Journal of Physiology & Pathology in Korean Medicine
/
v.23
no.6
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pp.1305-1313
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2009
Saengjihwangeum-ja (SJHEJ) was recorded in DongEuiBoGam as being able to be used for treatment of Sogal whose concept had been applied to Diabetes Mellitus (DM). Modification of proteins by long term circulation of glucose leads to the formation of advanced glycation end product(AGE). Recent immunological studies demonstrated that ligation of AGE play an important role in the development of diabetic complications including atherosclerosis, which includes activation, adhesion, and migration of monocytes. Also, AGE and Maillard reaction product(MRP) could augment monocyte inflammatory responses via ligation of AGE receptor. In this study, the effects of SJHEJ extracts on the expression of inflammatory response-related genes such as tumor necrosis factor-$\alpha$, monocyte chemoattractant protein-1, interferon-g-inducible protein-10, and cyclooxygenase-2 in the human monocyte cell line, THP-1 cells. Reverse transcriptase-polymerase chain reaction revealed that SJHEJ had inhibitory effects on the expression of the TNF-a, MCP-1, IP-10, COX2, IL-1b genes in MRP-induced THP-1 cells. Treatment with SJHEJ had reduced reactive oxygen production in THP-1 cells stimulated by MRP. These inhibitory effects might be exerted via prevention of oxidative stress in activated monocytes. In addition, radical scavenging activity of SJHEJ was increased. These results suggest that SJHEJ has a beneficial effects for improve diabetic vascular complication.
Fucoidan has been reported to exhibit various beneficial activities ranging from to antivirus and anticancer properties. However, little information is available about the effects of fucoidan on cerebral ischemia-reperfusion injury (IRI). Our study aimed to explore the effects of fucoidan on cerebral IRI, as well as the underlying mechanisms. Sprague-Dawley (SD) rats were randomly subjected to four groups: Sham, IRI+saline (IRI+S), IRI+80 mg/kg fucoidan (IRI+F80), and IRI+160 mg/kg fucoidan (IRI+F160). Fucoidan (80 mg/kg or 160 mg/kg) was intraperitoneally injected from 7 days before the rats were induced to cerebral IRI model with middle cerebral artery occlusion (MCAO) method. At 24 h after reperfusion, neurological deficits and the total infarct volume were determined. The levels of inflammation-associated cytokines (interleukin (IL)-$1{\beta}$, IL-6, myeloperoxidase (MPO), and tumor necrosis factor (TNF)-${\alpha}$), oxidative stress-related proteins (malondialdehyde (MDA) and superoxide dismutase (SOD)) in the ischemic brain were measured by enzyme-linked immunosorbent assay (ELISA). Besides, the levels of apoptosis-related proteins (p-53, Bax, and B-cell lymphoma (Bcl)-2) and mitogen-activated protein kinase (MAPK) pathway (phosphorylation-extracellular signal-regulated kinase (p-ERK), p-c-Jun N-terminal kinase (JNK), and p-p38) were measured. Results showed that administration of fucoidan significantly reduced the neurological deficits and infarct volume compared to the IRI+S group in a dose-dependent manner. Also, fucoidan statistically decreased the levels of inflammation-associated cytokines, and oxidative stress-related proteins, inhibited apoptosis, and suppressed the MAPK pathway. So, Fucoidan plays a protective role in cerebral IRI might be by inhibition of MAPK pathway.
Jeong, Da Hyun;Kang, Bo Kyeong;Kim, Koth Bong Woo Ri;Kim, Min Ji;Ahn, Dong Hyun
Journal of Applied Biological Chemistry
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v.57
no.3
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pp.227-234
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2014
The anti-inflammatory effect of Sargassum micracanthum water extract (SMWE) was investigated using lipopolysaccharide (LPS)-induced inflammatory response in this study. The murine macrophage cell line RAW 264.7 cells were used and MTT assay was performed to measure the cell proliferation ability. The secretion of nitric oxide (NO), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-6 (IL-6), and IL-$1{\beta}$ was measured in LPS-induced RAW 264.7 cells by ELISA. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear transcription factor-kappa B p65 protein was studied by immunoblotting. The Balb/c mice were used for an acute toxicity test, and imprinting control region mice were purchased to evaluate a croton oil-induced ear edema. As a result, there was no cytotoxicity in the macrophage proliferation treated with SMWE compared to the control. NO levels decreased with increasing concentration of SMWE and were inhibited over 50%. Moreover, the secretion of IL-6, TNF-${\alpha}$, and IL-$1{\beta}$ was suppressed in a dose-dependent manner, especially, IL-$1{\beta}$ inhibition activity was over 50% at 50 ${mu}g$/mL. The formation of ear edema of mice was reduced at the highest dose tested compared to that in the control. Moreover, in acute toxicity test, no moralities occurred in mice administered 5,000 mg/kg body weight of SMWE over 2 weeks observation period. These results suggested that SMWE may have significant effects on inflammatory factors and be potential anti-inflammatory therapeutic materials.
Yoo, Seon A;Kim, Ok Kyung;Nam, Da-Eun;Kim, Yongjae;Baek, Humyoung;Jun, Woojin;Lee, Jeongmin
Journal of the Korean Society of Food Science and Nutrition
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v.43
no.2
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pp.216-223
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2014
Curcuma longa L. (CL) is a well known traditional medicinal plant that is also used in curries and mustards as a coloring and flavoring agent. However, CL is not usually used as a food source due to its bitter taste. We investigated the immunomodulatory effect of CL fermented by Aspergillus oryzae (FCL) on RAW 264.7 cells. FCL was extracted with cold water (CW), hot water (HW), 20% ethanol (20% EtOH) and 80% ethanol (80% EtOH), after which its effects on phagocytic activity, tumor necrosis factor-alpha (TNF-${\alpha}$), nitric oxide (NO) production, natural killer (NK) cell activity and mRNA expression of LP-BM5 eco were investigated. Phagocytic activity was increased in HW and 20% EtOH when compared to the control. The secretion of nitric oxide (NO) from RAW 264.7 cells did not change significantly relative to the control. However, TNF-${\alpha}$ was significantly increased by the addition of FCL extracts. Moreover, FCL 20% ethanol extract showed a four fold increase in NK cell cytotoxity relative to the control group. Finally, we observed suppressed mRNA expression of LP-BM5 eco in FCL extracts, especially in the 20% ethanol extracts group. These results indicate that the FCL extracts can be used as a functional material due to their effective immunomodulating activities.
Kim, Seung-Ju;Chun, Jin-Mi;Yang, Won-Kyung;Cheon, Myeong-Sook;Sung, Yoon-Young;Park, Jun-Yeon;Kim, Ho-Kyoung
The Korea Journal of Herbology
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v.25
no.4
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pp.11-16
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2010
Objective : Oriental medicines have been combined oriental medical theory which based on the seven modes of emotions. Notopterygium incisum (N. incisum) and Clematis manshurica (C. manshurica) have been used as an anti-rheumatic and analgesic medicine for the treatment of rheumatism, headache, cold, etc. In this study, we evaluate the synergistic anti-inflammatory effect of N. incisum and C. manshurica. Method : To evaluate the synergistic anti-inflammatory effect of a herbal mixture N. incisum and C. manshurica, we examined the changed ear thickness in 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear edema model after topical application of herbal mixture. In addition, the levels of markers for inflammation, such as tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, prostaglandin $G_2$ ($PGE_2$), and nitric oxide (NO) were measured by ELISA assay and Griess reagent in lipopolysaccharide-stimulated Raw 264.7 cells. Results : Our results showed that aqueous extracts of N. incisum and C. manshurica combination significantly inhibited the mouse ear edema induced by TPA. Moreover, the aqueous extracts of N. incisum and C. manshurica combination exhibited synergistic effects in down-regulating TNF-${\alpha}$, IL-$1{\beta}$, $PGE_2$ level, but not NO. Conclusions : This study suggested that combined treatment of N. incisum and C. manshurica, based on seven methods in prescription compatibility, has a synergistic effect in down-regulating inflammatory response both in vitro and in vivo models.
BACKGROUND/OBJECTIVES: The present study investigated the hypothesis that a highly pure linear ${\beta}$-1,3-glucan produced by Agrobacterium sp. R259 enhances human natural killer (NK) cell activity and suppresses pro-inflammatory cytokines. SUBJECTS/METHODS: In an eight-week, double-blind, randomized, placebo-controlled clinical trial, 83 healthy adults with white blood cell counts of $4,000-8,000cells/{\mu}L$ were participated and randomly assigned to take two capsules per day containing either 350 mg ${\beta}$-1,3-glucan or placebo. Six participants withdrew their study consent or were excluded due to NK cell activity levels outside the normal range. NK cell activity and serum levels of immunoglobulin G (IgG) and cytokines, such as interferon (IFN)-${\gamma}$, interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12 and tumor necrosis factor (TNF)-${\alpha}$ were measured. RESULTS: NK cell activity and the serum levels of IL-10 were significantly higher from baseline to week 8 in the ${\beta}$-glucan group compared with the placebo group (P = 0.048, P = 0.029). Consumption of ${\beta}$-1,3-glucan also significantly increased NK cell activity compared with placebo after adjusting for smoking and stress status (P = 0.009). In particular, the effect of ${\beta}$-1,3-glucan on NK cell activity was greater in participants with severe stress than in those experiencing mild stress. However, the administration ${\beta}$-1,3-glucan did not significantly modulate the levels of IFN-${\gamma}$, IL-2, IL-4, IL-6, IL-12, TNF-${\alpha}$ and IgG compared with the placebo. CONCLUSION: The results showed that supplementation with bacterial ${\beta}$-1,3-glucan significantly increased NK cell activity without causing any adverse effects. Additionally, the beneficial effect of ${\beta}$-1,3-glucan on NK cell activity was greater in participants experiencing severe stress.
As nanomaterials might enter into cells and have high reactivity with intracellular structures, it is necessary to assay possible genotoxic risk of them. One of these approaches, we investigated possible genotoxic potential of gold nanoparticle (AuNP) using L5178Y cells. Four different sizes of AuNP (4, 15, 100 or 200 nm) were synthesized and the sizes and structures of AuNP were analyzed using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and stability was analyzed by a UV/Vis. Spectrophotometer. Cytotoxicity was assessed by direct cell counting, and cellular location was detected by dark field microscope at 6, 24 and 48 h after treatment of AuNP. Comet assay was conducted to examine DNA damage and tumor necrosis factor (TNF)-${\alpha}$ mRNA level was assay by real-time reverse transcription polymerase chain reaction. Synthetic AuNP (4, 50, 100 and 200 nm size) had constant characteristics and stability confirmed by TEM, SEM and spectrophotometer for 10 days, respectively. Dark field microscope revealed the location of AuNP in the cytoplasm at 6, 24 and 48 h. Treatment of 4 nm AuNP induced dose and time dependent cytotoxicity, while other sizes of AuNP did not. However, Comet assay represented that treatment of 100 nm and 200 nm AuNP significantly increased DNA damage compared to vehicle control (p <0.01). Treatment of 100 nm and 200 nm AuNP significantly increased TNF-${\alpha}$ mRNA expression compared to vehicle control (p<0.05, p<0.01, respectively). Taken together, AuNP induced DNA damage in L5178Y cell, associated with induction of oxidative stress.
Kim, Sang Suk;Park, Kyung Jin;Lee, Seung Eun;Lee, Jeong Hoon;Choi, Young Hun
Food Science and Preservation
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v.24
no.6
/
pp.842-848
/
2017
Hylotelephium erythrostictum is commonly used as a medicinal herb. In this study, H. erythrostictum leaf (HEL), branch (HEB), root (HER), and above ground (HEAG) extracts were evaluated for their antioxidant properties. The antioxidant activities were assayed by three methods based on scavenging of DPPH, ABTS and superoxide anion radical. HEAG extract showed the highest DPPH, ABTS, superoxide anion radical scavenging activities. HEAG extract also exhibited the highest phenolic content (230 mg/g gallic acid equivalent). In our research for anti-inflammatory ingredients, the extract of HEAG inhibited the generation of nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. To test the inhibitory effects of HEAG on pro-inflammatory cytokines, we conducted ELISA assay for the measuring the generation of tumor necrosis factor $(TNF)-{\alpha}$, IL (interleukin)-$1{\beta}$, and IL(interleukin)-6 in LPS-stimulated RAW264.7 macrophage cells. In these assays, HEAG ethanol extract showed a dose-dependent decrease in the production of $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6. Based on these results, extract of HEAG could be the efficient candidate for anti-inflammatory agents.
Background: The light-emitting diode (LED) curing light used is presumed to be safe. However, the scientific basis for this is unclear, and the safety of LED curing light is still controversial. The purpose of this study was to investigate the effect of LED curing light irradiation according to the conditions applied for the polymerization of composite resins in dental clinic on the cell viability and inflammatory response in Raw264.7 macrophages and to confirm the stability of LED curing light. Methods: Cell viability and cell morphology of Raw264.7 macrophages treated with 100 ng/ml of lipopolysaccharide (LPS) or/and LED curing light with a wavelength of 440~490 nm for 20 seconds were confirmed by methylthiazolydiphenyl-tetrazolium bromide assay and microscopic observation. The production of nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) was confirmed by NO assay and $PGE_2$ enzyme-linked immunosorbent assay kit. Expression of interleukin $(IL)-1{\beta}$ and tumor necrosis factor $(TNF)-{\alpha}$ in total RNA and protein was confirmed by reverse transcription polymerase chain reaction and Western blot analysis. Results: The LED curing light did not affect the viability and morphology of normal Raw264.7 cells but affected the cell viability and induced cytotoxicity in the inflammation-induced Raw264.7 cells by LPS. The irradiation of the LED curing light did not progress to the inflammatory state in the inflammation-induced Raw264.7 macrophage. However, LED curing light irradiation in normal Raw264.7 cells induced an increase in NO and $PGE_2$ production and mRNA and protein expression of $(IL)-1{\beta}$ and $(TNF)-{\alpha}$, indicating that it is possible to induce the inflammatory state. Conclusion: The irradiation of LED curing light in RAW264.7 macrophage may induce an excessive inflammatory reaction and damage oral tissues. Therefore, it is necessary to limit the long-term irradiation which is inappropriate when applying LED curing light in a dental clinic.
Objectives : ${\beta}$-Asarone (BAS) is an active ingredient in Acori Rhizoma. This study investigated anti-neuroinflammatory and memory ameliorating effects of BAS in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Methods : BAS was administered orally at doses of 7.5, 15, and 30 mg/kg for 3 days prior to LPS (3 mg/kg, intraperitoneal) injection. Pro-inflammatory cytokine mRNA, including tumor necrosis factor-${\alpha}$ (TNF-ㅍ), interleukin (IL)-$1{\beta}$ and IL-6, was measured in hippocampus tissue using real-time polymerase chain reaction at 4 h after the LPS injection. An ameliorating effect of 30 mg/kg BAS on learning and memory impairment in the LPS-treated mice was verified using the Morris water maze test. Results : BAS significantly attenuated up-regulation of TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 mRNA in hippocampus tissue of the LPS-treated mice. In acquisition training test, BAS improved learning performance of the LPS-treated mice with a significant decrease of escape latency to the platform. In memory retention test, BAS also ameliorated memory impairment of the LPS-treated mice with a significant increase of swimming time in zones neighboring to the platform, number of target heading, and memory score. Conclusion : The results suggest that inhibition of pro-inflammatory cytokines and neuroinflammation in the hippocampus by BAS could be one of the mechanisms for BAS-mediated ameliorating effect on learning and memory impairment in LPS-treated mice.
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