• 디지털융복합연구
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• 제13권4호
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• pp.387-393
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• 2015

본 연구는 12주간 비만 여성을 대상으로 규칙적인 복합운동과 policosanol 섭취 병행이 염증표지인자 LDH와 CPK, Leptin에 미치는 변화를 분석함으로써 복합운동과 policosanol 섭취 병행이 생체 방어반응과 지방세포 조절 호르몬 변화에 미치는 영향을 규명하는데 있다. 통제집단 12명, policosanol 섭취집단 12명, 복합운동집단 12명, 복합 처치 집단 12명으로 무선 배정하였고 주 2회는 근저항성 운동, 주2회는 걷기형태의 유산소운동을 실시하였다. 12주 후 LDH는 운동시기에서 유의한 차이를 보였고(p<.01), 운동시기와 그룹간의 상호작용 효과에서도 유의한 차이 (p<.05)를 나타냈다. 또한 leptin의 변화에서는 운동시기에 유의한 차이(p<.001)를 나타내었다. 이상의 결과를 종합하면 복합 운동이나, policosanol 섭취는 염증표지인자와 렙틴에 긍정적인 영향을 미치며, 복합운동과 policosanol 섭취의 병행은 그 효과를 더욱 증대시키는 것으로 사료된다.

• 통합자연과학논문집
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• 제7권4호
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• pp.234-240
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• 2014

C-C chemokine receptor type 4 (CCR4) is a chemokine receptor with seven transmembrane helices and it belongs to the GPCR family. It plays an important role in asthma, lung disease, atopic dermatitis, allergic bronchopulmonary aspergillosis, cancer, inflammatory bowel disease, the mosquito-borne tropical diseases, such as dengue fever and allergic rhinitis. Because of its role in wide spectrum of disease processes, CCR4 is considered to be an important drug target. Three dimensional structure of the protein is essential to determine the functions. In the present study homology modeling of human CCR4 was performed based on crystal structure of CCR5 chemokine receptor. The generated models were validated using various parameters. Among the generated homology models the best one is selected based on validation result. The model can be used for performing further docking studies to identifying the critical interacting residues.

• 대한지역사회영양학회지
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• 제14권4호
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• pp.451-461
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• 2009

The purpose of this study was to investigate the age-related changes of cardiovascular disease risk factors and inflammatory markers in non-obese Korean women. Subjects were 112 women over 20 years old with body mass index (BMI) less than $30 kg/m^2$ and were divided into 3 groups (< 40 years, $40{\sim}59$ years, ${\ge}60$ years). Mean weight and BMI in the oldest group were significantly higher than those in the other 2 younger groups (p < 0.05). Mean total cholesterol, triglyceride, LDL-cholesterol and apolipoprotein B/apolipoprotein A1 ratio (BAR) in the oldest group were significantly higher than those in the youngest group (p < 0.05), and mean HDL-cholesterol of the oldest group was significantly lower than that of the youngest group (p < 0.05). The older-aged group showed significantly higher mean values of atherogenic index (AI) and LDL/HDL ratio (p < 0.05) than the respective younger-aged group, and AI was significantly correlated with age, nitric oxide and thiobarbituric acid reactive substances (p < 0.01). In addition, mean vascular cell adhesion molecule-l (VCAM-1) tended to be higher in the older-aged group than the younger group. Tumor necrosis factor-${\alpha}$, a proinflammatory maker, was significantly positively correlated with serum homocysteine, a cardiovascular disease risk factor (p < 0.01). In addition, a significantly positive correlation was observed between C-reactive protein and BAR (p < 0.01). Overall results suggested that the aging might affect the increase of cardiovascular disease risk factors including the serum lipid profiles, weight and BMI, and age-related increases of weight and BMI might play a role in changes in certain biomarkers of inflammation. (Korean J Community Nutrition 14(4) : 451${\sim}$461, 2009)

• Biomolecules & Therapeutics
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• 제20권5호
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• pp.463-469
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• 2012

Atopic dermatitis is a chronic, inflammatory disease of the skin with increased transepidermal water loss. Both an abnormal inflammatory response and a defective skin barrier are known to be involved in the pathogenesis of atopic dermatitis. Protease activated receptor 2 (PAR2) belongs to a family of G-protein coupled receptors and is activated by both trypsin and a specific agonist peptide, SLIGKV-$NH_2$. PAR2 is expressed in suprabasal layers of the epidermis and regulates inflammatory responses and barrier homeostasis. In this study, we show that nordihydroguaiaretic acid (NDGA) inhibits the PAR2-mediated signal pathway and plays a role in skin barrier recovery in atopic dermatitis. Specifically, NDGA reduces the mobilization of intracellular $Ca^{2+}$ in HaCaT keratinocytes by down-regulating inflammatory mediators, such as interleukin-8, thymus and activation-regulated chemokine and intercellular cell adhesion molecule-1 in HaCaT keratinocytes. Also, NDGA decreases the protein expression of involucrin, a differentiation maker of keratinocyte, in both HaCaT keratinocytes and normal human epidermal keratinocytes. We examined NDGA-recovered skin barrier in atopic dermatitis by using an oxazolone-induced atopic dermatitis model in hairless mice. Topical application of NDGA produced an increase in transepidermal water loss recovery and a decrease in serum IgE level, without weight loss. Accordingly, we suggest that NDGA acts as a PAR2 antagonist and may be a possible therapeutic agent for atopic dermatitis.