• 한국식품영양학회지
• /
• 제23권3호
• /
• pp.306-310
• /
• 2010

This study was designed to investigate the protective effect of the combination of fucoidan and lutein against AAPH-induced oxidative stress in THP-1 cells. The combination of fucoidan and lutein existed significant antioxidant effect on AAPH-damaged THP-1 cells by using lipid peroxidation and cellular antioxidant capacity assay. Fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) did not affect at all the viability of THP-1 cells, but protected the AAPH-damage of THP-1 cells at the same concentration. The viability of THP-1 cells was 0% with 1 mM AAPH alone, the protective effect of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) was 37% and 36%, respectively. The combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) exhibited significant inhibitory effect of lipid peroxidation using TBARS assay and cellular antioxidant capacity using DCFH-DA assay. In lipid peroxidation, the TBARS value of 1 mM AAPH alone was $0.8{\pm}0.03\;nM$ MDA, its of the combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) was $0.2{\pm}0.05\;nM$ MDA. In cellular antioxidant capacity, the combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) exhibited significant cellular antioxidant capacity of 76%, whereas quercetin($10\;{\mu}M$) as positive control exhibited the cellular antioxidant capacity of 32%. These results indicate that the cotreatment of fucoidan and lutein protects against AAPH-induced THP-1 cell damage by inhibiting lipid peroxidation, increasing cellular antioxidant capacity.

• 미생물학회지
• /
• 제44권4호
• /
• pp.299-304
• /
• 2008

마이엘로이드 계열의 단핵세포는 인체세포거대바이러스(human cytomegalovirus, HCMV)의 잠복 부위로 알려져 있다. 다양한 세포에서 HCMV에 의한 세포주기의 촉진 또는 억제에 관한 연구는 많이 있었지만, 단핵세포에서의 연구는 거의 없는 상태이다. 이에 본 연구에서는 단핵세포에 HCMV가 감염되면 세포주기에 어떤 변화가 나타나는지 알아보고자 하였다. Propidium iodide를 이용한 유세포 분석을 통한 세포주기 분석에서 HCMV에 감염된 THP-1 세포에서는 G0-G1기가 증가하고, 그만큼 S가 감소함을 보았다. 반면 HL-60 세포에서는G0-G1기와 S기의 상대적인 비율에 큰 변화가 없었다. BrdU 유입 실험에서 THP-1세포의 DNA 합성이 HCMV 감염에 의해 억제됨을 알 수 있었다. 세포주기의 G1기에서 S기로의 전환을 억제하는 p21 단백질은HCMV에 감염된 THP-1 세포에서는 발현이 유도되었지만 HL-60 세포에서는 거의 발현이 되지 않았다. 따라서 HCMV는 promocyte THP-1 세포에서 p21 단백질의 유도에 의해 세포주기를 G0-G1기에서 억류함에 따라 세포중식을 억제하는 것으로 생각된다.

• 생명과학회지
• /
• 제32권2호
• /
• pp.142-147
• /
• 2022

Oxysterols은 콜레스테롤의 산화 유도체로서 죽상경화증(atherosclerosis)에서 병태생리학으로 큰 관련성을 가진다. 본 연구는 oxysterols 중 많은 양을 차지하는 7-ketocholesterol (7-KC)이 단핵구(monocyte)의 분화와 활성화에 미치는 영향을 인간 단핵구세포주 THP-1을 이용하여 조사하였다. 7-KC를 처리한 THP-1 세포는 세포독성 없이 약간의 세포증식이 감소하였고, 세포내 lipids의 양이 크게 증가함을 Nile red 염색에 의해 관찰하였다. 7-KC는 단독으로 세포의 부착능(adhesion)에 영향을 주지 않았지만, phorbol 12-myristate 13-acetate (PMA)로 자극한 THP-1 세포에서는 부착능의 뚜렷한 감소를 나타내었다. 그리고, 형광이 부착된 latex beads를 이용하여 7-KC의 phagocytosis (포식능)를 조사하였다. 7-KC는 PMA로 분화를 자극한 세포의 phagocytosis를 현저히 감소시켰다. 또한, 7-KC를 처리한 THP-1 세포는 대식세포(macrophage)의 막표면 인자인 ICAM-1, CD11a, scavenger receptor(SR, 청소수용체) SR-A1, SR-B2 (CD36)의 발현을 감소시켰다. 하지만, 7-KC는 단독으로 혹은 PMA로 자극한 세포에서도 SR-D1 (CD68)의 발현을 현저히 증가시켰다. 이를 종합하면, 7-KC는 단핵구를 sterols이 풍부한 거품세포(foam cell)로 변형시킴으로써 생리적 자극에 의한 정상적인 단핵구의 분화와 활성화를 저해한다는 것을 시사한다.

• 한국미생물·생명공학회지
• /
• 제50권2호
• /
• pp.293-300
• /
• 2022

Lipoteichoic acid (LTA) regulates the immune system, including inflammatory responses, through TLR2-mediated signaling pathways. LTA isolated from Staphylococcus aureus (aLTA) has been shown to induce apoptosis, but the detailed mechanism has not been identified. We found that aLTA induced apoptosis through an autocrine mechanism in the human monocyte-like cell line, THP-1. We observed that the expression level of the anti-apoptosis protein, Bcl2, was suppressed in LTA-treated THP-1 cells. In addition, the cytokines, TNF-α and IFN-γ, which have been shown to induce apoptosis in some cell lines, were involved in THP-1 cell death via the modulation of Bcl2. The suppression of Bcl2 by aLTA was recovered when the negative regulator, SOCS-1, was knocked down. Taken together, these results showed that aLTA induced apoptosis in THP-1 cells through an autocrine mechanism of cytokines and SOCS-1-mediated Bcl2 inhibition.

• 유기물자원화
• /
• 제29권4호
• /
• pp.99-106
• /
• 2021

본 연구는 혐기성 소화의 전처리로써 열가수분해와 고액분리가 결합된 공정의 성능을 평가하였다. 탈수케이크는 열가수분해를 통해 가용화되며, 이후 고액분리를 수행한다. 고액 분리된 액상은 혐기성 소화에 기질로써 이용되고 고형물은 열가수분해로 회수된다. 열가수분해의 가용화율(COD 기준)은 45.1-49.3%이며 고액분리와 결합한 공정은 76.1-77.6%로 나타났다. Dual-pool two-step model을 통해 도출된 메탄 발생 특성을 살펴보면 고액 분리된 액상의 전체 분해 가능한 물질 중 분해가 빠른 물질의 비(a)는 0.891-0.911로 열가수분해된 시료에 비해 높게 나타났다. 반면에 분해가 빠른 물질의 반응 속도(kF)는 유사하게 나타났다. 이를 통해 열가수분해와 고액분리가 결합한 공정은 열가수분해를 통해 분해가 빠른 물질을 생성하고, 고액분리를 통해 선별하는 것으로 나타났다.

• Journal of Periodontal and Implant Science
• /
• 제29권2호
• /
• pp.333-350
• /
• 1999

The modulation of leukocyte cell surface adhesion molecules may influence the development of cellular events that determine the course of the inflammatory process. Direct interaction between activated T cells and monocytes resulted in a large production of $IL-1{\beta}$ by monocytes. In this reactions, adhesion molecules play an important part, yet the role of them in Tmonocytes interaction remain unclear. This study was undertaken in an effort to elucidate, 1) the influence of 1.25(OH)$_2D_3-induced$ differentiation on the monocyte responsiveness to direct contact with T lymphocytes, and 2) the role of adhesion molecules on the T-monocyte direct interaction. Initially, I observed that direct contact of monocyte cell line THP-1 with stimulated fixed T cell line HuT78 markedly induces IL-1${\beta}$ production by THP-1. $IL-1{\beta}$ production was higher when THP-1 had been previously exposed to 1.25(OH)$_2D_3$ as compared to control, with ${\alpha}$- 1.25(OH)$_2D_3$ dose-dependent and exposure time-dependent manner. It was shown that 1.25(OH)$_2D_3$ also increased the expression of ${\beta}_2$ integrin adhesion receptor Mac-1(CD11b/CD18) dose- and timedependently, but did not increase the expression of human leukocyte antigen- D(HLA-D) and intercellular adhesion molecule-1(ICAM-1). The $IL-1{\beta}$ producing activity of THP-1 cells correlated well with the ability to induce the Mac-1 expression on THP-1 surface. Monoclonal antibody raised against relevant cell surface glycoproteins on THP-1 were tested for their ability to block the response of THP-1 to T cells. Antibody to Mac-1 only partially blocked $IL-1{\beta}$ production by THP-1, whereas antibodies to ICAM-1 and HLA-D did not. These data indicate that regulation of Mac-1 expression on THP-1 cells can alter the responsiveness of these cells to contact by activated T cells, however other unknown structures on the THP-1 cells may be involved in this process also.

• 미생물학회지
• /
• 제55권2호
• /
• pp.112-116
• /
• 2019

Thp1/PCID2 단백질은 전사와 연계되어 mRNA를 핵에서 세포질로 방출하는데 필요한, 진화적으로 보존된 TREX-2 복합체의 구성요소이다. 분열효모인 Schizosaccharomyces pombe에는 Thp1/PCID2 단백질의 이종상동체가 2개 존재한다. pci2(SPBC1105.07c) 유전자 이외에, SPAC1B3.08 유전자는 PCI 영역을 갖고 있으며 TREX-2 복합체의 구성요소로 추정되는 단백질을 암호화하고 있다. SPAC1B3.08을 과발현하면, 생장이 약간 느려지고 mRNA 방출에 결함을 보였다. Yeast two-hybrid와 공동침전 분석 실험에서 SPAC1B3.08 단백질은 TREX-2 복합체의 다른 구성요소인 Sac3, Dss1 단백질들과 상호작용하였다. 이와 같은 관찰들은 S. pombe의 SPAC1B3.08 단백질도 TREX-2 복합체의 구성요소로서 mRNA 방출에 관여할 가능성을 지지한다.

• 대한화학회지
• /
• 제32권1호
• /
• pp.60-64
• /
• 1988

배추좀나방의 성 유인물질인 (Z)-11-헥사데센-1-올, (Z)-11-헥사데센-1-알, (Z)-11-헥사데센-1-일 아세테이트를 합성하여 생물활성 시험을 수행하였다. 1-헥신의 리튬음이온을 10-브로모데칸-1-올 THP 에테르와 반응시켜 11-헥사데신-1-올 THP 에테르를 얻었다. 이를 수소환원시킨 후 (Z)-11-헥사데센-1-올 THP 에테르를 생성시킨 다음 보호기를 제거시켜 (Z)-11-헥사데센-1-올을 합성하였다. 아세틸화시켜 (Z)-11-헥사데센-1-일 아세테이트를 산화시켜 (Z)-11-헥사데센-1-알을 각각 합성하였다. 합성된 성 페로몬에 대한 배추좀나방 숫컷의 성 유인력을 시험해 본 결과 활성이 있음을 밝혀졌다.

• 생약학회지
• /
• 제47권3호
• /
• pp.197-203
• /
• 2016

Decursin is a major component of the root of Angelica gigas(Umbelliferae), which has been traditionally used in Korea as a tonic and to treat anemia, hemiplegia, and women's diseases. The objective of this study is to identify the anti-cancer mechanism induced by decursin on apoptosis of human leukemia and lymphoma cells. Cytotoxicity of decursin on U937, HL-60, MOLT-4, THP-1 cells showed the significant effects. First of all, $IC_{50}$ of decursin on four cell lines was 27.1, 32.4, 17.4, $15.1{\mu}M$, respectively. So $IC_{50}$ in THP-1 cells was the smallest among 4 cell lines treated with decursin($15.1{\mu}M$). In order to understand the apoptosis-mechanism by decursin, we examined the gene expression of bcl-2(anti-apoptotic), bax(pro-apoptotic) and p53(tumor suppressor)after treating the THP-1 cells with decursin(10, 50 and $100{\mu}M$). It was found bcl-2 gene was decreased dose dependently, the expression level of bax gene of THP-1 cells treated with $100{\mu}M$ of decursin was about 3 times higher than those of control, and p53 gene was increased In the same concentration($100{\mu}M$), p53 gene was increased dose dependent manner. In protein express, bcl-2 and p53 protein showed a tendency to decrease. bax was increased about 4 fold. Therefore decursin is a useful chemotherapeutic agent against leukemia.

• International Journal of Oral Biology
• /
• 제42권1호
• /
• pp.17-23
• /
• 2017

Background: Periodontitis is generally a chronic disorder characterized by the breakdown of tooth-supporting tissues. P. gingivalis, a Gram-negative anaerobic rod, is one of the major pathogens associated with periodontitis. Frequently, P. gingivalis infection leads to cell death. However, the correlation between P. gingivalis-induced cell death and periodontal inflammation remains to be elucidated. Among cell deaths, the death of immune cells appears to play a significant role in inflammatory response. Thus, the aim of this study was to examine P. gingivalis-induced cell death, focusing on autophagy and apoptosis in THP-1 cells. Methods: Human acute monocytic leukemia cell line (THP-1) was used for all experiments. Autophagy induced by P. gingivalis in THP-1 cells was examined by Cyto ID staining. Intracellular autophagic vacuoles were observed by fluorescence microscopy using staining Acridine orange (AO); and 3-methyladenine (3-MA) was used to inhibit autophagy. Total cell death was measured by LDH assay. Cytokine production was measured by an ELISA method. Results: P. gingivalis induced autophagy in an MOI-dependent manner in THP-1 cells, but 3-MA treatment decreased autophagy and increased the apoptotic blebs. P. gingivalis infection did not increase apoptosis compared to the control cells, whereas inhibition of autophagy by 3-MA significantly increased apoptosis in P. gingivalis-infected THP-1 cells. Inhibition of autophagy by 3-MA also increased total cell deaths and inflammatory cytokine production, including $IL-1{\beta}$ and $TNF-{\alpha}$. Conclusion: P. gingivalis induced autophagy in THP-1 cells, but the inhibition of autophagy by 3-MA stimulated apoptosis, leading to increased cell deaths and pro-inflammatory cytokines production. Hence, the modulation of cell deaths may provide a mechanism to fight against invading microorganisms in host cells and could be a promising way to control inflammation.