• Title/Summary/Keyword: inflammatory factors

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Anti-inflammaory effects of the MeOH extract of Gentianae Macrophyllae Radix in vivo (진교(秦艽)가 항염 효과에 미치는 영향)

  • Cho, Hwi-Chang;Jung, Ho-Jun;Lee, Jae-Geun;Jo, Mi-Jeong;Jee, Seon-Young
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.22 no.3
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    • pp.63-70
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    • 2009
  • Objectives : The present study was examined to evaluate the anti-inflammatory effects of the Gentianae Macrophyllae Radix MeOH extracts (GMR) in vivo. Methods : The effects of GMR on anti-inflammation were measured by production of NO, TNF-$\alpha$ (Tumor Necrosis Factor-alpha) and IL-$1{\beta}$ (Interleukin-$1{\beta}$), IL-6 in Raw 264.7 macrophage cells stimulated with LPS. Results : 1. All concentrations of GMR(0.10 mg/ml) had no significant cytotoxicity in Raw 264.7 cell during the entire experimental period. 2. The level of NO and iNOS in culture medium was dramatically increased by LPS application. However, these increases were dose-dependently(0.03 and 0.10 mg/ml) attenuated by treatment with GMR. 3. All concentrations of GMR significantly inhibited the production of IL-$1{\beta}$ in Raw 264.7 macrophage cells stimulated with LPS. Conclusions : These results provide evidences that therapeutic effect of GMR on heat syndrome, especially due to the acute inflammation, are partly due to the reduction of some of inflammatory factors by inhibiting iNOS and COX-2 through the suppression of $p-I{\kappa}B{\alpha}$. Moreover, it suggests that the mechanism of action of GMR comes from the suppression of inflammatory mediators, such as NO, PGE2 and pro-inflammatory cytokines.

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Anti-inflammatory effect of CGT in atopic dermatitis model mice (아토피피부염을 유발한 마우스에서 청기해독탕의 항염증 효과)

  • Sueng, Yun-Chel
    • Journal of Digital Convergence
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    • v.12 no.8
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    • pp.361-368
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    • 2014
  • In order to investigate the effect of CGT on atopic dermatitis, various anti-inflammatory factors were studied. In-vitro, inflammatory mediators, such as MTT and nitric oxide and ROS were detected after the addition of LPS with or without CGT in RAW 264.7 cells. In-vivo, in order to verify the effectiveness of CGT in atopic dermatitis animal model, its role in inflammation factors and histological changes were observed in NC/Nga mice. CGT showed cell viability of 100% or higher in all concentration in RAW 264.7 cells. CGT inhibited LPS-induced productions of inflammatory mediators nitric oxide and antioxidant activity reactive oxygen species production in RAW 264.7 cells. CGT treated group showed significant decrease in serum of the expression of IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ by 53%, 43% and 57% respectively. And CGT treated group showed decrease in serum of the expression of IgE by 56% respectively. Also, infiltration of adipocytes into skin was suppressed and the thickness of epidermis and dermis were relatively decreased in the CGT treated group. As a result, CGT has an anti-inflammatory effects in NC/Nga mouse. Thus, these results suggested a beneficial effect of CGT in treatment with Atopic dermatitis and inflammatory.

Anti-Inflammatory Potential of Probiotic Strain Weissella cibaria JW15 Isolated from Kimchi through Regulation of NF-κB and MAPKs Pathways in LPS-Induced RAW 264.7 Cells

  • Yu, Hyung-Seok;Lee, Na-Kyoung;Choi, Ae-Jin;Choe, Jeong-Sook;Bae, Chun Ho;Paik, Hyun-Dong
    • Journal of Microbiology and Biotechnology
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    • v.29 no.7
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    • pp.1022-1032
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    • 2019
  • Probiotics are known to provide the host with immune-modulatory effects and are therefore of remarkable interest for therapeutic and prophylactic applications against various disorders, including inflammatory diseases. Weissella cibaria JW15 (JW15) has been reported to possess probiotic and antioxidant properties. However, the effect of JW15 on inflammatory responses has not yet been reported. Therefore, the objective of the current study was to evaluate the anti-inflammatory potential of JW15 against lipopolysaccharide (LPS) stimulation. The production of pro-inflammatory factors and the cellular signaling pathways following treatment with heat-killed JW15 was examined in LPS-induced RAW 264.7 cells. Treatment with heat-killed JW15 decreased nitric oxide and prostaglandin $E_2$ production via down-regulation of the inducible nitric oxide synthase and cyclooxygenase-2. In addition, treatment with heat-killed JW15 suppressed the expression of pro-inflammatory cytokines, interleukin $(IL)-1{\beta}$, IL-6, and tumor necrosis factor-${\alpha}$. The anti-inflammatory properties of treating with heat-killed JW15 were associated with mitogen-activated protein kinase signaling pathway-mediated suppression of nuclear factor-${\kappa}B$. These results indicated that JW15 possesses anti-inflammatory potential and provide a molecular basis regarding the development of functional probiotic products.

The protective effect of methanol extract of Corni Fructus on brain injury caused by unilateral common carotid artery occlusion in mice (산수유(山茱萸) 메탄올 추출물이 편측 경동맥 폐색으로 유도된 생쥐의 허혈성 뇌손상에 미치는 영향)

  • Choi, Na Ri;Jo, Sung Hyeon;Lee, Se-Eun;Lee, Min Ji;Cho, Suin
    • The Korea Journal of Herbology
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    • v.35 no.1
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    • pp.1-8
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    • 2020
  • Objectives : This study was conducted to evaluate the effects of Corni Fructus, the dried fruits of Cornus officinalis Sieb., on unilateral common carotid artery occlusion (UCCAO) in mouse model. Methods : The Corni Fructus used in the experiment was extracted with anhydrous methanol, then filtered and freeze-dried. C57BL/6 mice used in the experiments were conducted left UCCAO surgery to set up UCCAO rodent model for mice. The mice were divided into five groups for evaluate the effect of methanol extract of Corni Fructus (COM) on UCCAO induced ischemic brain injury. The expression levels of nitric oxide in cerebrum and serum, body weight change were measured. To determine the effect of UCCAO and COM administration on brain neurons, morphological changes of the cerebrum through a microscope was conducted. And western blot was performed to confirm the underlying mechanism of neuroprotective effect of COM administration. Results : COM administered UCCAO groups (CO50, CO150, and CO500) had no significant effects on nitric oxide production in ipsilateral hemisphere proteins and sera. The CO500, 500 mg/kg COM administration, attenuated UCCAO-induced p38 inflammatory signaling pathway and inflammatory mediators such as iNOS and COX-2. The CO500 group showed resilient morphological changes of hippocampus neuronal cells about brain damage caused by decreased flow of blood. These group also showed decreased inflammation and cellular stress response in neuronal cells. Conclusions : From these results, COM has a neuroprotective property via moderating inflammatory factors and cellular stress inducing factors in brain cells.

Inhibitory effect of carvacrol on lipopolysaccharide-induced memory impairment in rats

  • Lee, Bombi;Yeom, Mijung;Shim, Insop;Lee, Hyejung;Hahm, Dae-hyun
    • The Korean Journal of Physiology and Pharmacology
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    • v.24 no.1
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    • pp.27-37
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    • 2020
  • Neuroinflammation is an important process underlying a wide variety of neurodegenerative diseases. Carvacrol (CAR) is a phenolic monoterpene commonly used as a food additive due to its antibacterial properties, but it has also been shown to exhibit strong antioxidative, anti-inflammatory, and neuroprotective effects. Here, we sought to investigate the effects of CAR on inflammation in the hippocampus and prefrontal cortex, as well as the molecular mechanisms underlying these effects. In our study, lipopolysaccharide was injected into the lateral ventricle of rats to induce memory impairment and neuroinflammation. Daily administration of CAR (25, 50, and 100 mg/kg) for 21 days improved recognition, discrimination, and memory impairments relative to untreated controls. CAR administration significantly attenuated expression of several inflammatory factors in the brain, including interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2. In addition, CAR significantly increased expression of brain-derived neurotrophic factor (BDNF) mRNA, and decreased expression of Toll-like receptor 4 (TLR4) mRNA. Taken together, these results show that CAR can improve memory impairment caused by neuroinflammation. This cognitive enhancement is due to the anti-inflammatory effects of CAR medicated by its regulation of BDNF and TLR4. Thus, CAR has significant potential as an inhibitor of memory degeneration in neurodegenerative diseases.

Pro-inflammatory Cytokine Production Inhibitory Effects of Frankincence in Murine Macrophage (마우스의 대식세포에서 프랑킨센스의 염증성 사이토카인 분비 억제작용)

  • Park, Jeong-Sook
    • Journal of the Korea Convergence Society
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    • v.8 no.1
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    • pp.239-243
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    • 2017
  • This study aims to demonstrate the inhibitory effect of proinflammatory cytokines by using Frankinsense. The present data was designed to determine the production of the frankincence on pro-inflammatory factors such as $TNF-{\alpha}$ and $IL-1{\beta}$ in lipopolysaccharide(LPS) stimulated RAW264.7 macrophages cell. The cell toxicity was identified by CellTiter 96 AQueous One solution cell proliferation assay. To evaluate of anti-inflammatory effect of frankincence, pro-inflammatory cytokines were measured by ELISA kit. As a result, the frankincence reduced NO and $TNF-{\alpha}$ production without cytotoxicity. As a result, Francincense was not cytotoxic at 10 ug / ml-1000 ug / ml and significantly inhibited the proinflammatory cytokines $TNF-{\alpha}$ and $IL-1{\beta}$. The secretion inhibition effect of proinflammatory cytokine is believed to be applicable to various physiological activity data and functional materials to demonstrate the anti - inflammatory properties of frankincense.

Anti-inflammatory Effect of Water Extract from Tuna Heart on Lipopolysaccharide-induced Inflammatory Responses in RAW 264.7 Cells (Lipopolysaccharide로 유도된 RAW 264.7 세포에 대한 참치심장 물 추출물의 항염증 효과)

  • Kim, Min-Ji;Bae, Nan-Young;Kim, Koth-Bong-Woo-Ri;Park, Ji-Hye;Park, Sun-Hee;Cho, Young-Je;Ahn, Dong-Hyun
    • KSBB Journal
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    • v.30 no.6
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    • pp.326-331
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    • 2015
  • The anti-inflammatory effect of tuna heart water extract (THWE) was investigated using lipopolysaccharide-induced inflammatory response in this study. Anti-inflammatory effect was detected by the cell proliferation and the production levels of nitric oxide, pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-$1{\beta}$, and tumor necrosis factor-alpha. As a result, there were no cytotoxic effects on proliferation of macrophages treated with THWE compared to the control. The production of pro-inflammatory cytokines was remarkably suppressed compared with that of the LPS only group. These results suggest that THWE exerts the anti-inflammatory property by inhibiting production of inflammatory factors and may be a potential material for anti-inflammatory therapy.

Effects of Ginsenosides Rg1 on Osteoblasts Cultured with Ti Particles

  • Lin, Yu;Wu, Yinsheng;He, Jiacheng;Huang, Yunmei;Lin, Yanping
    • Biomolecules & Therapeutics
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    • v.20 no.1
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    • pp.75-80
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    • 2012
  • The aim of this study was to explore the role and effect of ginsenosides Rg1 on osteoblasts cultured with Ti particles. Osteoblasts from neonatal rats were cultured with particles and different doses of Rg1, the main active ingredient in ginsenosides Rg1. We found that the COX-2, $PGE_2$, TNF-${\alpha}$, IL-1, and IL -6 concentrations in the medium of cells cultured with Ti particles significantly increased as compared with that of the control cells (p<0.05 or p<0.01). In addition, cells cultured with Ti particles alone exhibited the highest concentrations of these molecules. The $PGE_2$, TNF-${\alpha}$, IL-1, and IL-6 levels in the medium of cells cultured with Rg1 were in between those of the control cells and the cells cultured with Ti particles alone. The IL-1ra level in the group cultured with Ti and medium-dose Rg1 was the highest followed by the cells cultured with Ti and high-dose Rg1 and those cultured with Ti and low-dose Rg1 (p<0.05). In conclusion, ginsenosides can reduce the levels of infl ammatory cytokines produced by osteoblasts on induction with Ti particles and can prevent prosthesis loosening.

The venom of jellyfish, Chrysaora pacifica, induces neurotoxicity via activating Ca2+-mediated ROS signaling in HT-22 cells

  • Yang, Yoon-Sil;Kang, Young-Joon;Kim, Hye-Ji;Kim, Min-Soo;Jung, Sung-Cherl
    • Journal of Applied Biological Chemistry
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    • v.62 no.4
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    • pp.347-353
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    • 2019
  • Stings of jellyfish, which frequently occur in a warm season, cause severe pain, inflammation and sometimes irreversible results such as the death. Harmful venoms from jellyfish, therefore, have been studied for finding the therapeutic agents to relieve pain or to neutralize toxic components. However, it is still unclear if and how jellyfish venom reveal neuronal toxicity even though pain induction seems to result from the activation of nociceptors such as nerve endings. In this study, using HT-22 cell line, we investigated neurotoxic effects of the venom of Chrysaora pacifica (CpV) which appears in South-East ocean of Korea. In 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, CpV significantly reduced the viability of HT-22 cells in a dose-dependent manner. Additionally, in 2',7'-Dichlorofluorescin diacetate fluorescence test under the culture condition lacking dominant inflammatory factors, CpV remarkably increased the production of intracellular reactive oxygen species (ROS). Reduced responsive fluorescence to Rhodamine123 and increased expression of intracellular cytochrome c were also observed in HT-22 cells treated with CpV. These indicate that CpV-reduced viability of HT-22 cells may be due to the activation of apoptotic signalings mediated with oxidative stress and mitochondrial dysfunction. Furthermore, removing Ca2+ ion or adding N-acetyl-Lcystein remarkably blocked the CpV effect to reduce the viability of HT-22 cells. The findings in this study clearly demonstrate that CpV may activate Ca2+-mediated ROS signalings and mitochondrial dysfunction resulting in neuronal damage or death, and suggest that blocking Ca2+ pathway is a therapeutic approach to possibly block toxic effects of jellyfish venoms.

The Effect of Lonicera japonica Extract in Wound-induced Rats (창상을 유발한 흰쥐에서 금은화(金銀花) 추출물의 치료 효과)

  • Won, Je-Hoon;Woo, Chang-Hoon
    • Journal of Korean Medicine Rehabilitation
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    • v.30 no.1
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    • pp.47-61
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    • 2020
  • Objectives This study is carried out to investigate the effects of Lonicera japonica in wound-induced rats. Methods Rats were divided into 5 groups; normal (Nor), control (Veh), positive comparison (PC), Lonicera japonica 100 mg/kg (LL), Lonicera japonica 200 mg/kg (LH), each n=8. Total polyphenol and flavonoid were quantified. 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3 ethylbenzothiazoline-6-sulfonic acid) (ABTS) free radical scavenging activation were measured. Reactive oxygen species (ROS) was measured in serum. Antioxidant factors and inflammatory factors were measured in skin tissue, and also hydroxyproline content. Skin tissue was analyzed by Hematoxylin & Eosin and Masson's trichrome staining method. Results Total polyphenol and flavonoid were 32.86±0.14 mg/g and 67.17±0.57 mg/g. The IC50 values of DPPH and ABTS free radical scavenging activation were 26.69±1.50 ㎍/mL and 49.33±4.52 ㎍/mL. ROS was significantly lower in LL and LH groups. Nuclear factor-erythroid 2-related factor 2 (Nrf2) was significantly higher in LH group and higher in LL group but not significant. Superoxide dismutase 1 (SOD-1), catalase, and heme oxygenase 1 (HO-1) were significantly higher in LL and LH groups. Nuclear factor kappa-B p65 (NF-κBp65), phosphorylated iκBα (p-iκBα), cyclooxygenase 2 (COX-2), and tumor necrosis factor alpha (TNF-α) were significantly lower in LL and LH groups. Hydroxyproline was significantly higher in LL and LH groups. The histopathologic analysis showed that skin tissue had recovered further more in LL and LH groups than in Veh group. Conclusions These results suggest that Lonicera japonica has the anti-oxidant, anti-inflammatory and healing effects in wound-induced rats.