• Title/Summary/Keyword: Damaged DNA

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Potential Role of Hedgehog Signaling in Radiation-induced Liver Fibrosis (방사선에 의한 간섬유증에서 헤지호그의 잠재적 역할)

  • Wang, Sihyung;Jung, Youngmi
    • Journal of Life Science
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    • v.23 no.5
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    • pp.710-720
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    • 2013
  • Radiotherapy is commonly used in treating many kinds of cancers which cannot be cured by other therapeutic strategies. However, radiotherapy also induces the damages on the normal tissues. Radiation-induced fibrosis is frequently observed in the patients undergoing radiotherapy, and becomes a major obstacle in the treatment of intrahepatic cancer. Hedgehog (Hh) that is an essential in the liver formation during embryogenesis is not detected in the healthy liver, but activated and modulates the repair process in damaged livers in adult. The expression of Hh increases with the degree of liver damage, regulating the proliferation of hepatic progenitors and hepatic stellate cells (HSC). In addition, Hh induces epithelial-to-mesencymal transition (EMT) and activation of myofibroblasts. In the irradiated livers, up-regulated expression of Hh signaling was associated with proliferation of progenitors, EMT induction, and increased fibrosis. Female-specific expression of Hh leaded to the expansion of progenitors and the accumulation of collagen in the irradiated livers of female mice, indicating that gender disparity in Hh expression may be related with radiation-susceptibility in female. Hence, Hh signaling becomes a novel object of studies for fibrogenesis induced by radiation. However, the absence of the established experimental animal models showing the similar physiopathology with human liver diseases and fibrosis-favorable microenvironment hamper the studies for the radiation-induced fibrosis, providing a few descriptive results. Therefore, further research on the association of Hh with radiation-induced fibrosis can identify the cell and tissue-specific effects of Hh and provides the basic knowledge for underlying mechanisms, contributing to developing therapies for preventing the radiation-induced fibrosis.

Effect of Water Soluble Extract of Lichens on Weights of Various Organs, Blood Components and Activities of Transaminases and 5-Nucleotidase in Rat (지의류(地衣類)의 수용성 추출물이 흰쥐의 각 장기무게, 혈액성분 및 Transaminases와 5-Nucleotidase 활성에 미치는 영향(I))

  • Cho, Ok-Lang;Suh, Jung-Soon;An, Mi-Jung;Lee, In-Ja;Cho, Sung-Hee
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.14 no.2
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    • pp.137-144
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    • 1985
  • In order to evaluate the effect of water soluble extract of lichens (Physcia, Parmelia and Clandonia species) on liver damage, activities transaminase(GPT) and 5'-nucleotidase in serum and liver were measured in rats fed lichens extract. DNA and RNA were measured in liver and spleen, as well as various organ weights and blood components. Control group was fed water to compare with the lichen group. Three sets of experiments were conducted: the first set was done with normal rats, the second one with rats with liver damage induced by $CCl_4$ injection was divided into three subgroups. i.e. no treatment group, pre-treatment group and post-treatment group, and the third one was with rats with acute and chronic liver damage. In normal rats, lichens extract feeding reduced serum GOT and GPT activities. In liver damaged rats, both pre-and post-treatment had suppressing effect against increase of serum enzymes. In rats with acute and chronic liver damage, lichens fed group had lower activities of serum GOT, GPT and 5'-nucleotidase but higher activities of liver enzymes than control group. This effect was more pronounced in rats with acute liver damage. Liver weight increased considerably with lichens intake. Hemoglobin and hematocrit levels were also higher in lichens fed group. Nucleic acid contents in spleen but not in liver were increased in lichens fed group. The latter increase was more significant with chronic liver damage. It is suggested from the present study that water soluble lichens extract play protective and therapeutic roles in organs against infection and atrophic disease.

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