• YAKHAK HOEJI
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• v.38 no.6
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• pp.715-720
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• 1994

${\alpha}2-macroglobulin$ $({\alpha}2-M)$ has been shown to have a variety of activities. One of those activities is the suppression of immune response. Characterization of the immunosuppressive factor secreted by a T cell hybridoma showed that ${\alpha}2-M$ was produced and secreted from the T cell hybridoma. ${\alpha}2-M$ was produced abundantly from the T cell hybridoma when cultured as ascites. The isolation and identification of the ${\alpha}2-M$ were studied using affinity chromatography and N-terminal amino acid sequencing. The extended observations were that the ${\alpha}2-M$ produced by the T cell hybridoma suppresses mixed lymphocyte reaction.

• BMB Reports
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• v.46 no.12
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• pp.582-587
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• 2013

Adipocyte differentiation is a complex developmental process forming adipocytes from various precursor cells. The murine 3T3-L1 preadipocyte cell line has been most frequently used in the studies of adipocyte differentiation. Differentiation of 3T3-L1 preadipocytes includes a medium containing fetal bovine serum (FBS) with hormonal induction. In this study, we observed that differentiation medium containing adult bovine serum (ABS) instead of FBS did not support differentiation of preadipocytes. Impaired adipocyte differentiation was due to the presence of a serum protein factor in ABS that suppresses differentiation of preadipocytes. Using a proteomic analysis, alpha-2-macroglobulin and paraoxonase/arylesterase 1, which were previously shown to suppress differentiation of preadipocytes, were identified as anti-adipogenic proteins. Although their functional mechanisms have not yet been elucidated, the anti-adipogenic effects of these proteins are discussed.

• Natural Product Sciences
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• v.16 no.3
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• pp.159-163
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• 2010

A mixture of several detoxified bacterial strains ($Sterodin^{(R)}$) has been studied for anti-inflammatory effect in Wistar rats on carrageenin, dextran and prostaglandin $E_1$ ($PGE_1$) induced edema in acute model and cotton pellet and carrageenin induced sub-acute model, while, Freund's adjuvant induced chronic model. The bacterial strains showed strong inhibitory activity in acute, sub-acute and chronic models of inflammation. Further, it reduced ${\alpha}1$ acid glycoprotein and ${\alpha}2$ macroglobulin levels in serum and prostaglandin $E_2$ in inflamed paw. These results indicated that the bacterial strains probably act through prostaglandin mediatory pathways and may be useful in treatment of inflammation.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2001.10a
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• pp.47.1-47
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• 2001

One of the problems associated with in vitro culture of primordial gern cells (PGCs) is the large loss of cells during the initial period of culture. This study characterized the initial loss and determined the effectiveness of two classes of apoptosis inhibitors, protease inhibitors and antioxidants, on the ability of the porcine PGCs to survive in culture. Results from electron microscopic analysis and in situ DNA fragmentation assay indicated that porcine PGCs rapidly undergo apoptosis when placed in culture. Additionally, \ulcorner2-macroglobulin, a protease inhibitor and cytokine carrier, and N-acetylcysteine, an antioxidant, increased the survival of PGCs in vitro. While other protease inhibitors tested did not affect survival of PGCs, all antioxidants tested improved survival of PGCs (p<0.05). Further results indicated that the beneficial effect of the antioxidants was critical only during the initial period of culture. Finally, it was determined that in short-term culture, in the absence of feeder layer, antioxidants could partially replace the effect(s) of growth factors and reduce apoptosis. Collectively, these results indicate that the addition of \ulcorner2-macroglobulin and antioxidatns can increase the number of PGCs in vitro by suppressing apoptosis.

• Proceedings of the KSAR Conference
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• 2001.10a
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• pp.47-47
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• 2001

One of the problems associated with in vitro culture of primordial germ cells (PGCs) is the large loss of cells during the initial period of culture. This study characterized the initial loss and determined the effectiveness of two classes of apoptosis inhibitors, protease inhibitors and antioxidants, on the ability of porcine PGCs to survive in culture. Results from electron microscopic analysis and in situ DNA fragmentation assay indicated that porcine PGCs rapidly undergo apoptosis when placed in culture. Additionally,？ 2-macroglobulin, a protease inhibitor and cytokine carrier, and N-acetylcysteine, an antioxidant, increased the survival of PGCs in vitro. While other protease inhibitors tested did not affect survival of PGCs, all antioxidants tested improved survival of PGCs (p〈0.05). Further results indicated that the beneficial effect of the antioxidants was critical only during the initial period of culture. Finally, it was determined that in short-term culture, in the absence of feeder layers, antioxidants could partially replace the effect(s) of growth factors and reduce apoptosis. Collectively, these results indicate that the addition of ？2-macroglobulin and antioxidants can increase the number of PGCs in vitro by suppressing apoptosis.

• Korean Journal of Veterinary Research
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• v.59 no.1
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• pp.9-15
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• 2019

In canine acute pancreatitis (AP), inappropriate release and activation of zymogen proteases within the pancreas results in the consumption of serum antiproteases. The aim of this study was to examine whether the serum concentrations of ${\alpha}_2$-macroglobulin (A2MG), ${\alpha}_1$-antitrypsin (A1AT), and C-reactive protein (CRP) differ between dogs with AP and healthy dogs. Twenty healthy dogs and 20 dogs with AP were included in this study. Concentrations of A2MG, A1AT, and CRP were measured in the sera of healthy dogs and dogs diagnosed with AP. Serum A2MG and A1AT concentrations were significantly lower in dogs with AP than in healthy dogs, whereas the serum CRP concentration was significantly higher. In addition, the concentrations of A2MG and A1AT were significantly higher in AP survivors than in AP non-survivors, while the CRP concentration was significantly lower. However, in both AP survivors and non-survivors, the CRP concentrations showed a negative correlation with A2MG concentrations but not with A1AT. These findings indicate that serum antiproteases and CRP concentrations might be associated with the mortality rate of AP in dogs.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.124-124
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• 1993

녹용은 강심작용, 여성홀몬작용, 강장작용, 창상치유작용 등의 약리작용이 있는 것으로 보고되어 있는데 녹용의 상용량에서는 강장작용, 창상치유작용이 있는 것으로 알려져 있다. 녹용의 창상치유작용은 생체내 질소 평형이 음의 방향으로 되었을 때 이를 빠른 시간내에 정상적으로 회복시키는 약리효과에 기인하는 것으로 볼 수 있겠다. 본 연구에서도 흰쥐에 turpentineee oil (TPO)를 주사하여 acute-phase response를 일으켜 질소평형을 깨뜨린 실험 모델에서 녹용의 효과를 측정하였다. Acute-phase reactants중에서 $\alpha$$_2$-macroglobulin, $\alpha$$_1$-cysteine pretense inhibitor (T-kininogen), ceruloplasmin을 측정 하였는데 이 중에서 creuloplasmin의 측정이 재현성이 높았다. TPO로 급성염증을 유발시키면 2일 후에 ceruloplasmin의 혈청내 농도가 약 100% 증가하며 4일까지 지속하다가 5일째부터 감소하는데 이때 미리 녹용추출물을 투여한 군은 TPO주사 후 4일째에 50% 감소하였다. TPO로 염증을 유발하기 전에 녹용을 투여했을 때가 염증유발 후에 투여했을 때보다 녹용의 효과가 현저히 나타났다. 이러한 결과는 급성염증에 의해 깨어진 단백질 평형을 신속히 정상화시키는 효과가 있음을 나타내는 것으로 이러한 녹용의 효과를 지표로 하여 녹용의 유효성분 분리를 수행하고자 한다.

• Parasites, Hosts and Diseases
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• v.40 no.2
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• pp.93-99
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• 2002

The effect of a secretory proteinase from the pathogenic amoebae Acanthamoeba castellanii on host's defense-oriented or regulatory proteins such as immunoglobulins, interleukin-1, and protease inhibitors was investigated. The enzyme was found to degrade secretory immunoglobulin A (slgA), IgG, and IgM. It also degraded $interleukin-1{\alpha}$ ($IL-l{\alpha}$) and $IL-l{\beta}$. Its activity was not inhibited by endogenous protease inhibitors, such as ${\alpha}$2-macroglobulin, ${\alpha}l-trypsin$ inhibitor, and ${\alpha}2-antiplasmin$. Furthermore, the enzyme rapidly degraded those endogenous protease inhibitors as well. The degradation of host's defense-oriented or regulatory proteins by the Acanthanoeba proteinase suggested that the enzyme might be an important virulence factor in the pathogenesis of Acanthamoeba infection.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.425-431
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• 1996

Human neutrophil elastases (HNElastase, EC 3.4.21.37), a causative factor of inflammatory diseases, are regulated by plasma proteinase inhibitors, alpha-proteinase inhibitor and ${\alpha}_2-macroglobulin$. Under certain pathological conditions, however, released enzymes or abnormal function of inhibitors may cause various inflammatory disease. NSAIDs have been clinically applied for treatment of inflammatory diseases. Inhibition of cyclooxygenase is a known mechanism of action of NSAIDs in the treatment of inflammatory disease. In in vitro experiments, HNElastase was inhibited by naproxen, phenylbutazone, and oxyphenbutazone, but ibuprofen, ketoprofen, aspirin, salicylic acid, and tolmetin did not inhibit elastase. HNElastase was also inhibited by chelating agents, EDTA & EGTA, and tetracyclines. Removal of divalent metal ions by EDTA caused inhibition of elastase, and reconstitution of the metal ions recovered the enzyme activity to a certain level. Frequencies and contours in the Raman spectra of various conditions of human neutrophil elastase undergo drastic changes upon partial removal and/or reconstitution of calcium and zinc ions. The metal ion content dependent activities and change of the contour of the Raman spectrogram suggest us that the mechanism of action of a chelator or chelator-like agents on neutrophil elastase may be related to the conformational change at/or near the active site, especially -C=O radical or -COOH radical.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.62-70
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• 2001

Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques (SPs) and neurofibrillary tangles(NFTs). ${\beta}$-amyloid protein($A{\beta}$) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of $A{\beta}$ and tau formation are thought to be a final common pathway of AD. Acetylcholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and ${\alpha}$-macroglobulin increase risk of AD. In this article, we will review about the neurobiology of AD and some newly developed research areas.