang (SJ) and fermented Sipjundaebo-tang with Lactobacillus fermentum KFRI 164 (FSJ) using established HPLC-DAD method. The chromatogram of FSJ has shown that the contents of six bioactive compounds 5-HMF, paeoniflorin, ferulic acid, cinnam aldehyde, decursin, glycyrrhizin in SJ has decreased. And the contents of unknown compounds (1), (2), (3), (4) and (5) in FSJ were higher than each contents of SJ. The antioxidant activities of SJ and FSJ were conducted by DPPH free radical and Hydrogen peroxide ($H_2O_2$) scavenging assay. Electron donating activity (EDA, %) value of FSJ has shown higher than 21.9% and 14.5% at a concentration of 0.5 mg/ml for DPPH radical scavenging activity and $H_2O_2$ scavenging activity, respectively. Also, the neuroprotective activities of SJ and FSJ against glutamate-induced oxidative stress in a mouse hippocampal cell line (HT22) were evaluated by MTT assay. As a result, FSJ has shown higher neuroprotective activity than 56.5% comparing with SJ. In conclusion, the fermented SJ using microorganism could convert compounds in SJ and enhance antioxidant activity and neuroprotective activity.

• Bulletin of the Korean Chemical Society
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• v.31 no.11
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• pp.3327-3332
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• 2010

We investigated the effects of newly synthesized 4-[(butylsulfinyl)methyl]-1,2-benzenediol (SMBD) on the prevention of atherosclerosis in hypercholesterolemic rabbits. SMBD exhibited stronger inhibition of $Cu^{2+}$-induced low-density lipoprotein oxidation than that of ascorbic acid or simvastatin. Three-month-old rabbits were fed an atherogenic diet containing 0.5% cholesterol and 10% coconut oil, while other two groups were given an atherogenic diet with intravenous injection of either simvastatin or SMBD (0.33 mg/kg/day) for 4 weeks. The concentrations of plasma cholesterol and thiobarbituric acid reactive substances were significantly decreased in SMBD groups, compared to the control group. Also, aortic lipid level in the SMBD group significantly lower than that in the control group. Furthermore, compared with the control group, the SMBD group significantly inhibited the increase of aortic intimal thickness by 36% via reducing of aortic reactive oxygen species and cyclooxygenase-2 protein levels. We conclude that raised antioxidant effect of SMBD results in significant prevention against hypercholesterolemia.

• Journal of Veterinary Clinics
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• v.26 no.3
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• pp.200-204
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• 2009

This study was performed to evaluate the effects of reduced L-glutathione on the oxidant/antioxidant status(superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GPx), protein carbonyl and lipid hydroperoxide(LPO) concentration), renal function(blood urea nitrogen(BUN) and serum creatinine levels), and microscopy of renal tissues in pigs undergoing unilateral renal ischemia-reperfusion(I/R). Sixteen Landrace and Yorkshire mixed-breed pigs were divided randomly into two groups: untreated control group and reduced L-glutathione-treated group(4 mg/kg IV). Each group had 8 pigs. Pigs were unilaterally nephrectomized and the kidney was subject to 30 min of renal pedicle occlusion. Blood samples for biochemical assay were collected on days 1, 3, 5, 7, and 14 post nephrectomy. Renal I/R injury were evaluated histopathologically by the microscopic observation of renal tissue sections and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as SOD, GPx, CAT, protein carbonyl and LPO were measured. The elevation of creatine and BUN levels was lower in the treated group, compared with the control group. The activities of antioxidant-enzyme were higher in the treated group, compared with the control group. In histological findings, the severity of damage in the reduced L-glutathione treated group was less when compared to the control group.

• Molecules and Cells
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• v.43 no.7
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• pp.662-670
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• 2020

We have investigated the involvement of the pre-mRNA processing factor 4B (PRP4) kinase domain in mediating drug resistance. HCT116 cells were treated with curcumin, and apoptosis was assessed based on flow cytometry and the generation of reactive oxygen species (ROS). Cells were then transfected with PRP4 or pre-mRNA-processing-splicing factor 8 (PRP8), and drug resistance was analyzed both in vitro and in vivo. Furthermore, we deleted the kinase domain in PRP4 using Gateway™ technology. Curcumin induced cell death through the production of ROS and decreased the activation of survival signals, but PRP4 overexpression reversed the curcumin-induced oxidative stress and apoptosis. PRP8 failed to reverse the curcumin-induced apoptosis in the HCT116 colon cancer cell line. In xenograft mouse model experiments, curcumin effectively reduced tumour size whereas PRP4 conferred resistance to curcumin, which was evident from increasing tumour size, while PRP8 failed to regulate the curcumin action. PRP4 overexpression altered the morphology, rearranged the actin cytoskeleton, triggered epithelial-mesenchymal transition (EMT), and decreased the invasiveness of HCT116 cells. The loss of E-cadherin, a hallmark of EMT, was observed in HCT116 cells overexpressing PRP4. Moreover, we observed that the EMT-inducing potential of PRP4 was aborted after the deletion of its kinase domain. Collectively, our investigations suggest that the PRP4 kinase domain is responsible for promoting drug resistance to curcumin by inducing EMT. Further evaluation of PRP4-induced inhibition of cell death and PRP4 kinase domain interactions with various other proteins might lead to the development of novel approaches for overcoming drug resistance in patients with colon cancer.