• Title/Summary/Keyword: Necrosis Cell

Search Result 1,572, Processing Time 0.039 seconds

Cytotoxicity of Artemisia argyi Extract Against H9 (ATCC HTB 176) Cell and Antioxidant Enzyme Activities (황해쑥(Artemisia argyi)의 H9 (ATCC HTB176) 세포에 대한 세포독성 및 항산화효소 활성)

  • 김경하;정대영;민태진;박시원
    • YAKHAK HOEJI
    • /
    • v.43 no.5
    • /
    • pp.598-605
    • /
    • 1999
  • The hot water and mathanol extracts of Artemisia argyi showed considerable cytotoxicities against H9(ATCC HTB 176) cancer cell with IC50 values of $48.6{\;}\mu\textrm{g}/ml$ and $51.9{\;}\mu\textrm{g}/ml$, respectively. These cytotoxicities were found to be dependent on the extract concentrations and culture days. CuZnSOD and MnSOD activities were significantly increased in the cytoplasm and mitochondria fractions of cancer cell, and media in the presence of Artemisia argyi. Such enhanced SOD activities were generally in the range of two to threefolds. In contrast to SOD, catalase and glutathione peroxidase activities were not detected at all. These results suggest that Artemisia argyi have generated $O_2^-$ in the mitochondria and cytoplasm of H9 cancer cell with concurrent induction of CuZnSOD and MnSOD in situ, which dismutate $O_2^-{\}to{\;}H_2O_2$. Without coordinated actions of catalase and/or glutathione peroxidase $H_2O_2$ is easily converted to very toxic OH and these reactive oxygen species together might have induced necrosis and/or apoptosis of H9 cell.

  • PDF

Anti-tumor and Anti-inflammatory Activity of the Methanol Extracts from Adlay Bran

  • Lee, Ming-Yi;Tsai, Shu-Hsien;Kuo, Yueh-Hsiung;Chiang, Wenchang
    • Food Science and Biotechnology
    • /
    • v.17 no.6
    • /
    • pp.1265-1271
    • /
    • 2008
  • Adlay bran is a waste product previously thought to have no commercial value, Its methanolic extract was fractionated using n-hexane (ABM-Hex), ethyl acetate (ABM-EtOAc), 1-butanol (ABM-BuOH), and water (ABM-$H_2O$). The ABM-EtOAc fraction exhibited a strongest inhibition against growth of human lung cancer cell A549 and human colorectal carcinoma cells HT-29 and COLO 205. Inhibition of cell cycle progression at $G_0/G_1$ transition, increase of cells at the sub-$G_1$ phase, and DNA ladders were observed in cells treated with ABM-EtOAc. The ABM-BuOH fraction showed the strongest inhibition of proinflammatory cytokines tumor necrosis factor (TNF)-$\alpha$ and interlukin (IL)-$1{\beta}$ in stimulated RAW 264.7 macrophages. Further, ABM-EtOAc and ABM-BuOH inhibited cyclooxygenase (COX)-2 expression in A549 and HT-29 carcinoma cells, while COX-l expression was not affected. These results reveal that both ABM-EtOAc and ABM-BuOH may aid the prevention of cancers and the applications in cancer chemotherapy.

MODULATION OF IRRADIATION-INDUCED CELL DEATH BY INSULIN-LIKE GROWTH FACTOR-II IN MC3T3 OSTEOBLASTS (Insulin-like growth factor-II가 방사선에 의한 MC3T3 조골세포의 세포사멸에 미치는 영향)

  • Park, Kyeong-Lok
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
    • /
    • v.33 no.6
    • /
    • pp.617-624
    • /
    • 2007
  • Insulin-like growth factor(IGF) is the most abundant growth factor in bone matrix. Recent studies have shown that it can sensitize apoptotic cell death of osteoblasts. Thus, this study investigated whether IGF-II aggravates irradiation-induced cell death of osteoblasts. Cultured MC3T3 osteoblasts were irradiated and IGF-II was added at the concentration of 50 ng/ml immediately after the irradiation. Cell viability was measured by MTT assay. Changes in cell death and cell cycle were analyzed by flow cytometry. The expression of proapoptotic gene bax and antiapoptotic gene bcl-2 was quantified by real time RT-PCR and Western blot. A dose of 30 Gy caused G2/M arrest and increased cell death through both necrosis and apoptosis, while irradiation from 4 to 10 Gy little affected cell cycle and death. IGF-II treatment reduced cell viability without stimulating cell proliferation and changing cell cycle. Combined treatment of IGF-II with irradiation decreased cell viability and proliferation and increased cell death along with G2/M arrest. These effects were not different from those of irradiation only. At transcriptional and protein levels, IGF-II treatment did not affect bax and bcl-2 expression, whereas irradiation increased the expression ofbax without changes in bcl-2. IGF-II in combination with irradiation showed similar findings. These results suggest that IGF-II could modulate apoptotic cell death through mechanisms other than an imbalance between bax and bcl-2 gene expression, although its effect was overridden by irradiation.

Long-term Activation of c-Jun N-terminal Kinase through Receptor Interacting Protein is Associated with DNA Damage-induced Cell Death

  • Seok, Jeong-Ho;Park, Kyeong-Ah;Byun, Hee-Sun;Won, Min-Ho;Shin, Sang-Hee;Choi, Byung-Lyul;Lee, Hyun-Ji;Kim, Young-Rae;Hong, Jang-Hee;Park, Jong-Sun;Hur, Gang-Min
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.12 no.4
    • /
    • pp.185-191
    • /
    • 2008
  • Activation of c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is an important cellular response that modulates the outcome of the cells which are exposed to the tumor necrosis factor (TNF) or the genotoxic stress including DNA damaging agents. Although it is known that JNK is activated in response to genotoxic stress, neither the pathways to transduce signals to activate JNK nor the primary sensors of the cells that trigger the stress response have been identified. Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-${\beta}$-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation. Our findings revealed that this sustained JNK activation was not mediated by the TNF (tumor necrosis factor) receptor signaling, but it required a functional ATM (ataxia telangiectasia) activity. In addition, JNK inhibitor SP-600125 significantly blocked the Adr-induced cell death, but it did not affect the cell death induced by MNNG. These findings suggest that the sustained activation of JNK mediated by RIP plays an important role in the DNA damage-induced cell death, and that the duration of JNK activation relays a different stress response to determine the cell fate.

Effects of Cultured Acer tegmentosum Cell Extract Against Hepatic Injury Induced by D-galactosamine In SD-Rats (산겨릅나무 세포배양 추출물이 D-galactosamine 유도 급성 간손상에 미치는 보호 효과)

  • Park, Young Mi;Kim, Jin Ah;Kim, Chang Heon;Lim, Jae Hwan;Seo, Eul Won
    • Korean Journal of Plant Resources
    • /
    • v.28 no.5
    • /
    • pp.551-560
    • /
    • 2015
  • Here we report the protective activity of cultured Acer tegmentosum cell extract against liver damage in rat intentionally instigated by D-galactosamine. Local fat degeneration and infiltration of inflammatory cells were significantly decreased in cultured A. tegmentosum cell extract administered rat. In addition, acutely increased AST, ALT, LDH, ALP activities and lipid peroxidation and lipid content by liver damage were recovered in experimental rat administrated with A. tegmentosum extract. These results showed that cultured A. tegmentosum cell extract has a role in blood enzyme activation and lipid content restoration within damaged rat liver tissues. Moreover expression rate of TNF-α which accelerates inflammation and induces tissue damage and necrosis was significantly decreased. Also activities of antioxidant enzymes were more effectively upregulated comparing to those of the control group induced hepatotoxicity. All data that cultured A. tegmentosum cell extract has a preventive role against liver damages such as inflammation, tissue necrosis in rats by improving activities of blood enzymes, antioxidant enzymes and modulating expression of inflammation factor, suggest that cultured Acer tegmentosum cell extract is an effective medicinal resource for restoration of hepatotoxicity.

Gene Expression Profile of Lung Cancer Cells Following Photodynamic Therapy (폐암 세포주에서 광역학 치료에 의한 유전자 발현 분석)

  • Sung, Ji Hyun;Lee, Mi-Eun;Han, Seon-Sook;Lee, Seung-Joon;Ha, Kwon-Soo;Kim, Woo Jin
    • Tuberculosis and Respiratory Diseases
    • /
    • v.63 no.1
    • /
    • pp.52-58
    • /
    • 2007
  • Background: Photodynamic therapy is a viable option for lung cancer treatment, and many studies have shown that it is capable of inducing cell death in lung cancer cells. However, the precise mechanism of this cell death has not been fully elucidated. To investigate the early changes in cancer cell transcription, we treated A549 cells with the photosensitizer DH-I-180-3 and then we illuminated the cells. Methods: We investigated the gene expression profiles of the the A549 lung cancer cell line, using a DEG kit, following photodynamic therapy and we evaluated the cell viability by performing flow cytometry. We identified the genes that were significantly changed following photodynamic therapy by performing DNA sequencing. Results: The FACS data showed that the cell death of the lung cancer cells was mainly caused by necrosis. We found nine genes that were significantly changed and we identified eight of these genes. We evaluated the expression of two genes, 3-phosphoglycerate dehydrogenase and ribosomal protein S29. The expressed level of carbonic anhydrase XII, clusterin, MRP3s1 protein, complement 3, membrane cofactor protein and integrin beta 1 were decreased. Conclusion: Many of the gene products are membrane-associated proteins. The main mechanism of photodynamic therapy with using the photosensitizing agent DH-I-180-3 appears to be necrosis and this may be associated with the altered production of membrane proteins.

Fine Needle Aspiration Cytology of Metastatic Small Cell Carcinoma of Lymph Nodes - Comparison to Non-Hodgkin's Lymphoma on 5 Cases - (림프절의 전이성 소세포암종의 세침흡인 세포학적 소견 - 악성 림프종과의 감별을 중심으로 5예 분석 -)

  • Kim, Yeon-Mee;Cho, Hye-Je;Ko, Ill-Hyang
    • The Korean Journal of Cytopathology
    • /
    • v.7 no.1
    • /
    • pp.44-50
    • /
    • 1996
  • Small cell carcinoma of the lung is characterized by cells with finely stippled chromatin and scanty cytoplasm as well as a particularly aggressive clinical course and favorable response to the chemotherapy. Recently percutaneous fine needle aspiration (FNA) biopsy has become both widely established and highly respected for the diagnosis of lung cancer. However metastatic small cell carcinoma of lymph node should be cytologically differentiated from the small round cell tumor of particular sites, especially malignant lymphoma, because small ceil carcinoma of classic oat cell type nay simulate small cell non-Hodgkin's lymphoma. We report five cases of metastatic small cell carcinoma of in-termediate cell type diagnosed by FNA of the enlarged lymph nodes of the neck and axilla. The cytologic smears contained diffuse small neoplastic cells larger than lymphocytes with dense, pyknotic nuclei and extremely scanty cytoplasm. Apparently viable large tumor cells have vesicular nuclei with granular, sometimes very coarse chromatin. The characteristic cytologic features of small cell carcinoma as compared to malignant lymphoma were as follows.: 1) small cells with dense pyknotic nuclei are evenly distributed in the background of apparently viable larger tumor cells, admixed with mature lymphocytes and phagocytic macrophages. 2) small loose aggregates of cells with nuclear melding are indicative of small cell carcinoma rather than non-Hodgkin's lymphoma. 3) the cytoplasmic and nuclear fragments of tumor necrosis are more dominant in the smears of small cell carcinoma. 4) nuclear membrane and nucleoli are generally indistinct in small cell carcinoma due to condensation of chromatin.

  • PDF

Woodchuck Hepatitis Virus Infection

  • 정규식
    • Proceedings of the Korean Society of Veterinary Pathology Conference
    • /
    • 2002.11a
    • /
    • pp.9-9
    • /
    • 2002
  • Grossly, the liver exhibits marked cirrhotic changes characteristics of the pre-transformation phase of WHV. Microscopically, focal hepatocyte necrosis and inflammatory cells were observed in midzonal and periportal areas. Bridging portal fibrosis produced pseudolobulation due to entrapment of hyperplastic hepatocytes. Biliary hyperplasia, ductal cell proliferation, and increased amounts of fibrous connective tissue expanded portal areas and extended into periportal areas. Myofibroblasts stained positive for -SMA were detected in proliferating fibrotic tissue and sinusoids.

  • PDF

Synergistic effect of green tea polyphenol co-treated along with gamma radiation in leukemia cell necrosis (방사선 조사와 병행 처리한 녹차 Polyphenol의 혈구암세포 사멸 촉진 효과)

  • Lee Hong Su
    • Journal of The Korean Radiological Technologist Association
    • /
    • v.28 no.1
    • /
    • pp.39-48
    • /
    • 2002
  • The Green tea, one of the most popular and favorite drinks in eastern societies, has been reported to have various therapeutic properties. These includes anti-cancer, anti-oxident, anti-endocrine disrupter effects. Its anti-cancer effect was said to be ac

  • PDF