• Title/Summary/Keyword: 억제-유도 치료

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Identification of Matrix Mineralization-Related Genes in Human Periodontal Ligament Cells Using cDNA Microarray (cDNA microarray에 의한 치주인대세포의 광물화 결절형성에 관여하는 유전자들의 분석)

  • Shin, Jae-Hee;Park, Jin-Woo;Yeo, Shin-Il;Noh, Woo-Chang;Kim, Moon-Kyu;Kim, Jung-Chul;Suh, Jo-Young
    • Journal of Periodontal and Implant Science
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    • v.37 no.sup2
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    • pp.447-463
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    • 2007
  • Periodontal ligament (PDL) cells have been known as multipotential cells, and as playing an important rolesin periodontal regeneration. The PDL cells are composed of heterogeneous cell populations which have the capacity to differentiate into either cementoblasts or osteoblasts, depending on needs and conditions. Therefore, PDL cells have the capacity to produce mineralized nodules in vitro in mineralization medium which include ascorbic acid, ${\beta}$-glycerophosphate and dexamethasone. In spite of these well-known osteoblast like properties of PDL cells, very little is known about the molecules involved in the formation of the mineralized nodules in the PDL cells. In the present study, we analysed gene-expression profiles during the mineralization process of cultured PDL cells by means of a cDNA microarray consisting of 3063 genes. Nodules of mineralized matrix were strongly stained with alizarin red S on the PDL cells cultured in the media with mineralization supplements. Among 3,063 genes analyzed, 35 were up-regulated more than two-fold at one or more time points in cells that developed matrix mineralization nodules, and 38 were down-regulated to less than half their normal level of expression. In accord with the morphological change we observed, several genes related to calcium-related or mineral metabolism were induced in PDL cells during osteogenesis, such as IGF-II and IGFBP-2. Proteogycan 1, fibulin-5, keratin 5, ,${\beta}$-actin, ${\alpha}$-smooth muscle actin and capping protein, and cytoskeleton and extracellular matrix proteins were up-regulated during mineralization. Several genes encoding proteins related to apoptosis weredifferentially expressed in PDL cells cultured in the medium containing mineralization supplements. Dkk-I and Nip3, which are apoptosis-inducing agents, were up-regulated, and Btf and TAXlBP1, which have an anti-apoptosis activity, were down-regulated during mineralization. Also periostin and S100 calciumbinding protein A4 were down-regulated during mineralization.

Effects of Small Colored Potato Extracts by High-Pressure Extraction on Serum Lipid Levels in High Fat Diet Fed Rats (꼬마색깔감자 초고압 추출물이 고지방식이를 섭취한 흰쥐의 혈청지질농도개선 미치는 영향)

  • Rha, Young-Ah;Choi, Mi-Sook;Kwon, Min-Soo;Hwang, Young-Jeong;Park, Sung-Jin
    • Culinary science and hospitality research
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    • v.20 no.4
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    • pp.157-168
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    • 2014
  • We investigated the anti-obesity effects of small colored potato extracts by high pressure water extraction process on body weight, plasma lipid levels in high-fat diet-induced obese mice. Experimental groups were divided into basal diet only (Normal), high fat diet control (HFD), small colored potato water extracts (CP), and high-fat diet and small colored potato water high pressure extracts (HCP) groups. The levels of hematological variables were not significantly different among the four groups. Compared with the HFD group's serum total cholesterol level of $86.01{\pm}1.16mg/dL$, the levels of the CP and HCP groups were significantly lowered to $80.29{\pm}1.28$ and $77.21{\pm}4.21mg/dL$, respectively. Compared with the HFD group's LDL-cholesterol level of $18.92{\pm}2.44mg/dL$, the LDL-cholesterol levels of the CP and HCP groups were significantly lowered to $13.52{\pm}1.26$ and $12.93{\pm}1.26mg/dL$, respectively. Also, compared to the HFD group's serum triglyceride level of $82.71{\pm}3.94mg/dL$, the level of the HCP group was significantly lowered to $63.24{\pm}6.32mg/dL$. These results suggested that dietary supplementation of small colored potato extracts using high pressure water extraction does not have any adverse effects on the hematological variables, while improving the lipid content and reducing hepatic damage of the high-fat fed rats.

De novo Expression of Hepatic UCP3 Is Time-Dependently Related with Metabolic Function in Fenofibrate-Treated High Fat Diet Rats (고지방 섭취한 쥐에서 페노파이브레이트 복용에 의한 간 UCP3 발현 기간과 대사변화 관계)

  • Park, Mi-Kyoung;Kang, Ah-Young;Seo, Eun-Hui;Joe, Yeon-Soo;Kang, Soo-Jeong;Hong, Sook-Hee;Kim, Duk-Kyu;Lee, Hye-Jeong
    • Journal of Life Science
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    • v.19 no.1
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    • pp.15-20
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    • 2009
  • Uncoupling protein 3 (UCP3) is a mitochondrial protein that is expressed predominantly in skeletal muscle. It may play a role in altering metabolic function. However, its major physiological roles are not fully understood. Recently de novo expression of UCP3 in rat liver by fenofibrate was reported. We also reported previously that fenofibrate-induced de novo expression of UCP3 contributes to reduction of adipose tissue in obese rats. In the present study, we investigated that ienofibrate-induced expression of UCP3 in rat liver is related with metabolic function such as body weight and hepatic lipid content by time-dependent manner in high-fat diet rats. Eight-week-old male Sprague-Dawley rats were randomly divided into two groups; the high fat diet group (HF, n=16) and fenofibrate-treated high fat diet group (HFF, n=16). The mRNA expression of hepatic UCP3 was detected as early as 1 week of fenofibrate treatment by quantitative real-time PCR and the amount of mRNA was increased time-dependently. The mean body weight of the HFF group was significantly less com. pared with the HF group after 6 weeks of fenofibrate treatment, even though there was no difference of food intake between the two groups. Rectal temperature was increased during 4 to 6 weeks of fenofibrate treatment and body weight was decreased after 6 weeks of treatment. These results were corresponded with the increased amount of the expression of UCP3 mRNA and protein. We suggest that de novo expression of hepatic UCP3 is increased time-dependently with fenofibrate treatment and that the amount of expression is correlated with metabolic function.

Fermented Jeju Soybean Extract Promotes Hair Growth in Human Hair Follicle Organ Culture and Clinical Trial (모낭기관배양과 임상에서 제주푸른콩발효추출물의 육모 효능에 미치는 영향)

  • Lee, Yonghee;Shin, Seung Hyun;Kim, Sehyun;Jeong, Gyusang;Hong, Min Jung;Park, Hyeokgon;Kim, Seung Hun;Kim, Eun Joo;Kang, Young-Gyu;Park, Byung Cheol;Park, Won Seok;Kim, Su Na;Kim, Hyoung-June
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.47 no.3
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    • pp.255-263
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    • 2021
  • Soybean extract is known to play an important role in preventing and treating diseases associated with aging, cancer, obesity, and cardiovascular disease. A recent has revealed that soybean extract has a potent effect on hair growth in in vitro, in vivo, and clinical studies. Recently, it has been reported that their fermented extracts exhibit numerous and high efficacy, as compared to general extracts. However, the underlying mechanisms that induce hair growth after using fermented soybean extract are not well understood. The present study aimed to determine the effects of fermented Jeju soybean (FJS) extract on hair growth, with a focus on the underlying mechanisms similar to those of minoxidil. We conducted in vitro and ex vivo investigations and clinical studies. FJS extract enhanced dermal papilla cell proliferation, VEGF levels, and potassium channel opening. Moreover, it promoted human hair follicle elongation. These effects were comprehensively demonstrated in the clinical results, in which FJS extract-containing shampoo improved hair density after 24 weeks of utilization. Collectively, the results of this study demonstrate that FJS extract promotes hair growth and inhibits hair loss through a mechanism similar to that of minoxidil in hair follicles.

Inflammatory Reponse of the Lung to Hypothermia and Fluid Therapy after Hemorrhagic Shock in Rats (흰쥐에서 출혈성 쇼크 후 회복 시 저체온법 및 수액 치료에 따른 폐장의 염증성 변화)

  • Jang, Won-Chae;Beom, Min-Sun;Jeong, In-Seok;Hong, Young-Ju;Oh, Bong-Suk
    • Journal of Chest Surgery
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    • v.39 no.12 s.269
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    • pp.879-890
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    • 2006
  • Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.