• Korean Journal of Oriental Medicine
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• v.8 no.1
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• pp.65-74
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• 2002

Inflammation is a disease that continues to afflict large numbers of people and may cause other diseases, for example, rheumatoid arthritis, colon cancer, etc. prostaglandins(PGs), one of arachidonic acid metabolites, are major chemical mediators in the process of inflammation. In traditional herbal medicine, many kinds of herbal drugs have been widely used for the treatment of inflammation. So, we analyzed many publications until 2001 which worked on inhibition of $PGE_2$ synthesis by cyclooxygenase-2 (COX-2) with herbs and herb oriented single compounds. And then we tried to make interpretations of herbal traditional prescriptions for inflammation. There are significant correlations between herbal medicine prescribed and inhibitions of COX-2 activity. From our efforts and further researches, we expect to develop new-inflammatory herbal drugs which have more efficacy and fewer side effects.

• Journal of Haehwa Medicine
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• v.27 no.2
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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.

• The Journal of Internal Korean Medicine
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• v.28 no.1
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• pp.166-175
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• 2007

Objectives : This study was designed to evaluate the neuroprotective effect of Cirsium japonicum and Silibinin on lipopolysaccharide-induced inflammation in BV2 microglial cells. Methods : We studied on the neuroprotective effect of lipopolysaccharide-induced inflammation using MTS assay, western blot, and nitric oxide detection on mouse BV2 microglial cells. Results : Cirsium japonicum dose-dependently (50${\mu}g/ml$${\sim}$$250{\mu}g/ml$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglia and also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Silibinin dose-dependently (10${\mu}M$${\sim}$$100{\mu}M$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglial cells. Silibinin also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Conclusion : These effects of neuroprotection related to anti-inflammation suggest that Cirsium japonicum and Silibininmay be useful candidates for the development of a drug for related neurodegenerative diseases.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.2
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• pp.107-112
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• 2024

27-Hydroxycholesterol (27OHChol), a prominent cholesterol metabolite present in the bloodstream and peripheral tissues, is a kind of immune oxysterol that elicits immune response. Recent research indicates the involvement of 27OHChol in metabolic inflammation (meta-inflammation) characterized by chronic responses associated with metabolic irregularities. 27OHChol activates monocytic cells such that they secrete pro-inflammatory cytokines and chemokines, and increase the expression of cell surface molecules such as pattern-recognition receptors that play key roles in immune cell-cell communication and sensing metabolism-associated danger signals. Levels of 27OHChol increase when cholesterol metabolism is disrupted, and the resulting inflammatory responses can contribute to the development and complications of metabolic syndrome, including obesity, insulin resistance, and cardiovascular diseases. Since 27OHChol can induce chronic immune response by activating monocyte-macrophage lineage cells that play a crucial role in meta-inflammation, it is essential to understand the 27OHChol-induced inflammatory responses to unravel the roles and mechanisms of action of this cholesterol metabolite in chronic metabolic disorders.

• The Korean Journal of Pain
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• v.12 no.2
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• pp.171-176
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• 1999

Background: Effect of nitric oxide on the hyperalgesia induced by inflammation is controversial. From our previous experiment, NOS inhibitor, L-NAME given during the induction period decrease mechanical hyperalgesia occured by Freund's complete adjuvant induced inflammation. In addition, we attempted to analyze the effects of L-NAME on mechanical hyperalgesia after the development of inflammation by Freund's complete adjuvant in rat paw. Methods: Male Sprague Dawley rats were divided into four groups; control (normal saline), and three different doses of L-NAME (0.1 mg, 1 mg, 10 mg). Inflammation was induced in rats by injecting 0.15 ml of Freund's complete adjuvant (FCA) intraplantarly. Rats showed typical hyperalgesia within twelve hours after injection and maintained this for about one week. Tests were done 2 days after injection of FCA. After the baseline test either L-NAME or saline was injected under light halothane anesthesia. Effect of L-NAME on hyperalgesia was assessed by measuring mechanical hyperalgesia at 15, 30, 60, 90, 120 minutes. Same experients were repeated on normal rats. Results: When injected at the site of inflammation, L-NAME caused dose dependent decrease in mechanical hyperalgesia. However, normal rats also showed increased mechanical threshold after L- NAME injection. Conclusions: Although L-NAME reduces FCA induced mechanical hyperalgesia, this result may solely be due to inhibition of nitric oxide production and need to be further determined.

• BMB Reports
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• v.57 no.4
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• pp.200-205
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• 2024

We conducted a comprehensive series of molecular biological studies aimed at unraveling the intricate mechanisms underlying the anti-fibrotic effects of triamcinolone acetonide (TA) when used in conjunction with fully covered self-expandable metal stents (FCSEMS) for the management of benign biliary strictures (BBS). To decipher the molecular mechanisms responsible for the anti-fibrotic effects of corticosteroids on gallbladder mucosa, we conducted a comprehensive analysis. This analysis included various methodologies such as immunohisto-chemistry, ELISA, real-time PCR, and transcriptome analysis, enabling us to examine alterations in factors related to fibrosis and inflammation at both the protein and RNA levels. Overall, our findings revealed a dose-dependent decrease in fibrosis-related signaling with higher TA concentrations. The 15 mg of steroid treatment (1X) exhibited anti-fibrosis and anti-inflammatory effects after 4 weeks, whereas the 30 mg of steroid treatment (2X) rapidly reduced fibrosis and inflammation within 2 weeks in BBS. Transcriptomic analysis results consistently demonstrated significant downregulation of fibrosis- and inflammation-related pathways and genes in steroid-treated fibroblasts. Use of corticosteroids, specifically TA, together with FCSEMS was effective for the treatment of BBS, ameliorating fibrosis and inflammation. Our molecular biological analysis supports the potential development of steroid-eluted FCSEMS as a therapeutic option for BBS in humans resulting from various surgical procedures.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.305-317
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• 1990

The present study was performed to investigate modification in the electrophysiological characteristics of cat dorsal horn cells during neurogenic inflammation induced by mustard oil. The results obtained were summarized as follows: 1) Following subcutaneous injection of mustard oil the majority of wide dynamic range (WDR) cells (10/15 units) showed enhanced responses (80%) to brush, while the responses to all types of mechanical stiumli were enhanced in 3/15 units. One cell was further activated by pinch and the another was not affected at all after induction of inflammation. 2) The sensitization of WDR cell was resulted from subcutaneous injection of mustard oil either inside or outside of the receptive field (RF), whereas the spontaneous activity increased only after mustard oil was injected inside of the RF. 3) In the animal with inflammation the responses of high threshold (HT) cell to noxious stimulus were not altered, while HT cell responded to such mechanical stimulus as pressure which was usually ineffective in normal animals. 4) After induction of inflammation, low threshold (LT) cell appeared to be converted to WDR cell, showing responses not only to brush but also to pressure and pinch. 5) The mustard oil-induced inflammation enhanced responses of WDR and HT cells to the thermal stimuli and also resulted in a pronounced after-discharge in WDR cells. 6) After subcutaneous injection of lidocaine, the increased background activity of WDR cells due to inflammation was almost completely abolished. 7) A subcutaneous injection of mustard oil inside of the RF invariably desensitized the dorsal horn cells which receive sensory inputs from the inflamed RF. From the results of Present study it was revealed that a neurogenic inflammation induced by mustard oil resulted in an enhancement of responses of cat dorsal horn cells to mechanical and thermal stimuli.

• Herbal Formula Science
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• v.32 no.1
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• pp.39-49
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• 2024

Objectives : The purpose of this study was to investigate the molecular targets and pathways of anti-inflammatory effects of Jakyakgamchotang with corydalis tuber (JC) using network pharmacology. Methods : The compounds in constituent herbal medicines of JC were searched in TCM systems pharmacology (TCMSP). Target gene informations of the components were collected using chemical-target interactions database provided by Pubchem. Afterwards, network analysis between compounds and inflammation-related target genes was performed using cytoscape. Go enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on inflammation-related targets using DAVID database. Results : 70 active compounds related to inflammation were identified, and 295 target genes related to the anti-inflammatory activity of the compound of JC were identified. In the Go biological process DB and KEGG pathway DB, "inflammatory response", "cellular response to lipopolysaccharide", "positive regulation of interleukin-6 production", and "positive regulation of protein kinase B. signaling", "positive regulation of ERK1 and ERK2 cascade", "positive regulation of I-kappaB kinase/NF-kappaB signaling", "negative regulation of apoptotic process", and "PI3K-Akt signaling pathway" were found to be mechanisms related to the anti-inflammatory effects related to the target genes of JC. The main compounds predicted to be involved in the anti-inflammatory effect of JC were quercetin, licochalcone B, (+)-catechin, kaempferol, and emodin. Conclusions : This study provides the molecular targets and potential pathways of JC on inflammation. It can be used as a basic data for using JC for various inflammatory disease in traditional korean medicine clinic.

• The Korean journal of internal medicine
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• v.33 no.6
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• pp.1210-1223
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• 2018

Background/Aims: The co-occurrence of obesity aggravates asthma symptoms. Diet-induced obesity increases helper T cell (TH) 17 cell differentiation in adipose tissue and the spleen. The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin can potentially be used to treat asthma in obese patients by inhibiting interleukin 17 (IL-17) expression. This study investigated the combined effects of pravastatin and anti-IL-17 antibody treatment on allergic inflammation in a mouse model of obesity-related asthma. Methods: High-fat diet (HFD)-induced obesity was induced in C57BL/6 mice with or without ovalbumin (OVA) sensitization and challenge. Mice were administered the anti-IL-17 antibody, pravastatin, or both, and pathophysiological and immunological responses were analyzed. Results: HFD exacerbated allergic airway inflammation in the bronchoalveolar lavage fluid of HFD-OVA mice as compared to OVA mice. Blockading of the IL-17 in the HFD-OVA mice decreased airway hyper-responsiveness (AHR) and airway inflammation compared to the HFD-OVA mice. Moreover, the administration of the anti-IL-17 antibody decreased the leptin/adiponectin ratio in the HFD-OVA but not the OVA mice. Co-administration of pravastatin and anti-IL-17 inhibited airway inflammation and AHR, decreased goblet cell numbers, and increased adipokine levels in obese asthmatic mice. Conclusions: These results suggest that the IL-17-leptin/adiponectin axis plays a key role in airway inflammation in obesity-related asthma. Our findings suggest a potential new treatment for IL-17 as a target that may benefit obesity-related asthma patients who respond poorly to typical asthma medications.

• Tuberculosis and Respiratory Diseases
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• v.78 no.1
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• pp.8-17
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• 2015

Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.