| Project/Area Number |
14571583
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KEIO UNIVERSITY |
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Principal Investigator |
SUEOKA Kou Keio Univ., School of Medicine, Associate Professor, 医学部, 助教授 (90162833)
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| Co-Investigator(Kenkyū-buntansha) |
IWATA Soukichi Keio Univ., School of Medicine, Instructor, 医学部, 助手 (50203386)
KUJI Naoaki Keio Univ., School of Medicine, Assistant Professor, 医学部, 講師 (80169987)
YOSHIMURA Yasunori Keio Univ., School of Medicine, Professor, 医学部, 教授 (10129736)
MAEDA Taro Keio Univ., School of Medicine, Instructor, 医学部, 助手 (90327594)
TAJIMA Hiroto Keio Univ., School of Medicine, Instructor, 医学部, 助手 (30317193)
佐藤 健二 慶應義塾大学, 医学部, 助手 (50306825)
中林 章 慶應義塾大学, 医学部, 助手 (80306828)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | spermatogenesis / doxorubicin / c-kit / F-TRAP / telomerase / TUNEL / green tea extract (GTE) / apoptosis / Doxorubicin (DXR) / RT-PCR法 / mRNA発現 / テロメラーゼ活性 / c-kit mutant / WBB6F1(wild type)+ / + / hetero W^v / W / W^v / Apoptosis |
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| Research Abstract |
The implication of c-kit was examined on the aspect of gene expression and c-kit production at testicular germ cell by RT-PCR and immunohistochemistry in the mice testes damaged by doxorubicin (DXR) as a germ cell toxic model. And also the promoting effect of herbal medicine (TJ41, TJ7) and GTCs on telomerase activity and apoptosis were investigated. Apoptotic cells were labelled by the TdT-mediated dUDP nick-end labelling (TUNEL) assay. The weight of testes was significantly decreased to 55-64% by DXR exposure, while the combined treatment of GTCs with DXR resulted in parameters similar to the control. In the testes of DXR-exposed mice, germ cells in the testicular tubules of control were drastically reduced by about 80% by histological analysis. However, germ cell damage was significantly attenuated by TJ41 and GTCs coadministration. c-Kit and its gene expression were reduced in the DXR exposured testis, but not in the group with promoting agents. Although the telomerase activity evaluated by fluorescence-based TRAP assay was increased with coadministration of TJ41 and GTCs compared with control, that was decreased by DXR expoosure without these promoting agents. The promoting agents with DXR show a marked reduction in the number of apoptotic cells compared with DXR exposure without these agents. These results suggest that testicular dysfunction following exposure of toxic chemicals are determining at the mechanisms provoked by c-kit and its gene expression and TJ41 and GTCs may have eventful evidence of a protective effect against DXR-induced testicular toxicity via promoting telomerase activity by inhibition of testicular apoptosis.
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