• Title/Summary/Keyword: NIH 3T3세포

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Study of Whakijogyung-Tang about cytotoxicity in S-180 (화기조경탕(化氣調經湯)의 여러 가지 분획에 따른 S-180 암(癌) 세포주(細胞株) 억제(抑制) 효과(效果))

  • Kim, Dae-Su;Choi, Jeong-Hwa;Kim, Jong-Han;Park, Soo-Yeon
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.20 no.1 s.32
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    • pp.145-153
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    • 2007
  • Objecgtive : The aim of present study was to investigate inhibition effect of Whakijogyung-Tang(WJT) on the tumor cell lines. This study estimated the cytotoxicity of WJT about viability of S-180 and NlH3T3. Methods : The cytotoxicity of WJT about viability of cells were tested using a colorimetric tetrazoliun assay(MTT assay) Results and Conclusion : 1. Water extract of WJT had $IC_{50}$ of 863 ${\mu}g/ml$ in S-180 cell lines, but cytotoxicity of NIH3T3 was not significant difference compare with S-180. 2. n-Hexane fraction of WJT had similar cytotoxicity between S-180 and NIH3T3, but that could not have $IC_{50}$ in S-180 cell lines. 3. Ethyl acetate fraction of WJT had low degree cytotoxicity both S-180 and NIH3T3 cell lines. 4. Significantly, Butanol fraction of WJT had differenct citotoxicity between S-180 and NIH3T3. 5. $H_2O_2$ fraction of WJT had no cytotoxicity both S-180 and NIH3T3.

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Comparison of Ag-NORs stain and [3H]thymidine incorporation in antiproliferative effect of caffeine on NIH3T3 cells (Ag-NORs 염색법과 [3H]thymidine incorporation법에 의한 caffeine의 NIH3T3 세포증식 억제효과 비교측정)

  • Kim, Sung-ho;Lee, Cha-soo
    • Korean Journal of Veterinary Research
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    • v.30 no.4
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    • pp.459-464
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    • 1990
  • Inhibitory effect of caffeine on NIH3T3 cell proliferation was studied by using [$^3H$]thymidine incorporation and a modified one-step silver staining technique. The latter technique shows argyrophilic nucleolar organizer region-associated proteins (Ag-NORs), which are seen in nuclei as black dots. The result was compared with the counts of [$^3H$] thymidine incorporation. The results were summarized as follows; 1. The Ag-NORs numbers of NIH3T3 cells were $6.81{\pm}1.38$ at 24 hrs, $7.13{\pm}1.26$ at 48 hrs, $8.50{\pm}2.04$ at 72 hrs after incubation. 2. The numbers of Ag-NORs were significantly decrease in caffeine treated groups (p<0.01). 3. The counts of [$^3H$] thymidine incorporation were similar to the result of using Ag-NORs staining technique. It is concluded that Ag-NOR is a rapid, simple and compatible method to quantitate cell proliferation as compared with [$^3H$]thymidine incorporation.

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Antioxidative Effect of Chelidonium majus Extract on Cultured NIH3T3 Fibroblasts Injured by Cadmium Chloride of Toxicant (독성물질인 염화카드뮴으로 손상된 배양 NIH3T3 섬유모세포에 대한 애기똥풀 추출물의 항산화 효과)

  • Kim, Tae-Yoon;Jekal, Seung-Joo
    • Korean Journal of Clinical Laboratory Science
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    • v.48 no.1
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    • pp.1-7
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    • 2016
  • The aim of this study was to evaluate the cytotoxicity of cadmium chloride ($CdCl_2$), toxicant, and the protective effect of Chelidonium majus (CM) extract on $CdCl_2$-induced cytotoxicity in cultured NIH3T3 fibroblasts. Cell viability, the effect of butylated hydroxytoluene (BHT) against $CdCl_2$, and the antioxidative effects including DPPH-free radical scavenging activity, superoxide anion-radical scavenging activity (SSA), and lactate dehydrogenase (LDH) activity were assessed. $CdCl_2$ caused a significant dose-dependent decrease in cell viability, and $XTT_{50}$ value was determined at 38.7uM of $CdCl_2$. It was determined as highly-toxic by Borenfreund and Puerner' toxic criteria. BHT of antioxidant significantly increased cell viability severely damaged by $CdCl_2$-induced cytotoxicity in these cultures. In the protective effect of CM extract on $CdCl_2$-induced cytotoxicity, CM extract significantly increased cell viability, DPPH-free radical scavenging activity, SSA and inhibitory activity of LDH. From these results, it is suggested that oxidative stress is involved in the cytotoxicity of $CdCl_2$, and CM extract showed protective efficacy on $CdCl_2$-induced cytotoxicity via antioxidative effects. Conclusively, natural resources like CM extract may be a putative antioxidative agent for the detoxification or diminution of toxicity correlated with oxidative stress.

Decrease of Genotoxicity by Red Ginseng Root Extract (II) -Decrease of MMS- induced Genotoxicity by Red Ginseng Root Extract in Cul tared NIH3T3 Cells (홍삼 추출물에 의한 유전독성 감소효과(II) -배양 NIH3T3 세포에서 MMS에 의한 유전독성의 감소에 미치는 홍삼추출물 처리효과)

  • 차재영;유병수
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.24 no.1
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    • pp.87-99
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    • 1998
  • We have studied the effects of red ginseng root extract on the derease of MMS-induced gemotoxicity in cultured NIH3T3 cells. The increase in survival and the recovery from DNA synthesis inhibition in MMS-treated cells as a function of normal medium incubation time was potentiated, at a rate higher than those in UV-irradiated cells, by the presence of the ginseng extract. The extract also increased the MMS-induced excision repair as determined by unscheduled DNA synthesis. The amount of MMS-induced DNA single strand breads that are accumulated by polymerase inhibitors was increased, but as a rate lower rate than in UV-induced strand break, by the presence of the extract. These results suggest that the red ginseng extract increase MMS-induced repair and could be used as a reagent for protectiong alkylating agent-induced genotoxicity and cytotoxicity.

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Over-Expression of Phospholipase D Isozymes Down-Regulates Protein Kinase CKII Activity via Proteasome-Dependent CKIIβ Degradation in NIH3T3 Cells

  • Yoon, Soo-Hyun;Min, Do Sik;Bae, Young-Seuk
    • Molecules and Cells
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    • v.27 no.3
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    • pp.299-305
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    • 2009
  • Over-expression of phospholipase D (PLD) 1 or PLD2 down-regulated CKII activity in NIH3T3 cells. The same results were found with catalytically inactive mutants of PLD isozymes, indicating that the catalytic activity of PLD is not required for PLD-mediated CKII inhibition. Consistent with this, 1-butanol did not alter CKII activity. The reduction in CKII activity in PLD-over-expressing NIH3T3 cells was due to reduced protein level, but not mRNA level, of the $CKII{\beta}$ subunit. This PLD-induced $CKII{\beta}$ degradation was mediated by ubiquitin-proteasome machinery, but MAP kinase and mTOR were not involved in $CKII{\beta}$ degradation. PLD isozymes interacted with the $CKII{\beta}$ subunit. Immunocytochemical staining revealed that PLD and $CKII{\beta}$ colocalize in the cytoplasm of NIH3T3 cells, especially in the perinuclear region. PLD binding to $CKII{\beta}$ inhibited $CKII{\beta}$ autophosphorylation, which is known to be important for $CKII{\beta}$ stability. In summary, the current data indicate that PLD isozymes can down-regulate CKII activity through the acceleration of $CKII{\beta}$ degradation by ubiquitin-proteasome machinery.

Cytotoxicity of Paraquat or Bentazone and Compensatory Effects of 3-Methylcholanthrene on the Rat Liver (Paraquat 및 Bentazone의 세포독성과 흰쥐 간에서 3-Methylcholanchrene의 독성경감효과)

  • Rim, Yo-Sup;Han, Du-Seok
    • Korean Journal of Environmental Agriculture
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    • v.20 no.3
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    • pp.155-161
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    • 2001
  • This study was carried out to investigate cytotoxicity of paraquat or bentazone on NIH 3T3 fibroblasts, toxicity of paraquat or bentazone, and compensatory effects of 3-Methylcholanthrene(3-MC) on the rat liver. In order to MTT assay, the $5.0{\times}10^4$ cell/mL of NIH 3T3 fibroblast in each well of 24 multidish were cultured. After 24 hours, the cells were treated with solution of paraquat or bentazone(1, 25, 50, 100 ${\mu}M$ respectively). After the NIH 3T3 fibroblast of all groups were cultured in same condition for 48 hours. MTT assay were performed to evaluate the cytotoxicity of cell organelles. Paraquat or bentazone $MTT_{50}$ were 1668.97 ${\mu}M$ and 1506.97 ${\mu}M$, respectively. These $IC_{50}$ of paraquat or bentazone were decided low cytotoxicity by Borenfreund. In order to observe the toxicity and compensatory effects of paraquat or bentazone on the rat liver, Sprague-Dawley male rats were used as experimental animals and divided into paraquat or bentazone only treated group and simultaneous application group of paraquat or bentazone and 3-MC. At 30 min and 1, 3, 6, 12, 24, 48 and 96 hrs interval after each treatment, the animals were sacrificed by decapitation and liver were immediately removed, immersed in fixatives, and processed with routine method for light microscopic study. Paraffin sections were stained with H-E, PAM and Best Carmine. Under the light microscope, degenerative changes of hepatic lobules were frequently observed in portal area from 3 hrs after paraquat or bentazone treatment. All hepatic cells were induced degenerative change at 12 hrs and more severe degenerative change at 48 hrs after paraquat or bentazone treatment. Especially, hepatic cells of bentazone only treated group were distinctly showed pyknotic. Glycogen granules were increased in portal area at 3 hrs, all hepatic cells at 12 hrs and remarkably increased at 48 hrs after paraquat or bentazone treated group. But hepatic cells of bentazone only treated group were regeneration at 48 hrs from portal area and glycogen granules of hepatic cells of paraquat or bentazone and 3-MC combination treated group showed in central area only at 48 hrs. The results indicate that 3-MC may be decrease paraquat or bentazone cytotoxicity on the rat liver.

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Decrease of Genotoxicity by Red Ginseng Root Extract (I) - Decrease of UV -induced Genotoxicity by Red Ginseng Root Extract in Cultured NIH3T3 Cells (홍삼 추출물에 의한 유전독성 감소효과 (I) - 배양 NIH3T3 세포에서 자외선에 의한 유전독성의 감소에 미치는 홍삼추출물 처리효과)

  • 김완주;유병수
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.24 no.1
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    • pp.74-86
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    • 1998
  • We have studied the effects of red ginseng root extract on the decrease of UV-induced genotoxicity in cultured NIH3T3 cells. The increase in survival and the recovery from DNA synthesis inhibition in UV-irradiated cells as a function of normal medium incubation time was potentiated by the presence of the ginseng extract. The extract also increased the UV-induced excision repair as determined by unscheduled DNA synthesis. The amount of UV-induced DNA single strand breaks that are accumulated by polymerase inhibitors was significantly increased by the presence of the extract. These results suggest that the red ginseng extract activates the incision/excision step of UV-induced repair and could be used as a reagent for protecting UV-induced genotoxicity and cytotoxicity.

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Fabrication of PDMS Stencil using Gas Blowing for Micropatterned 3T3 Cell Culture (가스 블로잉을 이용한 PDMS 스텐실 제작 및 3T3 세포의 마이크로 패터닝)

  • Choi, Jin Ho;Kim, Gyu Man
    • Journal of the Korean Society for Precision Engineering
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    • v.30 no.2
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    • pp.236-240
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    • 2013
  • In this presentation, we propose a fabrication method of PDMS stencil to apply into a localized culture of NIH/3T3 cells. PDMS stencil was fabricated by nitrogen gas blowing and soft lithography from preparing SU-8 master mold by photolithography. PDMS stencil pattern was production of the circle size 20 to $500{\mu}m$. In the culture test of PDMS stencil, a stencil was placed on a glass disk. The NIH/3T3 cells were successfully cultured into micropatterns by using the PDMS stencil. The results showed that cells could be cultured into micropatterns with precisely controlled manner at any shapes and specific size for bioscience study and bioengineering applications.

Effect of fisetin on UVB-induced apoptosis and DNA single strand breaks in NIH3T3 cells (NIH3T3 세포에서 UVB에 의한 세포고사와 DNA 단사절단에 미치는 fisetin의 효과)

  • Jeong, Se-Jin;Kim, Don-Young;Han, Seol-Hee;Shin, Sang-Min;Cha, Jae-Young;Park, Nou-Bog;Lee, Jung-Sup;Park, Jong-Kun
    • Journal of Life Science
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    • v.17 no.1 s.81
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    • pp.64-69
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    • 2007
  • In the present study, we have investigated the effect of fisetin on the apoptosis and DNA single strand breaks in ultraviolet light B (UVB)-exposed NIH3T3 cells. Exposure of cells to UVB light $(200J/m^2)$ and post-incubation in growth medium for 48 hr resulted in about 50% of cells with apoptotic nuclear fragmentation. Addition of various concentrations of fisetin in the postincubation medium, however, significantly reduced the apoptotic nuclear fragmentation as compared with the values expected when the effects are additive and independent. DNA single strand breaks induced by UVB exposure were also significantly decreased by postincubation with fisetin. By Western blot analysis, fisetin post-incubation was shown to attenuate the p53 upregulation upon UVB exposure. Furthermore, the decrease of proliferating cell nuclear antigen (PCNA) level upon UVB exposure was alleviated by fisetin postincubation. These results suggest that fisetin decrease the apoptosis and increae DNA repair in a possible association with alteration of p53 and PCNA levels in UVB-exposed cells.