RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제
      • 좁혀본 항목 보기순서

        • 원문유무
        • 원문제공처
        • 등재정보
        • 학술지명
        • 주제분류
        • 발행연도
        • 작성언어
        • 저자
          펼치기

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Protective Effect of Schisandra chinensis Polysaccharides Against the Immunological Liver Injury in Mice Based on Nrf2/ARE and TLR4/NF-κB Signaling Pathway

        Yingying Shan,Bin Jiang,Jiahui Yu,Jiaye Wang,Xiaoli Wang,He Li,Chunmei Wang,JianGuang Chen,Jinghui Sun 한국식품영양과학회 2019 Journal of medicinal food Vol.22 No.9

        We have previously demonstrated the hepatoprotective effect of Schisandra chinensis polysaccharides (SCP) against the liver injury induced by alcohol, high-fat diet, and carbon tetrachloride in mice. In this study, we investigated the effect of SCP against the immunological liver injury induced by concanavalin A (Con A) in mice. The results showed that SCP could significantly reduce the level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the serum of mice with immunological liver injury. SCP could significantly decrease the content of malondialdehyde (MDA) and nitric oxide (NO) and increase the activity of superoxide dismutase (SOD) and glutathione (GSH) in the liver tissue. SCP could significantly increase the number of CD4+ and decrease the number of CD8+ in the peripheral blood, and elevate the ratio of CD4+/CD8+. SCP could significantly downregulate the expression of Kelch-like ECH-associated protein 1 (Keap1) and upregulate the expression of nuclear factor-erythroid 2-related factor2 (Nrf2) and downstream gene heme oxygenase-1 (HO-1), and downregulate the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), and nuclear factor-kappa B (NF-κB) proteins. This study indicates that SCP can reduce the release of a large number of inflammatory factors to inhibit the oxidative stress in mice with the immunological liver injury induced by Con A, and its mechanism is closely related to the regulation of Nrf2/antioxidant response element and TLR4/NF-κB signaling pathways.

      • KCI등재

        UBE2W Interacts with FANCL and Regulates the Monoubiquitination of Fanconi Anemia Protein FANCD2

        Yingying Zhang,Peitang Huang,Xiaowei Zhou,Lixia Zhao,Chao Li,Hengqi Zhu,Long Xu,Liran Shan,Xiang Liao,Zekun Guo 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.2

        Fanconi anemia (FA) is a rare cancer-predisposing ge-netic disease mostly caused by improper regulation of the monoubiquitination of Fanconi anemia complementation group D2 (FANCD2). Genetic studies have indicated that ubiquitin conjugating enzyme UBE2T and HHR6 could regulate FANCD2 monoubiquitination through distinct mechanisms. However, the exact regulation mechanisms of FANCD2 monoubiquitination in response to different DNA damages remain unclear. Here we report that UBE2W, a new ubiquitin conjugating enzyme, could regulate FANCD2 monoubiquitination by mechanisms different from UBE2T or HHR6. Indeed, UBE2W exhibits ubiquitin conjugating enzyme activity and catalyzes the monoubiquitination of PHD domain of Fanconi anemia complementation group L (FANCL) in vitro. UBE2W binds to FANCL, and the PHD domain is both necessary and sufficient for this interaction in mammalian cells. In addition, over-expression of UBE2W in cells promotes the monoubiquitination of FANCD2 and down-regulated UBE2W markedly reduces the UV irradia-tion-induced but not MMC-induced FANCD2 monoubiquiti-nation. These results indicate that UBE2W regulates FANCD2 monoubiquitination by mechanisms different from UBE2T and HRR6. It may provide an additional regulatory step in the activation of the FA pathway.

      • KCI등재

        Melatonin prevents lung injury by regulating apelin 13 to improve mitochondrial dysfunction

        Lu Zhang,Fangli Liu,Xiaomin Su,Yue Li,Yining Wang,Ruonan Fang,Yingying Guo,Tongzhu Jin,Huitong Shan,Xiaoguang Zhao,Rui Yang,Hongli Shan,Haihai Liang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

        Pulmonary fibrosis is a progressive disease characterized by epithelial cell damage, fibroblast proliferation, excessive extracellular matrix (ECM) deposition, and lung tissue scarring. Melatonin, a hormone produced by the pineal gland, plays an important role in multiple physiological and pathological responses in organisms. However, the function of melatonin in the development of bleomycin-induced pulmonary injury is poorly understood. In the present study, we found that melatonin significantly decreased mortality and restored the function of the alveolar epithelium in bleomycin-treated mice. However, pulmonary function mainly depends on type II alveolar epithelial cells (AECIIs) and is linked to mitochondrial integrity. We also found that melatonin reduced the production of reactive oxygen species (ROS) and prevented apoptosis and senescence in AECIIs. Luzindole, a nonselective melatonin receptor antagonist, blocked the protective action of melatonin. Interestingly, we found that the expression of apelin 13 was significantly downregulated in vitro and in vivo and that this downregulation was reversed by melatonin. Furthermore, ML221, an apelin inhibitor, disrupted the beneficial effects of melatonin on alveolar epithelial cells. Taken together, these results suggest that melatonin alleviates lung injury through regulating apelin 13 to improve mitochondrial dysfunction in the process of bleomycin-induced pulmonary injury.

      • KCI등재

        Deformation path and springback behavior in double-curved bending at high temperature

        Po Liu,Taichao Zhang,Bin Guo,Li Yang,Debin Shan,Yingying Zong 대한기계학회 2019 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.33 No.9

        In this work, integrated double-curved bending–sizing–unloading is simulated for a Ti6Al4V titanium alloy sheet. Bending radii R30 mm × R30 mm and R30 mm × R15 mm are used in the bending tests at 700 °C and 750 °C, respectively. A holding time of 0–600 s is applied to explore the effect of sizing time on forming accuracy. Similar experimental tests are performed for comparison with the finite element analysis results. Results show that bending behavior varies remarkably with the bidirectional radii. As for equal bidirectional curvature, bending along each direction occurs simultaneously. Given that bidirectional radii are different, the sheet consecutively experiences single small-, single large-, and double-curved bending. The deformation path results in nonuniform plastic strain distribution. The springback amount increases from the center to the marginal middle zone. Sizing at 700 °C or 750 °C in 600 s or 180–600 s can remarkably reduce the springback amount, respectively. The springback prediction via finite element method is consistent with that of the experiment.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼