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Effects of Aspirin on the Pathogenesis of Acute Lung Injury in Rats Subjected to Hemorrhage (출혈성 쇼크로 인한 급성 폐손상의 발병기전과 아스피린의 효과)

  • Park, Yoon-yub;Lee, Young Man
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.1
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    • pp.83-91
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    • 2006
  • Background : For unknown reasons, the serum ferritin concentrations are higher in patients with acute lung injury. A pretreatment with aspirin reduces the acute lung injury in rats subjected severe hemorrhage, and increases the rate of ferritin synthesis in vitro. This study investigated the effect of aspirin on the serum ferritin changes in rats subjected to severe hemorrhage. Methods : Hemorrhagic shock was induced by withdrawing blood (20 ml/kg of B.W.) through the femoral artery for 5 min. The rats were pretreated with aspirin (10 mg/kg, i.v.) 30 min before hemorrhage. Results : The protein content and leukocyte count in the bronchoalveolar lavage fluid, lung tissue myeloperoxidase activities were significantly higher after hemorrhage. The aspirin pretreatment prevented these changes. The serum and lavage fluid ferritin concentrations were elevated higher after hemorrhage. These were also attenuated by the aspirin pretreatment. Conclusion : The changes in the serum and lung lavage ferritin level might be closely related to the severity of hemorrhage-induced acute lung injury. Therefore, the serum and lavage ferritin concentrations can be a useful biomarker for patients with precipitating conditions.

Role of Lysyl Oxidase Family during Odontoblastic Differentiation of Human Dental Pulp Cells Induced with Odontogenic Supplement (인간치수세포에서 상아모세포의 분화과정 동안 Lysyl Oxidase Family의 역할)

  • Lee, Hwa-Jeong;Han, Soo-Yeon
    • Journal of dental hygiene science
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    • v.13 no.3
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    • pp.296-303
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    • 2013
  • Lysyl oxidase (LOX), extracellular matrix enzyme, is catalyzing lysine-derived crosslinks in collagen and elastin. Recently, several LOX-like proteins (LOXL, LOXL2, LOXL3 and LOXL4) have been identified in human but their specific functions are still largely unknown. The purpose of this study was to evaluate the function of the LOX family genes during odontoblastic differentiation of human dental pulp (HDP) cells induced with odontogenic supplement (OS). The messenger RNA (mRNA) expression of LOX family genes and differentiation markers was assessed by reverse transcriptase polymerase chain reaction analysis (RT-PCR). The formation of mineralization nodules was evaluated by alrizarin red S staining. Amine oxidase activity of HDP cells was measured by peroxidase-coupled fluormetric assay. The expressions of differentiation markers, such as alkaline phosphatase (ALP), osteopontin (OPN), osteocalcin (OCN), dentin matrix protein1 (DMP1), dentin sialophosphoprotein (DSPP) in HDP cells were increased after treatment with OS media. The LOX and LOXL mRNA expression were gradually increased in OS media, whereas LOX enzyme activities were markedly detected on day 7. The mRNA expression and LOX enzyme activity of collagen type I was very similar to the pattern of LOX gene. In this study, the expression of LOX and its isoforms, and activity of LOX were highly regulated during odontoblastic differentiation. Thus, these results suggest that LOX plays a key role in odontoblastic differentiation of HDP cells.

Betaine Induces Epidermal Differentiation by Enhancement of Autophagy through an mTOR-independent Pathway (Betaine의 mTOR 비의존적 자가포식 작용 촉진에 의한 표피 분화 유도 효과)

  • Choi, Seon-Guk;Kim, Mi-Sun;Kim, Jin-Hyun;Park, Sun Gyoo;Lee, Cheon Koo;Kang, Nae-Gyu
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.44 no.1
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    • pp.95-101
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    • 2018
  • The epidermis which is stratified by epithelial tissue renewal based on keratinocyte differentiation protects the organism from various environmental insults by forming a physical barrier. Autophagy is a mechanism which mediates lysosomal delivery and degradation of protein aggregates, damaged organelles and intracellular microorganisms. Recent reports have shown that autophagy has critical roles for proper terminal differentiation to stratum corneum via removing metabolic organelles and nuclei. However, whether increasing autophagy can activate epidermal differentiation is unknown. Here, we screened a library of natural single compounds and discovered that betaine specifically increased the LC3 positive cytosolic punctate vesicles and LC3-I to LC3-II conversion in HaCaT human keratinocyte cell line, indicating increased autophagy flux. mTOR pathway, which negatively regulates autophagy, was not affected by betaine treatment, suggesting betaine-induced autophagy through an mTOR-independent pathway. Betaine-induced autophagy was also observed in primary human keratinocyte and skin equivalent. Furthermore, epidermal thickness was increased in skin equivalent under betaine treatment. Overall, our finding suggests that betaine as a novel regulator of autophagy may induce epidermal turnover and improve the skin barrier abnormality of the aged epidermis.

Effects of propofol-induced autophagy against oxidative stress in human osteoblasts

  • Kim, Eun-Jung;Choi, In-Seok;Yoon, Ji-Young;Park, Bong-Soo;Yoon, Ji-Uk;Kim, Cheul-Hong
    • Journal of Dental Anesthesia and Pain Medicine
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    • v.16 no.1
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    • pp.39-47
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    • 2016
  • Background: Oxidative stress occurs during the aging process and other conditions such as bone fracture, bone diseases, and osteoporosis, but the role of oxidative stress in bone remodeling is unknown. Propofol exerts antioxidant effects, but the mechanisms of propofol preconditioning on oxidative stress have not been fully explained. Therefore, the aim of this study was to evaluate the protective effects of propofol against $H_2O_2$-induced oxidative stress on a human fetal osteoblast (hFOB) cell line via activation of autophagy. Methods: Cells were randomly divided into the following groups: control cells were incubated in normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) without propofol. Hydrogen peroxide ($H_2O_2$) group cells were exposed to $H_2O_2\;(200{\mu}M)$ for 2 h, propofol preconditioning (PPC)/$H_2O_2$ group cells were pretreated with propofol then exposed to $H_2O_2$, 3-methyladenine (3-MA)/PPC/$H_2O_2$ cells were pretreated with 3-MA (1 mM) and propofol, then were exposed to $H_2O_2$. Cell viability and apoptosis were evaluated. Osteoblast maturation was determined by assaying bone nodular mineralization. Expression levels of bone related proteins were determined by western blot. Results: Cell viability and bone nodular mineralization were decreased significantly by $H_2O_2$, and this effect was rescued by propofol preconditioning. Propofol preconditioning effectively decreased $H_2O_2$-induced hFOB cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol. In western blot analysis, propofol preconditioning increased protein levels of collagen type I, BMP-2, osterix, and TGF-${\beta}1$. Conclusions: This study suggests that propofol preconditioning has a protective effect on $H_2O_2$-induced hFOB cell death, which is mediated by autophagy activation.

Apoptotic Response of Human Oral Squamous Carcinoma Cells to Etoposide (Etoposide에 대한 사람구강편평상피암종세포의 세포자멸사 반응)

  • Kim, Gyoo-Cheon;Lee, Kyoung-Duk;Park, Jae-Hyun;Kim, Duk-Han;Park, Jeong-Kil;Park, June-Sang;Park, Bong-Soo
    • Journal of Oral Medicine and Pain
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    • v.30 no.2
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    • pp.231-238
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    • 2005
  • Anti-cancer drugs have been shown to target diverse cellular functions in mediation cell death in chemosensitive tumors. Most antineoplastic drugs used in chemotherapy of leukemias and solid tumors induce apoptosis in drug-sensitive target cells. However, the precise molecular requirements that are central for drug-induced cell death are largely unknown. Etoposide is used for the treatment of lung and testicular cancer. This study was performed to examine whether etoposide promote apoptosis in human oral squamous carcinoma cells (OSC9) as well as in lung and testicular cancer. Etoposide had a significant dose- and time-dependent inhibitory effect on the viability of OSC9 cells. TUNEL assay showed the positive reaction on condensed nuclei. Hoechst stain demonstrated that etoposide induced a change in nuclear morphology. The expression of p53 was increased at 48 hour, suggesting that the nuclear of OSC9 cell was damaged, thereby inducing apoptosis. Etoposide treatment induced caspase-3 cleavage and activation. Intact PARP protein 116-kDa and 85-kDa cleaved product were observed. The activated caspase-3 led cleavage of the PARP. These results demonstrate that etoposide-induced apoptosis in OSC9 cells is associated with caspase-3 activation.

Reproductive Physiology of Pineal Hormone Melatonin (송과선 호르몬 멜타토닌의 생식 생리학)

  • 최돈찬
    • The Korean Journal of Zoology
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    • v.39 no.4
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    • pp.337-351
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    • 1996
  • Melatonin Is a multifunctional hormone secreted from the pineal gland in the middle of cerebrum and cerebellum. Its synthesis and release reflect photopedod;Photopedod is a yearly predictable ambient factor that most animals utilize as an environmental cue for maximum survival. Hamsters maintaln reproductive activity in summer during which day length exceeds night time. Upon the advent of autumnal equinox they undergo gonadal regression. The photoperiodic effects are prevented by removal of the pineal gland and restored by the timed repiacument of melatonin. The results suggest that melatonin constitutes part of control mechanism whereby environmental information is transduced to neuroendocrine signal responsIble for the functional integrity of the reproductive system. From the studies for the action site of melatonin following the treatment of photopedod or melatonin in the lesion of a spedflc portion of hypothalamus, suprachiasmatic nuclei and pars tuberalis are shown to be a consensus site for melatonIn. The action of melatonin. In the regulation of reproduction is largely unknown. It is mainly due to the lack of acute effect of melatonin on gonadotropin secretion. However, reduction of the gonadotropln release and augmentation of the hypothalamic gonadotropin-releasing hormone (GnRH) content by long-term treatment of melatonln Indicate that constant presence of melatonln may partidpate in the regulation of sexual activity via the GnRH neuronal system. The action mechanism by which melatonin exerts Its effect on GnRH neuron needs to be eluddated. The inability of opiold analogues to affect the reproductive hormones in sexually regressed animals by inhibftory photopedod and melatonin suggests that the opioldergic neuron may be a prime intervening mediator. Recent cloning of melatonin receptor will contribute to investigate its anatomical Identification and the action mechanism of melatonin on target tissues at the molecular level.

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MicroRNA-3200-5p Promotes Osteosarcoma Cell Invasion via Suppression of BRMS1

  • Li, Gen;Li, Li;Sun, Qi;Wu, Jiezhou;Ge, Wei;Lu, Guanghua;Cai, Ming
    • Molecules and Cells
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    • v.41 no.6
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    • pp.523-531
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    • 2018
  • Tumour metastasis is one of the most serious challenges of cancer as it is the major cause of mortality in patients with solid tumours, including osteosarcoma (OS). In this regard, anti-metastatic genes have potential for metastasis inhibition strategies. Recent evidence showed the importance of breast cancer metastasis suppressor 1 (BRMS1) in control of OS invasiveness, but the regulation of BRMS1 in OS remains largely unknown. Here, we used bioinformatics analyses to predict BRMS1-targeting microRNAs (miRNAs), and the functional binding of miRNAs to BRMS1 mRNA was evaluated using a dual luciferase reporter assay. Among all BRMS1-targeting miRNAs, only miR-151b, miR-7-5p and miR-3200-5p showed significant expression in OS specimens. Specifically, we found that only miR-3200-5p significantly inhibited protein translation of BRMS1 via pairing to the 3'-UTR of the BRMS1 mRNA. Moreover, we detected significantly lower BRMS1 and significantly higher miR-3200-5p in the OS specimens compared to the paired adjacent non-tumour bone tissues. Furthermore, BRMS1 and miR-3200-5p levels were inversely correlated to each other. Low BRMS1 was correlated with metastasis and poor patient survival. In vitro, overexpression of miR-3200-5p significantly decreased BRMS1 levels and promoted OS cell invasion and migration, while depletion of miR-3200-5p significantly increased BRMS1 levels and inhibited OS cell invasion and migration. Thus, our study revealed that miR-3200-5p may be a critical regulator of OS cell invasiveness.

Analysis of Pine Nut Oil Composition and Its Effects on Obesity (잣기름 성분분석 및 비만 예방효과 연구)

  • Kim, Kyoung Kon;Kang, Yun Hwan;Kim, Dae Jung;Kim, Tae Woo;Choe, Myeon
    • Korean Journal of Food Science and Technology
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    • v.46 no.5
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    • pp.630-635
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    • 2014
  • Pine nut oil (PNO) is well known to impart beneficial effects in overweight individuals, but the mechanisms underlying PNO-mediated weight loss remain unclear. To investigate how PNO promotes weight loss, its composition was determined by gas chromatography coupled with mass spectrometry (GC-MS). In addition, the effects of PNO on cytotoxicity, lipid accumulation, expression of lipid metabolism-related biomarkers, and leptin secretion were assessed in 3T3-L1 cells. GC-MS analyses revealed that PNO contains several components, including linoleic acid, oleic acid, palmitic acid, and stearic acid. Moreover, PNO did not have a cytotoxic effect on 3T3-L1 cells. However, it inhibited the expression of peroxisome proliferator-activated receptor (PPAR) and adipocyte protein 2 (aP2). Finally, PNO significantly increased leptin secretion in a dose-dependent manner. Taken together, these results support the notion that PNO is useful for weight management in overweight individuals.

Analysis of Amino Acid, Fatty Acid, and Vitamin in Korean Pine (Pinus koraiensis) Seeds (잣 종자(種子)의 아미노산(酸), 지방산(脂肪酸), 비타민 분석(分析))

  • Han, Sang Sup;Hwang, Byung Ho
    • Journal of Korean Society of Forest Science
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    • v.79 no.4
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    • pp.345-351
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    • 1990
  • The seeds of Korean pine, Pinus koraiensis, had been used as one of edible fruits for long time, but its chemical analysis of the nutrient components was extremely limited. The purpose of this study is to analyze the content of chemical components of Korean pine seeds. The results obtained are as follows : 1. In general analysis of Korean pine seeds, moisture is 4.4%, crude protein 18.3%, crude fat 67.3%, crude fiber 4.7%, ash 2.2%, and nitrogen-free extract 3.4%, respectively, 2. The Korean pine seed contained 18 different kinds of amino acid : lysine, histidine, arginine, aspartic acid, threonine, serine, glutamic acid, proline, glycine, alanine, valine, methionine, isoleucine, leucine, tyrosine, phenylalanine, cysteic acid, and tryptophan. The glutamic acid is highest content among 18 kinds of amino acid. 3. The Korean pine seed contains all the essential amino acids such as arginine, histidine, lysine, threonine, valine, methionine, isoleucine, leucine, phenylalanine, and tryptophan. 4. The Korean pine seed contains 13 different kinds of fatty acid such as myristic acid, palmitic acid, palmitoleic acid, stearic acid, oleic acid, linoleic acid, linolenic acid, arachidic acid, 9-icosenoic acid, 9, 11-icosenoic acid, 8, 11, 14-icosatrienoic acid, and tn-o unknown substances. Also it contains all the essential fatty acids as linoleic acid and linolenic acid. The linoleic acid is highest content among 13 kinds of fatty acid. 5. The Korean pine seed contained 5 different kind., of vitamin such as vitamin A, vitamin $B_1$, vitamin $B_2$, vitamin E and niacin. The content of vitamin E is the largest among 5 kinds of vitamin.

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The effect of scopoletin on Aβ-induced neuroinflammatory response in microglial BV-2 cells

  • Mun, Hui-Jin;Cho, Hyun-Jeong
    • Journal of the Korea Society of Computer and Information
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    • v.25 no.6
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    • pp.165-170
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    • 2020
  • In this paper, it was confirmed that scopoletin inhibits neuroinflammation induced by amyloid beta oligomer (Aβ1-42) in microglial BV-2. The mechanisms of inflammatory cytokines and inflammatory mediators by scopoletin were identified. Alzheimer's disease is the most common neurodegenerative disease, but it is a disease whose specific etiology is unknown, and many studies are trying to solve it. We first measured the cell viability with the CCK-8 assay method to confirm that scopoletin and Aβ1-42 are toxic to BV-2 cells. Expression levels of interleukin 1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nuclear factor-κB (NF-κB) in inflammatory reactions induced by Aβ1-42 with western blot were analyzed. The ANOVA assay was used to compare protein expression differences between BV-2 cells treated with Aβ1-42 alone and BV-2 cells pretreated with Aβ1-42 and scopoletin. Therefore, this study suggested that scopoletin is worth developing as a neuroinflammatory protection agent for Alzheimer's disease in the future.