백서의 폐포 및 복강 대식세포의 세포독성에 대한 연구

이홍렬(Hong Lyeol Lee),김세규(Se Kyu Kim),장준(Joon Chang),김성규(Sung Kyu Kim),이원영(Won Young Lee),조철호(Chul Ho Cho) 대한내과학회 1992 대한내과학회지 Vol.43 No.4

N/A Background: Mechanisms involved in host resistance against malignant tumors have been found to be mediated mainly by cellular effectors. These effector mechanisms include activated macrophages, killer T-cells, natural killer cells and antibody-dependent cellmediated cytotoxicity. Activated macrophages can sup- press DNA synthesis of tumor cells and kill tumor cells in a selective but nonspecific fashiori in vitro. Lipopolysaccharides (LPS) can enhance the cytotoxicity of macrophages and the lipid A which is produced by mild acid hydrolysis of LPS, is responsible for the LPS effect on macrophages. The mechanism by which LPS modifies macrophage physiology is not known, but it is suggested that it acts at the level of the macrophage plasma membrane. LPS may make macrophages tumoricidal by altering the membrane composition or by transmitting a necessary signal from the membrane to the vacuolar system. Methods: We isolated alveolar and peritoneal macrophages by bronchoalveolar and peritoneal lavage in rats. Rat sarcoma cell line (XC) was used as the target cell. As recommended commonly we controlled the effector cell: target cell ratio at 10:1, Three groups were divided as folows; no LPS added group, LPS 5μg/ml added group and LPS 10μg/ml added group, We focused the assay of cytotoxicity on the cytolysis rather than cytostasis by measuring the [3H] thymidine released and calculated the percentage specific cytalysis, By this experiment, we examined the stimulation effect of LPS an the macrophage cytotoxicity and compared the cytotoxicity between alveolar and peritoneal macrophages. Results: The cytotoxicity of alveolar and peritoneal macrophages was significantly enhanced when stimulated both with 5μg/ml and 10μg/ml of LPS. There was no significant difference in macrophage cytotoxicity between two groups each stimulated with 5μg/ml and 10μg/ml of LPS. We could not observe the significant difference in cytotoxicity between the alveolar and peritoneal macrophages, Conclusion: Cytotoxicity was significantly enhanced by stimulation of LPS, in hoth alveolar and peritoneal macrophages but there was no significant difference in cytotoxicity enhancement between 5μg/ml and 10μg/ ml of LPS. Also there was no significant difference in cytotoxicity between alveolar and peritoneal macrophages.

Effects of Non-Cytotoxic Concentration of Anticancer Drugs on Doxorubicin Cytotoxicity in Human Breast Cancer Cell Lines

Lee, Yoon-Ik,Lee, Young-Ik Korean Society for Biochemistry and Molecular Biol 1996 Journal of biochemistry and molecular biology Vol.29 No.4

The effects of non-cytotoxic concentrations of tamoxifen, verapamil, and trifluoperazine on doxorubicin cytotoxicity in five human breast cancer cell lines were studied. A non-cytotoxic concentration of tamoxifen resulted in enhanced doxorubicin cytotoxicity in HTB-123, HTB-26, and MCF-7. In these three cell lines, a combination of tamoxifen with verapamil resulted in even more increased doxorubicin cytotoxicity. Addition of verapamil or trifluoperazine alone did not influence the doxorubicin cytotoxicity significantly. Only in HTB-19 did coincubation with verapamil increase the doxorubicin cytotoxicity. In HTB-123, combination of tamoxifen with trifluoperazine increased the doxorubicin cytotoxicity significantly. In the cell lines where co-incubation with tamoxifen increased doxorubicin sensitivity, high estrogen receptor expression was detected. However, HTB-20, where tamoxifen did not enhance doxorubicin action, was also estrogen receptor positive. None of the cell lines had multidrug resistance related drug efflux and drug retention was not increased by the treatment with tamoxifen and verapamil. Cell cycle traverses were not altered by incubation with tamoxifen, verapamil or combinations thereof. These observatlons suggest mechanism of non-cytotoxic concentrations of tamoxifen and verapamil on doxorubicin cytotoxicity may involve one or more other cellular processes besides those of interference of estrogen binding to its receptor, cell cycle perturbation, or drug efflux blocking.

MiR-30c facilitates natural killer cell cytotoxicity to lung cancer through targeting GALNT7

Gao Fei,Han Jianjun,Jia Li,He Jun,Wang Yun,Chen Mi,Liu Xiaojun,He Xia 한국유전학회 2023 Genes & Genomics Vol.45 No.2

Background MicroRNAs (miRNAs) have been reported to play important roles in regulating natural killer (NK) cell cytotoxicity to cancer cells. Objective This study aimed to investigate the effects and potential mechanism of miR-30c in regulating NK cell cytotoxicity to lung cancer cells. Methods Primary NK cells were derived from the peripheral blood of lung cancer and normal participants. Exosomes were isolated and validated via transmission electron microscopy and nanoparticle tracking analysis. The levels of miR-30c, polypeptide N-acetylgalactosaminyltransferase 7 (GALNT7) and proteins in PI3K/AKT pathway were determined using quantitative real-time polymerase chain reaction or western blot. Tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) levels and the cytotoxicity of effector NK cells to target lung cancer cells were measured via enzyme linked immunosorbent assay, cell apoptosis or xenograft experiments. The relationship between miR-30c and GALNT7 was analyzed by luciferase activity, RNA pull-down and RNA immunoprecipitation assays. And a xenograft mice model was established to verify the effect of miR-30c in regulating NK cell cytotoxicity to lung cancer cells in vivo. Results NK cell-derived exosomes carrying miR-30c, and miR-30c level was significantly downregulated in primary NK cells of lung cancer patients. MiR-30c overexpression promoted TNF-α and IFN-γ secretion and enhanced the cytotoxicity of interleukin 2 (IL-2)-treated NK cells to lung cancer cells, while knockdown of miR-30c played an opposite effect in regulating the cytotoxicity of NK cells to lung cancer cells. GALNT7 was a target of miR-30c and was negatively regulated by miR-30c. Besides, miR-30c targeted GALNT7 to exert its function in regulating NK cell cytotoxicity. Furthermore, GALNT7 prompted the activation of PI3K/AKT pathway in NK cells. Additionally, miR-30c overexpression enhanced NK cell cytotoxicity to lung cancer cells and inhibited tumor growth in vivo. Conclusion miR-30c enhanced NK cell cytotoxicity to lung cancer cells via decreasing GALNT7 and inactivating the PI3K/AKT pathway, suggesting that regulating miR-30c expression maybe a promising approach for enhancing NK cell-based antitumor therapies.

Protective Effect of Kaempferol on Cultured Neuroglial Cells Damaged by Induction of Ischemia-like Condition

Young-Woo Son,Yu-Ran Choi,Young-Mi Seo 대한의생명과학회 2017 Biomedical Science Letters Vol.23 No.4

This study was performed to evaluate the cytotoxicity induced by ischemia-like condition (ILC) in cultured neuroglial cells (C6 glioma cells). The protective effect of kaempferol (KAE), flavonoid against the cytotoxicity induced by ILC induction was assessed. In addition, antioxidative effects of KAE were done by colorimetric assays. Cell viability and the antioxidative effects such as DPPH-radical scavenging activity, superoxide dismutase (SOD)-like activity and inhibitory activity of lipid peroxidation (LP) were analyzed. ILC induction decreased cell viability in a dose-dependent manner, and the XTT90 value (low cytotoxicity value) and XTT50 value (high cytotoxicity value) were determined during ILC induction for 15 and 40 minutes, respectively. The butylated hydroxytoluene (BHT) antioxidant significantly increased cell viability damaged by the ILC-induced cytotoxicity. In the protective effect of KAE on ILC-induced cytotoxicity, KAE protected the ILC-induced cytotoxicity by the significant increase of cell viability, and also it showed DPPH-radical scavenging ability, SOD-like ability and inhibitory ability of LP. From these results, it is suggested that ILC induction showed cytotoxicity in these cultures and the oxidative stress is involved in the ILC-induced cytotoxicity. While, KAE prevented ILC-induced cytotoxicity by antioxidative effects. In conclusion, natural products like KAE may be a putative therapeutic agent for the treatment of disease associated with oxidative stress such as ischemia.

Protective Effect of Aster tataricus L. Extract on the Dermal Cytotoxicity Induced by Sodium Bromate, Oxidant of Hair Dye

Jung-Hwa Chung,Gyoung-Wan Lee,Young-Mi Seo 대한의생명과학회 2019 Biomedical Science Letters Vol.25 No.4

This study evaluated the dermal cytotoxicity of sodium bromate (NaBrO₃) and the protective effect of Aster tataricus L. (AT) extract against NaBrO₃-induced cytotoxicity in the cultured NIH3T3 fibroblasts. For this study, it was done the antioxidative effects such as electron donating (ED) activity and lipid peroxidation (LP) activity as well as cell viability. NaBrO₃ significantly decreased cell viability in a dose-dependent manner and its XTT50 value was measured at a concentration of 54.4 μM in these cultures. The cytotoxicity of NaBrO₃ was determined as highly-toxic by Borenfreund and Puerner"s toxic criteria. The quercetin, antioxidant significantly increased cell viability against NaBrO₃-induced cytotoxicity. Regarding the protective effect of Aster tataricus (AT) L. extract on NaBrO₃-induced cytotoxicity, AT extract significantly increased the cell viability, the ED ability and the inhibitory ability of LP. From these findings, it suggested that the oxidative stress is involved in the cytotoxicity of NaBrO₃, and AT extract effectively protected NaBrO₃-induced cytotoxicity by antioxidative effects. Conclusively, the natural component like AT extract may be a putative therapeutic agent for the diminution or treatment of the cytotoxicity correlated with oxidative stress like hair dye component, NaBrO₃.

재생방법에 따른 교정용 브라켓의 세포독성에 관한 실험적 연구

임용규,양원식 대한치과교정학회 1993 대한치과교정학회지 Vol.23 No.2

The purpose of this stuy was to evaluated the cytotoxicity of brackets shich were recycled thermally or chemically. New brackets and used brackets which had been in mouth for at least 2 years were used as samples and human gingival cell culture and agar overlay technique was used to evaluate the cytotoxicity. From the experiment the following results were obtained : 1. New brackets in the as received state showed mild cytotoxicity. 2. Thermally recycled brackets except the used bracket not electropolished showed moderate cytotoxicity and among them new brackets showed greater cytotoxicity than used ones. 3. Used brackets which were thermally recycled without electropolishing showed mild cytotoxicity. 4. Among thermally recycled brackets, electropolished brackets showed greater cytotoxicity than not electropolished ones. 5. Chemically recycled brackets showed moderate cytotoxicity, and among them, new brackets appeared to be more cytotoxic than used ones.

보문 : 염모제 성분인 FeSO4의 세포독성에 대한 산사 추출물의 항산화 효과

정재윤 ( Jai Yun Jung ),서영미 ( Young Mi Seo ),정인주 ( In Ju Jung ) 대한미용학회(구 대한미용과학회) 2013 대한미용학회지 Vol.9 No.4

To clarify the antioxidative effect of Crataegi Fructus (CF) extract on the cytotoxicity induced by FeSO4, hair dye component, antioxidative effects such as DPPH-radical scavenging activity and lactate dehydrogenase (LDH) activity as well as cell viability by XTT assay were performed. Cell viability and LDH activity were assessed after NIH3T3 fibroblasts were cultured in media containing various concentrations of FeSO4. And also, the effect of antioxidant, vitamin E on FeSO4-induced cytotoxicity was evaluated. For the protective effect of CF extract on FeSO4-induced cytotoxicity, cell viability was measured after NIH3T3 fibroblasts were pretreated with 130 or 160 μg/mL of CF extract for 2 hours, and also, DPPH-radical scavenging activity and the inhibitory activity of LDH were assessed on CF extract. In this study, FeSO4 significantly decreased cell viability in dose-dependently compared with control, and XTT50 value was calculated at 33.4 μM of FeSO4. In the protective effect of vitamin E, it significantly increased cell viability damaged by FeSO4-induced cytotoxicity. In the protective effect of CF extract on FeSO4-induced cytotoxicity, CF extract significantly increased cell viability which was decreased by FeSO4, and also it showed DPPH-radical scavenging activity and the inhibitory effect of LDH activity. From these results, it is suggested that the oxidative stress is involved in the cytotoxicity of FeSO4, and also, CF extract effectively prevented FeSO4-induced cytotoxicity by antioxidative effect. Conclusively, the natural plant extract such as CF may be a putative resources for beauty by the prevention or diminution of the cytotoxicity of hair dye component such as FeSO4 correlated with oxidative stress.

보문 : 피부염 유발제인 삼산화크롬(CrO3)으로 손상된 배양 NIH3T3 섬유모세포에 대한 조개나물 추출물의 항산화 효과

정재윤 ( Jai Yun Jung ),오성균 ( Seung Kyun Oh ),박신희 ( Shin Hee Park ),윤미영 ( Mi Young Yoon ),유영월 ( Yeong Wol Yu ),임요섭 ( Yo Sup Rim ),정인주 ( In Ju Jung ) 대한미용학회(구 대한미용과학회) 2014 대한미용학회지 Vol.10 No.1

This study was to evaluate the protective effect of Ajuga multiflora BUNGE(AMB) extract on the cytotoxicity induced by chromium trioxide (CrO3), dermatitis inducer. For this study, the cytotoxicity induced by CrO3 was assessed by colorimetric assay after NIH3T3 fibroblasts were cultured in media containing various concentrations of CrO3. And also, the effect of vitamin E was assessed on the CrO3-induced cytotoxicity. For the protective effect of AMB extract on CrO3- induced cytotoxicity, NIH3T3 fibroblasts were pretreated with 60 or 80 μg/mL of AMB extract for 2 hours, and also, antioxidative effects of ABM extract were analysed via electron donating ability (EDA) and lactate dehydrogenase (LDH) activity. In this study, CrO3 significantly decreased cell viability in a dose-dependent manner, and the XTT50 value was calculated at 28.4 μM. In the effect of vitamin E, it significantly increased cell viability decreased by CrO3-induced cytotoxicity. In the protective effect of AMB extract on CrO3-induced cytotoxicity, it significantly increased cell viability which was decreased by CrO3-induced cytotoxicity, and also it showed EDA and LDH inhibitory activity. From these results, it is suggested that the cytotoxicity of CrO3 is involved in oxidative stress, and also, AMB extract effectively prevented CrO3-induced cytotoxicity by the antioxidative effect. Conclusively, the natural plant component like AMB may be a putative agent for the prevention of the cytotoxicity induced by dermatitis inducer correlated with oxidative stress.

염모제 성분인 FeSO4의 세포독성에 대한 산사 추출물의 항산화 효과

정재윤,정인주,서영미 대한미용학회 2013 대한미용학회지 Vol.9 No.4

To clarify the antioxidative effect of Crataegi Fructus (CF) extract on the cytotoxicity induced by FeSO4, hair dye component,antioxidative effects such as DPPH-radical scavenging activity and lactate dehydrogenase (LDH) activity as well as cell viability by XTT assay were performed. Cell viability and LDH activity were assessed after NIH3T3 fibroblasts were cultured in media containing various concentrations of FeSO4. And also, the effect of antioxidant, vitamin E on FeSO4-induced cytotoxicity was evaluated. For the protective effect of CF extract on FeSO4-induced cytotoxicity, cell viability was measured after NIH3T3 fibroblasts were pretreated with 130 or 160 μg/mL of CF extract for 2 hours, and also,DPPH-radical scavenging activity and the inhibitory activity of LDH were assessed on CF extract. In this study, FeSO4significantly decreased cell viability in dose-dependently compared with control, and XTT50 value was calculated at 33.4μM of FeSO4. In the protective effect of vitamin E, it significantly increased cell viability damaged by FeSO4-induced cytotoxicity. In the protective effect of CF extract on FeSO4-induced cytotoxicity, CF extract significantly increased cell viability which was decreased by FeSO4, and also it showed DPPH-radical scavenging activity and the inhibitory effect of LDH activity. From these results, it is suggested that the oxidative stress is involved in the cytotoxicity of FeSO4, and also, CF extract effectively prevented FeSO4-induced cytotoxicity by antioxidative effect. Conclusively, the natural plant extract such as CF may be a putative resources for beauty by the prevention or diminution of the cytotoxicity of hair dye component such as FeSO4 correlated with oxidative stress. 장미과(Rosaceae)에 속하는 산사(Crataegi Fructus, CF) 추출물이 염모제 성분인 FeSO4에 미치는 영향을 조사하기 위하여 NIH3T3 섬유모세포를 배양한 후 FeSO4의 세포독성과 이에 대한 산사 추출물의 영향을 항산화 측면에서 조사하였다. 본 연구에서 배양 NIH3T3 섬유모세포에 FeSO4를 처리한 결과 세포생존율을 유의하게 감소시켰으며, XTT50값이 33.4μM에서 나타났다. 한편, 항산화제인 vitamin E는 FeSO4의 세포독성에 의하여 감소된 세포생존율을 유의하게 증가시킴으로서 FeSO4의 세포독성을 방어하였다. 한편, 산사 추출물이 FeSO4의 세포독성에 미치는 영향의 조사에 있어서, 산사 추출물은 FeSO4만의 처리에 비하여 세포생존율을 유의하게 증가시켰다(p<0.01). 이와 동시에, 산사 추출물은 DPPH-라디칼 소거능과 lactate dehydrogenase(LDH) 활성을 억제함으로서 항산화능을 보였다. 이상의 결과로부터 FeSO4의 세포독성에 산화적 손상이 관여하고 있으며, 또한 산사 추출물은 항산화에 의하여 염모제 성분인 FeSO4의 세포독성을 효과적으로 방어하였음을 제시하였다. 따라서, 산사 추출물과 같은 천연물질을 대상으로 FeSO4와 같이 산화적 손상과 관련된 미용제 성분의 독성을 항산화 측면에서 방어 내지는 경감할 수 있는 미용소재로서의 개발적 가치가 크다고 생각된다.

배양 골모세포에 있어서 골다공증의 유발물질인 카드뮴에 대한 우슬 추출물의 보호 효과

최유란,강민정,손영우 한국인간·식물·환경학회 2012 인간식물환경학회지 Vol.15 No.5

골다공증의 유발제인 카드뮴(cadmium, Cd)에 대한 세포 독성과 이에 대한 우슬(Achyranthis radix, AR) 추출물의 영향을 배양 골모세포(HFOB-1)를 재료로 항산화 측면에서 조사하여 다음과 같은 결과를 얻었다. 본 연구에서 Cd의 일종인 CdCl2는 처리 농도에 비례하여 배양 HFOB-1세포의 생존율(cell viability)을 유의하게 감소시킴으로서 세포 독성을 나타냈다. 한편, 항산화제인 superoxide dismutase(SOD)와 butylated hydroxytoluene(BHT)는 CdCl2에 의해 감소된 세포 생존율을 유의하게 증가시킴으로서 CdCl2에 의한 세포독성을 방어하였다. 한편, CdCl2의 세포 독성에 대한 AR 추출물의 영향에 있어서, AR 추출물은 CdCl2에 의하여 감소된 세포 생존율을 유의하게 증가시킴으로서 CdCl2에 의한 세포 독성을 방어하였으며, 또한 전자공여능(electron donating activity, EDA)과 지질과산화(lipid peroxidation, LP) 억제능을 보였다. 이상의 결과에서 CdCl2의 세포 독성에 산화적 손상이 관여하고 있으며 CR 추출물은 CdCl2에 의하여 감소된 세포생존율의 증가는 물론, EDA 및 LP 억제능과 같은 항산화 효과(antioxidative effect)에 의하여 세포 독성을 방어한 것으로 나타났다. 따라서 AR 추출물과 같은 천연성분은 뇌졸중(stroke)이나 허혈(ischemia)과 같이 산화적 손상으로 매개되는 난치성 질환의 치료적 접근을 위한 소재로서의 적용가치가 클 것으로 생각된다. To evaluate the cytotoxicity of osteoporosis-induced agent, cadmium (Cd) and the protective effect of Achyranthis radix (AR) extract on the Cd-induced cytotoxicity in cultured osteoblasts (HFOB-1). Cultured HFOB-1 cells were treated or pretreated with cadmiun chloride (CdCl2) or AR extract. In this study, CdCl2 significantly decreased cell viability compared with control, and XTT50 value (midcytotoxicity value, MCV) was determined at a concentration of 42.0uM. The CdCl2 was toxic by the significant decrease of cell viability. While, CdCl2-induced cytotoxicity was prevented by superoxide dismutase (SOD) or butylated hydroxytoluene (BHT), the antioxidative agents. In the protective effect of AR extract on CdCl2-induced cytotoxicity, AR extract prevented CdCl2-induced cytotoxicity by the significant increase of cell viability decreased by CdCl2-induced cytotoxicity. And also, AR extract showed antioxidative effects such as electron donating activity (EDA) and inhibitory effect of lipid peroxidation (LP). From these results, it is suggested that CdCl2 showed toxic effect on cultured osteoblasts, and the cytotoxicity of CdCl2 was involved in oxidative stress. And also, AR extract was effective in blocking CdCl2-induced cytotoxicity by antioxidative effect. Conclusively, the natural components such as AR extract may be a useful resources for preventing diseases mediated by reactive oxygen species (ROS) such as stroke or ischemia.