• Journal of Microbiology and Biotechnology
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• 제34권4호
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• pp.940-948
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• 2024

Codium fragile has been traditionally used in oriental medicine to treat enterobiasis, dropsy, and dysuria, and it has been shown to possess many biological properties. Atopic dermatitis (AD) is one of the types of skin inflammation and barrier disruption, which leads to chronic inflammatory skin diseases. In the current investigation, the protective effects of C. fragile extract (CFE) on anti-inflammation and skin barrier improvement were investigated. In LPS-stimulated RAW 264.7 cells, nitric oxide generation and the expression levels of interleukin (IL)-1β, IL-4, IL-6, iNOS, COX-2, and tumor necrosis factor-alpha (TNF)-α were reduced by CFE. CFE also inhibited the phosphorylation of NF-κB-p65, ERK, p-38, and JNK. Additionally, CFE showed inhibitory activity on TSLP and IL-4 expression in HaCaT cells stimulated with TNF-α/interferon- gamma (IFN-γ). Enhanced expression of factors related to skin barrier function, FLG, IVL, and LOR, was confirmed. These findings implied that CFE may be used as a therapeutic agent against AD due to its skin barrier-strengthening and anti-inflammatory activities, which are derived from natural marine products.

• KSBB Journal
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• 제30권1호
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• pp.38-43
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• 2015

In this study, we investigated the anti-inflammatory effects of fermented Hizikia fusiformis extracts in lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse macrophages. The fermentation was performed using Lactobacillus casei in mixture of carbon source at $30^{\circ}C$ for 30 days. The sample groups were prepared with/without L. casei group in order to demonstrate the anti-inflammatory activity of fermented H. fusiformis in regard to lactic acid bacteria. As a result, we confirmed the inhibitory effect of H. fusiformis extracts on LPS-stimulated NO production and expression of $TNF{\alpha}$, while it had no regulatory effect on the expression of iNOS, COX-2, $IL-1{\beta}$ and IL-6 as important inflammatory factors. However, L. casei fermented group significantly suppressed the expression of the above factors. In particular, the difference between the two groups in the matter of mRNA expression of iNOS, which is directly associated with NO production, indicated that the fermentation with lactic acid bacteria effectively suppressed NO production by regulating iNOS expression. Also, effective suppression of pro-inflammatory cytokines showed that the fermentation using L. casei may provide an increment towards extraction of active ingredients that are effective anti-inflammatory agents.

• 대한한의학방제학회지
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• 제29권3호
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• pp.127-145
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• 2021

Objectives : The purpose of this study was to evaluate the effects of Daeganghwal-tang on knee cartilage in monosodium iodoacetate(MIA)-induced osteoarthritis rats. Methods : Forty SD rats were randomly divided into five groups(n=8/group): normal group was SD rats group injected with normal saline at left knee joint and administrated orally distilled water, control group was MIA-induced osteoarthritis SD rats group administrated orally distilled water, Indomethacin group was MIA-induced osteoarthritis SD rats group administrated orally indomethacin 2 mg/kg, DGHT(L) group was MIA-induced osteoarthritis SD rats group administrated orally 1280 mg/kg of Daeganghwal-tang, and DGHT(H) group was MIA-induced osteoarthritis SD rats group administrated orally 2560 mg/kg of Daeganghwal-tang. After orally administration of drugs for 4 weeks, gross appearance and histological analysis were used to evaluate the degree of knee cartilage damage. In addition, pro-inflammatory cytokines, bone degrade factor and bone defence factors were analyzed to investigate the anti-inflammatory and cartilage protection effects of Daeganghwal-tang. Also, hematological test, biochemical test, and liver and kidney tissue were analyzed to determine the safety of Daeganghwal-tang. Results : Daeganghwal-tang inhibited the damage of the knee cartilage, and significantly prevented the reduction in cartilage thickness. In addition, the pro-inflammatory cytokines and the bone degrade factor significantly decreased, and the bone defence factors significantly increased. In the safety assessment of Daeganghwal-tang, there were no significant differences among the experimental groups and no abnormal findings were observed. Conclusions : Daeganghwal-tang has anti-inflammatory effect, inhibits cartilage damage, and protects cartilage in MIA-induced osteoarthritis rats.

• 생약학회지
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• 제42권4호
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• pp.348-353
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• 2011

The aim of the present study is to investigate the cytokine production inhibitory effect of a Dictamni Radicis Cortex (DRC). DRC has been commonly used as important medicinal herb in China and it used to control eczema, atopic dermatitis, fever and inflammatory diseases. Inflammation, such as a bacterial infection in vivo metabolites, such as external stimuli or internal stimuli to the defense mechanisms of the biological tissue a variety of intracellular regulatory factors deulin inflammatory TNF-${\alpha}$, IL-$1{\beta}$, IL-6, IL-8, such as proinflammatory cytokines, prostagrandin, lysosomal enzyme, free radicals are involved in a variety of mediators. The present study was designed to determine the effect of the DRC on proinflammatory factors such as NO, iNOS expression and TNF-${\alpha}$, IL-$1{\beta}$, IL-6 in lipopolysaccharide (LPS) - stimulated RAW264.7 cells. The cell toxicity was determined by MTS assay. To evaluate of anti-inflammatory effect of DRC, amount of NO was measured using the NO detection kit and the iNOS expression was measured by reverse transcriptase polymerase chain reaction (RT-PCR). And proinflammatory cytokines were measured by ELISA kit. As a result, the DRC reduced NO, iNOS expression and TNF-${\alpha}$, IL-$1{\beta}$, IL-6 production without cytotoxicity. Our results suggest that the DRC may have an anti-inflammatory property through suppressing inflammatory mediator productions.

• BMB Reports
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• 제36권1호
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• pp.95-109
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• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• 대한본초학회지
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• 제35권3호
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• pp.17-24
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• 2020

Objectives : The objective of this study was to evaluate the gastric protective effect of Curcuma Longae Rhizoma (CLR) in 150 mM HCl/60% ethanol induced gastric ulcer (GU) in mice. Methods : Forty ICR mice were divided into five groups (n=8/Group): Nor group; Normal, Veh group; GU control, SC group; GU + sucralfate 10 mg/kg, CL; GU + CLR 30% ethanol extract 100 mg/kg, CH group; GU + CLR 30% ethanol extract 200 mg/kg. Then, mice were orally administered with 150 mM HCl/60% ethanol and caused GU. After 1 hr, mice were sacrificed, and blood and stomach tissue were collected. Results : CLR showed significance scavenging effects in 1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azinobis-3-ethyl-benzothiazoline-6-sulfonic acid (ABTS) radical scavenging activities (DPPH IC₅₀; 78.18 ± 0.60 ㎍/㎖, ABTS IC₅₀; 55.91 ± 1.86 ㎍/㎖). CLR significance reduce inflammatory-related factors such as cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin-6 (IL-6) via nuclear factor kappa B (NF-κB) inactivation. In addition, the activation of nuclear factor erythroid2-related factor 2 (Nrf2) significantly led to up-regulation of anti-oxidant enzymes including factors heme oxygenase-1 (HO-1), super oxide dismutase (SOD), and glutathione peroxidase-1/2 (GPx-1/2). Conclusions : Our discovery provides that CLR possesses anti-oxidant and anti-inflammatory effects. Hence, CLR may ameliorate the development of gastric ulcer though the inhibition of NF-κB inflammatory pathway and the elevation of Nrf2 anti-oxidant pathway.

• 한방안이비인후피부과학회지
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• 제22권3호
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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.

• Genomics & Informatics
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• 제9권3호
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• pp.114-120
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• 2011

Chronic inflammation has been implicated as one of the important etiological factors in insulin resistance and type 2 diabetes mellitus (T2DM). To investigate the role of anti-inflammatory cytokines in the development of T2DM, we conducted a case-control study to assess the association between IL4/IL4R polymorphisms and disease risk. We firstly identified single nucleotide poly-morphisms (SNP) at IL4 and IL4RA loci by sequencing the loci in Korean participants. Case-control studies were conducted by genotyping the SNPs in 474 T2DM cases and 470 non-diabetic controls recruited from community-based cohorts. Replication of the associated signals was performed in 1,216 cases and 1,352 controls. We assessed effect of IL4 -IL4RA interaction on T2DM using logistic regression method. The functional relevance of the SNP associated with disease risk was determined using a reporter expression assay. We identified a strong association between the IL4 promoter variant rs2243250 and T2DM risk (OR=0.77; 95% CI, 0.67~0.88; p=$1.65{\times}10^{－4}$ in the meta-analysis). The reporter gene expression assay demonstrated that the presence of rs2243250 might affect the gene expression level with ~1.5-fold allele difference. Our findings contribute to the identification of IL4 as a T2D susceptibility locus, further supporting the role of anti-inflammatory cytokines in T2DM disease development.

• 대한의생명과학회지
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• 제19권1호
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• pp.61-69
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• 2013

The aim of this study was to evaluate the effect of exercise-based cardiac rehabilitation on pro- and anti-inflammatory markers in patients with acute coronary syndrome (ACS). ACS patients who underwent percutaneous coronary intervention (PCI) and took medicine during phase II of rehabilitation were recruited for study. Subjects were divided into two groups; exercise group (EX, n=21) and a non-exercise group (non-EX, n=13). Supervised exercise program in hospital consisted of treadmill and bicycle exercise was performed three times per week for 6 weeks. Patients of EX received individual counseling, including knowledge of heart disease, risk factor modification, and physical training. Cardiopulmonary fitness, body composition, and biochemical blood factors were analyzed before and after experiment. There was no significant difference in serum levels of hs-CRP and TGF-${\beta}1$ between groups, and between time intervals. But there was a significant decrease in serum levels of IL-18 (P<.001). And there was a significant increase in ratio of IL-18 to IL-10 (P<.01) and serum levels of IL-10 (P<.001). After cardiac rehabilitation, there was significant increase in exercise duration (P<.001), maximal oxygen uptake ($VO_{2peak}$; P<.001) and decrease in submaximal rate-pressure product (sRPP; P<.05) in EX. In conclusion, exercise-based cardiac rehabilitation during phase II in patients with ACS after PCI decreased serum IL-18 (pro-inflammatory) content and ratio of IL-18 to IL-10 in serum (highly related with disease recurrence), and increased serum IL-10 (anti-inflammatory) content. In addition, it led to improved cardiopulmonary fitness.

• 혜화의학회지
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• 제27권2호
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• pp.11-20
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• 2018

Objectives : Coronary and cerebrovascular disease with high mortality is a major factor in arteriosclerosis. Pro-inflammatory cytokines damage vascular endothelial cells, leading to vascular inflammation. These vascular inflammation can build up cholesterol and thrombus to cause atherosclerosis. Methods : In this study, we researched the effect of ChungHyul-Plus for vascular inflammation in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$). Change in mRNA expression of inflammatory cytokines (CCL5, CXCL8, CX3CL1, and MCP-1), cell adhesion molecules (VCAM-1 and ICAM-1), and anti-inflammation modulators (KLF2 and eNOS) were quantified by qRT-PCR. Results : ChungHyul-Plus decreased expression of inflammatory cytokines and cell adhesion molecules and increased anti-inflammation modulators expression in $TNF-{\alpha}$ stimulated HUVECs. Conclusions : These results suggest that ChungHyul-Plus can be used in the treatment and prevention of vascular inflammation and arteriosclerosis.