• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.1-9
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• 2017

Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

• Journal of Nutrition and Health
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• v.50 no.6
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• pp.578-584
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• 2017

Purpose: Excess intake of sodium is a major diet-related risk factor for human diseases including hypertension and cancer as well as obesity and inflammation. However, findings are still controversial, and evidence is lacking in Koreans. Therefore, for better understanding of the role of dietary sodium intake in disease etiology, this study investigated the effects of dietary sodium intake on adiposity, inflammation, and hormones in Koreans. Methods: A total of 80 males and females joined the study. The general characteristics and dietary intake data were investigated by trained interviewers using a questionnaire and 24-h dietary recall, respectively. For the markers of adiposity, body weight, body mass index, percent of body fat, visceral fat area, and waist and hip circumference were measured. For the inflammation and hormone markers, leptin, adiponectin, insulin, tumor necrosis $factor-{\alpha}$, and interleukin-6 were also analyzed. Results: Multivariate linear regression analyses suggested that dietary sodium intake was not associated with adiposity. However, dietary sodium showed a significant association with insulin level: Plasma insulin concentration increased with sodium intake independent of other dietary intake or percent of body fat (${\beta}=0.296$, adjusted $r^2=0.276$, p < 0.01). Other markers for inflammation and hormonal responses were not associated with dietary sodium intake. Conclusion: Findings suggested that dietary sodium intake may be a critical modifying factor in the level of plasma insulin. However, it showed a limited effect on obesity and other inflammation markers and hormone levels. These findings should be confirmed in larger, well-designed investigations.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.1
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• pp.16-22
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• 2010

Purpose: The purpose of this study was not only to evaluate the relative mRNA expression of interleukin-$1{\beta}$(IL-$1{\beta}$), cyclooxygenase2 (COX-2) and prostaglandin E2 (PGE2) by RT-PCR analysis but to observe pattern of edema by light microscopic and electron microscope after topical apply of hyaluronic acid in inflammation-guided mouse. Material and methods: Mice of this study were devided into 4 groups: Control group (no inflammation guided), Positive control (inflammation guided + vaselin apply), Protopic group (inflammation guided + protopic apply), Hyaluronic group (inflammation guided + hyaluronic acid apply). Results: Hyaluronic group showed less expressions of IL-$1{\beta}$, COX-2, PGE2 than those of positive control & protopic group. Hyaluronic group revealed a decreased inflammation than positive control & protopic group in Light Microscope. Hyaluronic group appeared decreased edema of ear compare to positive control & protopic group in Elecron Microscope. Conclusion: It was considered that hyaluronic acid has an antiinflammatory effect for intercepting the gene expression of cytokines related to inflammation.

• Journal of Acupuncture Research
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• v.34 no.1
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• pp.23-30
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• 2017

Objectives : In this study, the roles of Interleukin (IL)-4 and Signal transducer and activator of transcription 6 (STAT6), which have been reported to play a role in the pathogenesis of inflammation and cancer, were evaluated in snake venom toxin (SVT)-induced apoptosis. Methods : Inflammation was induced in human HaCaT kerationocytes, by lipopolysaccharide (LPS; $1{\mu}g/mL$) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), followed by treatment with SVT (0, 1, or $2{\mu}g/mL$). Cell viability was assessed by MTT assays after 24 h, and the expression of levels of IL-4, STAT6, and the apoptosis-related proteins p53, Bax, and Bcl-2 were evaluated by western blotting. Electro mobility shift assays (EMSAs) were performed to evaluate the DNA binding capacity of STAT6. Results : MTT assays showed that inflammation-induced growth of HaCaT cells following LPS or TNF-${\alpha}$ stimulation was inhibited by SVT. Western blot analysis showed that p53 and Bax, which promote apoptosis, were increased, whereas that of Bcl-2, an anti-apoptotic protein, was decreased in a concentration-dependent manner in LPS- or TNF-${\alpha}$-induced HaCaT cells following treatment with SVT. Moreover, following treatment of HaCaT cells with LPS, IL-4 concentrations were increased, and treatment with SVT further increased IL-4 expression in a concentration-dependent manner. Western blotting and EMSAs showed that the phosphorylated form of STAT6 was increased in HaCaT cells in the context of LPS- or TNF-${\alpha}$-induced inflammation in a concentration-dependent manner, concomitant with an increase in the DNA binding activity of STAT6. Conclusion : SVT can effectively promote apoptosis in HaCaT cells in the presence of inflammation through a pathway involving IL-4 and STAT6.

• International Journal of Oral Biology
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• v.41 no.3
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• pp.125-131
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• 2016

The aim of the present study was to develop an animal model for evaluation of temporomandibular (TMJ) nociception under TMJ inflammation. We also investigated the participation of $IL-1{\beta}$ in inflammation-induced TMJ nociception. Experiments were carried out using male Sprague-Dawley rats. Intra-articular injection of 3% formalin was administered to evaluate hyperalgesia 3 days after CFA injection. Intra-articular injection of 3% formalin did not produce nociceptive behavior in normal rats. Although intra-articular injection of 3 doses of CFA produced TMJ inflammation, only 1:3 diluted CFA produced hyperalgesia when formalin was injected intra-articularly 3 days after CFA injection. Co-administration of IL-1 receptor inhibitor with formalin into the TMJ cavity 3 days after CFA injection was performed. Co-administration of IL-1 receptor inhibitor significantly inhibited formalin-induced hyperalgesia in rats with CFA-induced TMJ inflammation. These results suggested that intra-articular injection of formalin produced hyperalgesia under chronic TMJ inflammation. Moreover, $IL-1{\beta}$ plays an important role in TMJ hyperalgesia under chronic inflammation and blockade of $IL-1{\beta}$ is a potential therapeutic target for inflammatory TMJ pain.

• 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.

• Journal of Radiopharmaceuticals and Molecular Probes
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• v.1 no.2
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• pp.104-108
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• 2015

Human serum albumin (HSA) has potential for diagnosis and therapy in clinical setting. The purpose of experiments was to develop and evaluate $^{68}Ga$-HSA as a PET agent for diagnosis of acute inflammation. NOTA-HSA was synthesized by conjugating 2-(p-isothiocyanatobenzyl)-1,4,7-triazacyclononane-1,4,7-triacetic acid to HSA in 0.1 M sodium carbonate buffer (pH 9.5) and then purified using a PD-10 size-exclusion column. NOTA-HSA was labeled with $^{68}Ga$ at room temperature for 10 min, and 8.4% sodium hydrogen carbonate buffer was added for neutralization. $^{68}Ga$-NOTA-HSA was purified using alumina N plus light cartridge and $0.22{\mu}m$ syringe filter. Labeling efficiency and radiochemical purity were determined by ITLC-SG with 0.1 M citric acid. Biodistribution study was performed in a male BALB/c mice model of Carrageenan-induced acute inflammation. Animal PET study was performed in acute inflammation mice model after tail vein injection of $^{68}Ga$-HSA. This radiotracer showed high labeling efficiency (>99%) around pH 7. Biodistribution study showed higher inflamed footpad uptake than control footpad uptake. Animal PET study revealed 2 times higher uptake on inflamed footpad compared to control footpad. In these experiments, we developed $^{68}Ga$-HSA for acute inflammation PET imaging and evaluated it in a mouse disease model. The results demonstrated that $^{68}Ga$-HSA has potential as a PET imaging agent for diagnosis of acute inflammation.

• Journal of Korean Neurosurgical Society
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• v.30 no.sup1
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• pp.170-173
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• 2001

Germinoma associated with chronic granulomatous inflammation of pineal gland has been rarely reported in the literature. The mechanism of chronic granulomatous inflammation is not understood well. We report a case of chronic granulomatous inflammation in pineal germinoma. In a 17 year-old male who suffered from headache and diplopia for six months, the mass of pineal gland was detected by brain MRI and removed through occipital transtentorial approach. The pathological specimen revealed the mass was predominantly composed of chronic granulomatous inflammation associated with small portion of germ cell tumor nests In the pathological interpretation of chronic granulomatous inflammation of pineal mass, it would be obliged to search for the presence of germ cell component.

• Clinical and Experimental Pediatrics
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• v.64 no.1
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• pp.37-43
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• 2021

Background: Animal studies have shown that a leukocyte influx precedes the development of bronchopulmonary dysplasia (BPD) in premature sheep. The CXC chemokine receptor 2 (CXCR2) pathway has been implicated in the pathogenesis of BPD because of the predominance of CXCR2 ligands in tracheal aspirates of preterm infants who later developed BPD. Purpose: To test the effect of CXCR2 antagonist on postnatal systemic and pulmonary inflammation and alveolarization in a newborn Sprague-Dawley rat model of BPD. Methods: Lipopolysaccharide (LPS) was injected intraperitoneally (i.p.) into the newborn rats on postnatal day 1 (P1), P3, and P5 to induce systemic inflammation and inhibit alveolarization. In the same time with LPS administration, CXCR2 antagonist (SB-265610) or vehicle was injected i.p. to investigate whether CXCR2 antagonist can alleviate the detrimental effect of LPS on alveolarization by attenuating inflammation. On P7 and P14, bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) were collected from the pups. To assess alveolarization, mean cord length and alveolar surface area were measured on 4 random nonoverlapping fields per animal in 2 distal lung sections at ×100 magnification. Results: Early postnatal LPS administration significantly increased neutrophil counts in BALF and PB and inhibited alveolarization, which was indicated by a greater mean cord length and lesser alveolar surface area. CXCR2 antagonist significantly attenuated the increase of neutrophil counts in BALF and PB and restored alveolarization as indicated by a decreased mean cord length and increased alveolar surface area in rat pups exposed to early postnatal systemic LPS. Conclusion: CXCR2 antagonist preserved alveolarization by alleviating pulmonary and systemic inflammation induced by early postnatal systemic LPS administration. These results suggest that CXCR2 antagonist can be considered a potential therapeutic agent for BPD that results from disrupted alveolarization induced by inflammation.