• Journal of Periodontal and Implant Science
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• v.43 no.5
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• pp.215-220
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• 2013

Purpose: Cigarette smoking is a major risk factor in periodontal diseases. The pathogenesis of periodontal diseases may be affected by alterations of the inflammatory response by smoke. Nitric oxide (NO) is a gaseous, colorless, highly reactive, short-lived free radical with a pivotal role in the regulation of various physiological and pathological mechanisms in the body. It is important in host defense and homeostasis, on the one hand, whereas, on the other hand, it modulates the inflammatory response in periodontitis, leading to harmful effects. The aim of this study was to assess the levels of NO in both the serum and saliva of smokers and nonsmokers having chronic periodontitis and to compare them with periodontally healthy controls. Methods: Sixty subjects participated in the study and were divided into three groups: group I, healthy nonsmoking subjects; group II, nonsmoking patients with chronic periodontitis; group III, smoking patients with chronic periodontitis. Each group consisted of twenty subjects. The biochemical estimation of NO in the collected serum and in the saliva was performed using the Griess colorimetric reaction. Results: The results showed that the mean value of the salivary and serum NO was greater in group II than in group I, and also greater in group III than in group II. Conclusions: NO appears to play an important and rather complex role in the immuno-inflammatory process and in the remodeling and maintenance of osseous structures. It is therefore logical that modulation of this mediator has potential for the treatment of a number of inflammatory conditions including periodontal disease.

• Biomolecules & Therapeutics
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• v.25 no.6
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• pp.634-640
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• 2017

Atopic dermatitis (AD) is a common inflammatory skin disorder mediated by inflammatory cells, such as macrophages and mast cells. Rifampicin is mainly used for the treatment of tuberculosis. Recently, it was reported that rifampicin has anti-inflammatory and immune-suppressive activities. In this study, we investigated the effect of rifampicin on atopic dermatitis in vivo and in vitro. AD was induced by treatment with 2, 4-dinitrochlorobenzene (DNCB) in NC/Nga mice. A subset of mice was then treated with rifampicin by oral administration. The severity score and scratching behavior were alleviated in the rifampicin-treated group. Serum immunoglobulin E (IgE) and interleukin-4 (IL-4) levels were also ameliorated in mice treated with rifampicin. We next examined whether rifampicin has anti-atopic activity via suppression of mast cell activation. Rifampicin suppressed the release of ${\beta}$-hexosaminidase and histamine from human mast cell (HMC)-1 cultures stimulated with compound 48/80. Treatment with rifampicin also inhibited secretion of inflammatory mediators, such tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) and prostaglandin $D_2$ ($PGD_2$), in mast cells activated by compound 48/80. The mRNA expression of cyclooxygenase 2 (COX-2) was reduced in the cells treated with rifampicin in a concentration-dependent manner. These results suggest that rifampicin can be used to treat atopic dermatitis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2007.11a
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• pp.67-73
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• 2007

There have been various inflammatory skin disorders in humans including atopic dermatitis, eczema and psoriasis. Although some drugs have been used for these disorders, there is an urgent need for safer and more effective topical anti-inflammatory agents. Plant flavonoids possess anti-inflammatory activity and some of them have multiple pharmacological mechanisms, inhibition of eicosanoid metabolizing enzymes, histamine release and/or down-regulation of pro inflammatory gene expression. These properties of flavonoids may be suitable for treating chronic skin inflammatory disorders. Especially, wogonin, some prenylated flavonoids and biflavonoids have a strong potential as new anti-inflammatory agents by topical application.

• The Journal of Internal Korean Medicine
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• v.39 no.1
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• pp.76-83
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• 2018

Objectives: This case study reports on one patient presenting atypical and chronic disorders after being diagnosed with $Guillain-Barr{\acute{e}}$ Syndrome (GBS). Methods: One patient was treated by Yeongseonjetong-eum-gami, Taklisodok-eum-gami, electroacupuncture, and physical therapy. Any improvement in symptoms was assessed by measuring changes in the motor grade of upper limb weakness, the numerical rating scale (NRS) of lower limb numbness, and GBS scores. Results: After 24 days of treatment, the patient's symptoms of GBS showed little improvement. Conclusions: Traditional Korean medical treatment appeared to be effective in reducing GBS symptoms, but more research is required to confirm these results. When treating GBS patients, the clinician should put effort into distinguishing GBS from other nervous disorders, such as acute onset Chronic Inflammatory Demyelinating Polyneuropathy (CIDP).

• The Journal of Korean Medicine
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• v.39 no.4
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• pp.126-135
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• 2018

Objectives: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and irreversible airflow. This study aimed to evaluate the effects of GHX02 in a COPD-induced mouse model. Methods: The COPD mouse model was established by exposure to cigarette smoke extract and lipopolysaccharide which were administered by intratracheal injection three times with a 7 day interval. GHX02 (100, 200, 400 mg/kg) and all other drugs were orally administrated for 14 days from Day 7 to Day 21. Results: GHX02 significantly decreased the neutrophil counts in bronchoalveolar lavage fluid (BALF) and the number of $CD4^+$, $CD8^+$, $CD69^+$, and $CD11b^+/GR1^+$ cells in BALF and lung cells. GHX02 also suppressed the secretion of tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-17A, macrophage inflammatory protein 2 (MIP2), and chemokine (C-X-C motif) ligand 1 (CXCL-1) in BALF and ameliorated the lung pathological changes. Conclusions: Thus, GHX02 effectively inhibited airway inflammation by inhibiting migration of inflammatory cells and expression of pro-inflammatory cytokines. Therefore, GHX02 may be a promising therapeutic agent for COPD.

• Journal of Microbiology and Biotechnology
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• v.16 no.12
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• pp.1954-1960
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• 2006

The effects of the exopolymers of Aureobasidium pullulans SM-2001 containing $\beta$-1,3/1,6-glucan on formalin-induced chronic inflammation were observed. Doses of 62.5, 125, and 250 mg/kg of the exopolymers were orally administered once a day for 10 days to formalin-induced chronic inflammatory mice (0.02 ml of 3.75% formalin was subaponeurotically injected into the left hind paw), and then the bilateral hind-paw thickness and volume were measured daily, while the paw wet-weight, histological profiles, and histomorphometrical analyses were conducted at termination. The results were compared with those for diclofenac, indomethacin, and dexamethasone (intraperitoneally injected) 15 mg/kg-dosed groups. All the animals were sacrificed 10 days after dosing. As a result of the formalin injection, a marked increase in the difference between the intact and formalin-induced paw thickness and volume was detected in the formalin-injected control compared with that in the intact control with time, plus at the time of sacrifice, the difference in the paw wet-weights was also dramatically increased. In a histological and histomorphometrical analysis, severe histological profiles of chronic inflammation were detected in the formalin-injected control with a marked increase in the thickness of the skin of the dorsum pedis. However, these formalin-induced chronic inflammatory changes were significantly and dose-dependently decreased by the exopolymer treatment. In conclusion, the exopolymer treatment inhibited the chronic inflammatory response induced by formalin injection in the mice. However, somewhat low efficacies were detected compared with those for the diclofenac-, indomethacin-, and dexamethasone-treated groups.

• Clinical and Experimental Pediatrics
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• v.48 no.10
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• pp.1038-1049
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• 2005

Asthma is characterized by a chronic inflammatory disorder of the airways that leads to tissue injury and subsequent structural changes collectively called airway remodelling. Characteristic changes of airway remodelling in asthma include goblet cell hyperplasia, deposition of collagens in the basement membrane, increased number and size of microvessels, hypertrophy and hyperplasia of airway smooth muscle, and hypertrophy of submucosal glands. Apart from inflammatory cells, such as eosinophils, activated T cells, mast cells and macrophages, structural tissue cells such as epithelial cells, fibroblasts and smooth muscle cells can also play an important effector role through the release of a variety of mediators, cytokines, chemokines, and growth factors. Through a variety of inflammatory mediators, epithelial and mesenchymal cells cause persistence of the inflammatory infiltrate and induce airway structural remodelling. The end result of chronic airway inflammation and remodelling is an increased thickness of the airway wall, leading to a increased the bronchial hyperresponsiveness and fixed declined lung function.

• Journal of Haehwa Medicine
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• v.17 no.2
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• pp.155-160
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• 2008

Pelvic inflammatory disease (PID) is a general term that refers to infection of the internal reproductive organs such as the female uterus, fallopian tubes, and ovaries. PID is caused by germs that invade the genital organs, causing the acute inflammatory reaction, and chronic PID is to have a recurrence of PID because of the lack of effective treatment of acute PID. Symptoms of PID include pelvic pain, fever, leukorrhea, infertility, and fatigue. Treatments for PID can be improved by combining herb medicine therapy, intestinal irrigation, or the therapy that put herb medicine on the abdominal region with antibiotics, or analgesic drugs.

• Hanyang Medical Reviews
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• v.33 no.1
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• pp.27-32
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• 2013

Inflammatory bowel diseases(IBD), including Crohn's disease and ulcerative colitis, are chronic inflammatory states of the intestinal tract. While the exact mechanisms inducing chronic inflammation are still unclear, it is hypothesized that the inflammation is caused in part by an inappropriate immune response to the intestinal microflora. Although inflammatory diseases are not directly linked to patient survival, symptoms of these diseases significantly decrease quality of life. The incidence rate is higher in western people than eastern people, but the incidence rate of IBD in eastern people, including Korean, is increasing. Recently, it has been reported that IL-17 is an important factor that appears to be involved in IBD induction and progression. This report reviews many recent papers reporting the relationship between IBD and IL-17, which may provide an understanding leading to new means of prevention and treatment for IBD.

• IMMUNE NETWORK
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• v.22 no.6
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• pp.46.1-46.25
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• 2022

T-helper-17 (Th17) cells and related IL-17-producing (type17) lymphocytes are abundant at the epithelial barrier. In response to bacterial and fungal infection, the signature cytokines IL-17A/F and IL-22 mediate the antimicrobial immune response and contribute to wound healing of injured tissues. Despite their protective function, type17 lymphocytes are also responsible for various chronic inflammatory disorders, including inflammatory bowel disease (IBD) and colitis associated cancer (CAC). A deeper understanding of type17 regulatory mechanisms could ultimately lead to the discovery of therapeutic strategies for the treatment of chronic inflammatory disorders and the prevention of cancer. In this review, we discuss the current understanding of the development and function of type17 immune cells at the intestinal barrier, focusing on the impact of microbiota-immune interactions on intestinal barrier homeostasis and disease etiology.