• Nutrition Research and Practice
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• v.10 no.4
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• pp.371-376
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• 2016

BACKGROUND/OBJECTIVES: Chronic ultraviolet (UV) exposure-induced reactive oxygen species (ROS) are commonly involved in the pathogenesis of skin damage by activating the metalloproteinases (MMP) that break down type I collagen. Adenophora remotiflora (AR) is a perennial wild plant that inhabits Korea, China, and Japan. The present study investigated the protective effects of AR against UVB-induced photo-damage in keratinocytes. MATERIALS/METHODS: An in vitro cell-free system was used to examine the scavenging activity of 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical and nitric oxide (NO). The effect of AR on ROS formation, antioxidant enzymes, elastase, MMP-1 level, and mRNA expression of MMP-1 were determined in UVB-irradiated human keratinocyte HaCaT cells. RESULTS: AR demonstrated strong DPPH free radical and NO scavenging activity in a cell-free system exhibiting $IC_{50}$ values of 1.88 mg/mL and 6.77 mg/mL, respectively. AR pretreatment dose-dependently attenuated the production of UVB-induced intracellular ROS, and antioxidant enzymes (catalase and superoxide dismutase) were enhanced in HaCaT cells. Furthermore, pretreatment of AR prevented UVB-induced elastase and collagen degradation by inhibiting the MMP-1 protein level and mRNA expression. Accordingly, AR treatment elevated collagen content in UVB-irradiated HaCaT cells. CONCLUSION: The present study provides the first evidence of AR inhibiting UVB-induced ROS production and induction of MMP-1 as a result of augmentation of antioxidative activity in HaCaT human keratinocytes. These results suggest that AR might act as an effective inhibitor of UVB-modulated signaling pathways and might serve as a photo-protective agent.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.1
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• pp.29-36
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• 2011

Nardostachyts chinensis (N. chinensis) belonging to the family Valerianaceae has been used to elicit stomachic and sedative effects. The MAPKs are serine/threonine kinases involved in the regulation of various cellular responses, such as cell proliferation, differentiation and apoptosis. The PKC also plays a key role in regulating the response of hematopoietic cells to both physiological and pathological inducers of proliferation and differentiation. This study investigated the signaling pathways on the U937 cell differentiation induced by N. chinensis. N. chinensis induced the differentiation of U937 cells, as shown by increased of differentiation surface antigen CD11b. Activation of ERK increased time-dependently in differentiation of U937 cells induced by N. chinensis, but activations of JNK and p38 were unaffected. Inhibitor of ERK (PD98059) significantly reduced CD11b expression induced by N. chinensis in U937 cells. In addition, N. chinensis increased protein level of PKC ${\beta}$I and PKC ${\beta}$II isoforms, but the protein level of PKC ${\alpha}$ and PKC ${\gamma}$was constant. PKC inhibitors (GF 109203X and H-7) inhibited U937 cell differentiation and the ERK activation induced by N. chinensis. These results indicated that PKC and ERK may be involved in U937 cell differentiation induced by N. chinensis.

• The Korean Journal of Pain
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• v.19 no.2
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• pp.137-141
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• 2006

Background: It has been known that melatonin is involved in the modulation of nociceptive transmission. However, the effect of melatonin administered spinally has not been examined. Therefore, we examined the effect of melatonin on the formalin-induced or thermal-induced nociception at the spinal level. Methods: Intrathecal catheter was inserted into the subarachnoid space of male Sprague-Dawley rats. Pain was assessed by formalin test (induced by injection of $50{\mu}l$ of a 5% formalin solution to the hindpaw) or Hot-Box test (induced by radiant heat application to the hindpaw). The effect of intrathecal melatonin was examined on flinching behavior in the formalin test or withdrawal response in Hot-Box test. Results: Intrathecal melatonin produced a limited, but dose-dependent reduction of the flinching response during phase 1 and 2 in the formalin test. In addition, melatonin delivered at evening also decreased the flinching response in both phases of the formalin test. Melatonin restrictively increased the withdrawal latency in Hot-Box test. Conclusions: These results suggest that melatonin is active against the formalin- and thermal-induced nocicpetion at the spinal level, but the effect is limited.

• Natural Product Sciences
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• v.15 no.1
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• pp.37-43
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• 2009

Oxidative stress is caused by an imbalance between the production of reactive oxygen and an ability of a biological system, to readily detoxify the reactive intermediates or easily repair the resulting damage. It has been suggested that developmental alloxan-induced liver damage is mediated through increases in oxidative stress. The anti-diabetic effect and antioxidant activity of Phaleria macrocarpa (PM) fractions were investigated in alloxan-induced diabetic rats. After two weeks administration of PM, the liver antioxidant enzyme and hyperglycemic state were evaluated. The results showed that oral administration of PM treatments reduced blood glucose levels in diabetic rats by oral administration (P < 0.05). Serum glutamic-oxaloacetic transaminase (sGOT) and serum glutamic-pyruvate-transaminase (sGPT) were also diminished by PM supplementation. The superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GPx) activities, and glutathione (GSH) level in the alloxan-induced diabetic rats were significantly decreased (P < 0.05) compared to those in the normal rats but were restored by PM treatments. PM fractions also repressed the level of malondialdehyde (MDA) in the liver. Glutathione reductase (GR), glutathione-S-transferase (GST) and $\gamma$-glutamylcysteine synthase (GCS) were also reduced in alloxan-induced diabetic rats. PM fractions could restore the GR and GST activities, but the GCS activity was not affected in rat livers. From the results of the present study, the diabetic effect of the butanol fraction of PM against alloxan-induced diabetic rats was concluded to be mediated either by preventing the decline of hepatic antioxidant status or due to its indirect radical scavenging capacity.

• The Journal of Korean Medicine
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• v.16 no.2 s.30
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• pp.281-298
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• 1995

The following results were made by observation GOT, GPT, ALP, total cholesterol and higlyceride in serum to research the effects of medicines which are Injinsaryungsan(Sample- A) and another medicine(Sample-B) of which Injin(Artemisiae Capillaris Herba)was increased in quantity on liver damaged by $CCl_4$ and d-galactosamine in rats. 1. The high concentrated extracts of Sample A group and Sample- B group showed significant inhibltory effects on the increase of serum GPT, ALP, LDH, total cholesterol and triglyceride levels induced by $CCl_4$ and d-galactosamine. 2. The high concentrated extracts of sample A group and Sample B group showed more significant inhibitory effects(P〈0.001) than the low ones' effects(P〈0.01) on the increase of serum triglyceride level induced by $CCl_4$ 3. Sample-A group showed significant inhibitory effects on the increase of serum GOT, GPT. ALP, total cholesterol and triglyceride levels, but no significance on the increase of serum LDH level induced by d-galactosamine. 4. Sample-B group showed very significant inhibitory effects on the increase of serum GOP, GPT, ALP, LDH, total cholesterol and triglyceride levels induced by d-galactosamine. 5. As compared with Sample-A group, Sample-B group of which Injin was increased in quantity showed more significant inhibitory effects on all items of this experiment induced by $CCl_4$ and d-galactosamine. As mentioned above. it seemed that both Injinsaryungsan and another medicine of which Injin was increased in quantity had effects protecting liver and anti-fatty liver induced by $CCl_4$ and d-galactosamine in rats. Specially Sample-B group had very significant effects on liver damage as compared with Sample-B group. Therefore it seems that more researches on variation according to the increase of Injin dose must be continued for curing liver diseases.

• Advances in Traditional Medicine
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• v.4 no.1
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• pp.28-36
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• 2004

The purpose of this study was to investigate the pharmacological effects of low-esterified pectin on carbon tetrachloride $(CCL_4)-induced$ hepatotoxicity in rats. The study included two experiments. In the first experiment the animals were given daily $CCL_4$ through gavage for 7 days and then 10, 50, or 250 mg/kg b.w. of pectin for 21 days. At the end of experiment rats were killed within 24 hours. The increased bilirubin level, enhanced alanine aminotransferase and aspartate aminotransferase activity in plasma induced by $CCL_4$ were partly normalized by pectin administration in a dose-dependent manner. The pectin treatment also resulted in significant recovery of $CCL_4-induced$ decrease of the liver glycogen content. In addition, pectin significantly improved $CCL_4-induced$ alterations of pro-oxidant and antioxidant biochemical parameters in liver and plasma compared to those of rats administered $CCL_4$. In the second experiment the animals were given daily 10, 50 or 250 mg/ kg b.w. of pectin for 21 days before a 7-day administration of $CCL_4$. Rats were killed 24 hours after the end of experiment. Pretreatment with pectin before $CCL_4$ administration resulted in significantly inhibited increase of the blood enzymatic activities of alanine and aspartate aminotransferases and bilirubin level in a dose-dependent manner. Also, preliminary administration of pectin prevented elevation of malondialdehyde and conjugated diene levels in liver and plasma as well as a reduction of glutathione content in liver of rats given $CCL_4$. These results suggest that low-esterified pectin exert healing and preventive effects on $CCL_4-induced$ hepatotoxicity in rats.

• Journal of Ginseng Research
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• v.39 no.4
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• pp.376-383
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• 2015

Background: Panax ginseng has a wide range of biological activities including anti-inflammatory, antioxidant, and immunomodulatory functions. Wild ginseng cambial meristematic cells (CMCs) were obtained from P. ginseng cambium. This study examined the protective mechanism of wild ginseng CMCs against $\small{D}$-galactosamine (GalN)-induced liver injury. GalN, a well-known hepatotoxicant, causes severe hepatocellular inflammatory damage and clinical features similar to those of human viral hepatitis in experimental animals. Methods: Hepatotoxicity was induced in rats using GalN (700 mg/kg, i.p.). Wild ginseng CMCs was administered orally once a day for 2 wks, and then 2 h prior to and 6 h after GalN injection. Results: Wild ginseng CMCs attenuated the increase in serum aminotransferase activity that occurs 24 h after GalN injection. Wild ginseng CMCs also attenuated the GalN-induced increase in serum tumor necrosis factor-${\alpha}$, interleukin-6 level, and hepatic cyclooxygenase-2 protein and mRNA expression. Wild ginseng CMCs augmented the increase in serum interleukin -10 and hepatic heme oxygenase-1 protein and mRNA expression that was induced by GalN, inhibited the increase in the nuclear level of nuclear factor-kappa B, and enhanced the increase in NF-E2-related factor 2. Conclusion: Our findings suggest that wild ginseng CMCs protects liver against GalN-induced inflammation by suppressing proinflammatory mediators and enhancing production of anti-inflammatory mediators.

• Journal of Korean Clinical Nursing Research
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• v.19 no.2
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• pp.298-308
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• 2013

Purpose: The purpose of this study was to identify factors influencing chemotherapy-induced peripheral neuropathy among colorectal cancer patients receiving oxaliplatin. Methods: A total of 132 patients hospitalized for chemotherapy were surveyed at K University Hospital in Seoul, Korea. This study was a descriptive causal relationship study using a self-report questionnaire survey method. Correlation and multiple regression analysis between the factors were performed using SPSS 18.0. Results: The regression model was significant (F=31.64, p<.001), which meaned that the experience of chemotherapy-induced peripheral neuropathy among the participants was statistically significant. The factors influencing the chemotherapy-induced peripheral neuropathy were depression (${\beta}=.34$, p<.001), followed by anxiety (${\beta}=.32$, p<.001), medical staff support (${\beta}=-.17$, p=.037) and the level of knowledge of anticancer drugs (${\beta}=-.16$, p=.045). The explanatory power of these factors on the chemotherapy-induced peripheral neuropathy of colorectal cancer patients was 69%. Conclusion: The factors influencing the chemotherapy-induced peripheral neuropathy of colorectal cancer patients receiving oxaliplatin were identified as depression, anxiety, level of knowledge of anticancer drugs and medical staff support.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.10a
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• pp.65-65
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• 2019

In this study, we evaluated the anti-inflammatory effect of extracts of leaves (LCLE) and branches (LCBE) from L. caerulea in LPS-stimulated RAW264.7 cells. Inhibitory effect of LCLE and LCBE against LPS-induced overproduction of NO, iNOS and $IL-1{\beta}$ was higher than LCFE. Furthermore, LCLE and LCBE significantly inhibited the overexpression of COX-2, IL-6 and $TNF-{\alpha}$ in LPS-stimulated RAW264.7 cells. LCLE and LCBE did not inhibited LPS-induced degradation of $I{\kappa}B-{\alpha}$, but blocked the nuclear accumulation of p65. LCLE did not inhibited LPS-induced phosphorylation of ERK1/2 and p38, while LCBE significantly attenuated phosphorylation level of p38. LCLE and LCBE increased HO-1 protein level and decrease of iNOS and $IL-1{\beta}$ expression by LCLE and LCBE was inhibited by HO-1 knockdown. The inhibition of p38 by SB203580 and ROS by NAC blocked HO-1 expression by LCLE and LCBE. LCLE and LCBE increased p38 phosphorylation and the inhibition of ROS by NAC blocked p38 phosphorylation LCLE and LCBE. LCLE and LCBE induced nuclear accumulation of Nrf2, but this was significantly reversed by the inhibition of p38 and ROS. In addition, LCLE and LCBE increased ATF3 expression and decrease of iNOS and $IL-1{\beta}$ expression by LCLE and LCBE was inhibited by ATF3 knockdown. Collectively, LCLE and LCBE inhibited LPS-induced $NF-{\kappa}B$ activation by blocking p65 nuclear accumulation, increased HO-1 expression by ROS/p38/Nrf2 activation, and increased ATF3 expression. Furthermore, LCBE inhibited LPS-induced p38 phosphorylation.

• Journal of the Korea Society for Simulation
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• v.30 no.2
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• pp.33-40
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• 2021

The situation of high-altitude electromagnetic pulses (HEMP) arises from high-altitude nuclear explosions. The HEMP situation can be simulated through the threat level investigation (TLI). In this paper, the induced voltage according to the antenna type of the tactical mobile radio communication system was measured and analyzed by TLI. Under the influence of HEMP, electronic equipment can be paralyzed or damaged. HEMP protection filters are commercially available for power lines and signal lines. However, commercialization of HEMP filters for antennas is insufficient, and even some of them exist for lightning protection. In order to make an appropriate HEMP protection filter according to the frequency and type of the antenna, the induced voltage was measured and the maximum induced voltage was analyzed through extrapolation. It was found that the measured induced voltage decreased as the frequency increased, such as in the HF, VHF and UHF bands of the measurement results.