| Co-Investigator(Kenkyū-buntansha) |
SASAKI Ryohei KOBE UNIV.GRAD.SCHMED, RES.ASSOC., 大学院・医学系研究科, 助手 (30346267)
SOEJIMA Toshinori KOBE UNIV.GRAD.SCHMED, ASST.RPOF, 大学院・医学系研究科, 助教授 (20231384)
SUGIMURA Kazuro KOBE UNIV.GRAD.SCHMED, PROF, 大学院・医学系研究科, 教授 (00136384)
KISHI Kazufumi KOBE UNIV.GRAD.SCHMED, RES.ASSOC., 大学院・医学系研究科, 助手 (70254547)
DOTO Akinobu KOBE UNIV.GRAD.SCHMED, ASSITPROF, 大学院・医学系研究科, 助教授 (70283885)
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| Research Abstract |
It is a well-known fact that there iis a great difference in radiosensitivity between actively replicating tumor cell and differentiated neurons without replicating activity. In this research project, we focused on cyclo-oxygenase 2 (COX-2) inhibitors, whose inhibitory action of cell replication is recognized in many tumor cell linse, and carboxypeptidase B (HBCPB) which exhibits inhibitory activity for cell toxicity be dissociation of beta-amyloid oligomer, and snslyzed their functions with regard to apoptosis induction.
COX-2 study : Using human hemangiosarcoma cell line (ISO-HAS), following analyses were performed.
Effects in tumor growth and angiogenesis by co-usage of irradiation and NS-389, a selective COX-2 inhibitor.
Relationship of COX-2 effect and VEGF protein expression.
As for results, cell viability was decreased by NS-389 in a dose dependent fashion, and the VEGF-protein expression was increased by irradiation also in a dose-dependent manner, which was inhibited by co-usage of NS-398. Therefore, it seems that NS-389 has a co-usage effect with irradiation, and its cell growth inhibitory effect is relevant to VEGF.
HBCPB study : As a typical example of non-replicating cell, using rat hippocampus primary neuron culture system was used. In this system, neuro-toxicity of beta-amyloid 1-42 oligomer, and its dissociation by human brain carboxypeptidase B (HBCPB) were analyzed especially with respect to apoptosis induction.
As a result, this system induced no effects in the COX-2 prostaglandin lineage, and suggests that these are independent regulation system for selective cell death to keep homeostasis.
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