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@PHDTHESIS{ZhouStache:56880,
      author       = {Zhou-Stache, Jingfang},
      othercontributors = {Büttner, Reinhard},
      title        = {{I}nvestigation of the effects of chinese herb medicine on
                      {TNF}-[alpha] induced apoptosis in {H}uvec and {J}urkat
                      cells and their antioxidative effects},
      address      = {Aachen},
      publisher    = {Publikationsserver der RWTH Aachen University},
      reportid     = {RWTH-CONV-118957},
      pages        = {III, 84 S. : Ill., graph. Darst.},
      year         = {2002},
      note         = {Aachen, Techn. Hochsch., Diss., 2002},
      abstract     = {The Chinese herb, Radix Salviae Miltiorrhizae (RSM), is
                      being used in traditional Chinese medicine as a treatment
                      for cardiovascular and cerebrovascular diseases. Several
                      components of the plant extract from Salvia Mitorrhiza Bunge
                      have been determined previously, two of which are
                      protocatechuic acid (PAC) and protocatechuic aldehyde (PAL).
                      Since anti-apoptotic therapies have been proposed to limit
                      tissue damage in cardiovascular and cerebrovascular
                      diseases, PAC and PAL effects on cell protection from
                      apoptosis were investigated in this thesis. XTT assays were
                      first used to quantify cell viability. We found that PAC and
                      PAL inhibited TNF-alpha induced apoptosis of human umbilical
                      vein endothelial cells (Huvec) and Jurkat cells in a
                      concentration of 100 µM and 1mM respectively, when applied
                      2 hours prior to TNF-alpha exposition. To investigate
                      molecular consequences on cellular signal transduction
                      pathways, NF-kappaB reporter gene and DNA binding activities
                      were investigated by luciferase assay and gel shift assay.
                      Degradation of IkBalpha was determined by western blotting.
                      The molecular studies revealed that PAC activated NF-kappaB
                      with a maximal effect after 30 min of treatment. Inhibition
                      of NF-kappaB action by MG132 and NF-kappaB inhibitory
                      peptide suppressed the anti-apoptotic effect of PAC.
                      Further, degradation of IkBalpha occurred in response to PAC
                      treatment. Our results provide evidence that activation of
                      NF-kappaB plays an important role in mediating the
                      anti-apoptotic effect of PAC on HUVEC and Jurkat cells.
                      Nevertheless, PAL protection from apoptosis triggered by
                      TNF-alpha could not prevented by the treatment of MG132.
                      Additionally, PAL did not induce IkappaBalpha degradation.
                      The results implied that the anti-apoptotic action of PAL
                      may be mediated by a molecular mechanism other than
                      activation of NF-kappaB. In addition, a computer controlled
                      flow channel system (Elias-c-) was tested in this thesis to
                      study antioxidative capacities of herbal medicine. Effects
                      of herbal extracts and single components on oxidatively
                      impaired red blood cell (RBC) stiffness and relaxation time
                      as well as on oxidative damage (H2O2, 2 mM) induced
                      RBC-endothelial cell (EC) adhesion were investigated.
                      Following H2O2 treatment (20 min), RBC became significantly
                      stiffer and the relaxation time was reduced as compared with
                      control. These changes were irreversible after re-incubating
                      oxidatively damaged RBC in HEPES buffer. However, when
                      oxidatively damaged RBC were re-incubated with 88.5 µM
                      Tetramethylpyrazine (TMP), the H2O2-induced reduction in
                      relaxation time turned back to control levels whereas the
                      RBC stiffening did not. As mechanism we hypothesize, that
                      TMP applied to hydrogen peroxide damaged RBC may partially
                      reverse the hydrogen peroxide mediated formation of
                      hemoglobin-spectrin complexes possibly leading to a
                      normalization of the membrane viscosity. In the RBC-EC
                      adhesion tests, a maximum (about three-fold as compared to
                      control) increase in RBC-EC adhesion was obtained when both
                      RBC and EC were treated with H2O2. This increase in adhesion
                      was almost completely inhibited by 50 µM
                      3,4-dihydroxyphenyl lactate (Dhpl), when applied either
                      prior to or after treatment with H2O2. The mechanism of the
                      protection may be addressed in part to a direct free radical
                      scavenging effect of antioxidants dissolved in the EC
                      membrane. From a methodological point of view, the Elias-c
                      in combination with appropriate cell types and experimental
                      designs can be seen as a cellular bioassays to test herbal
                      extracts with high laboratory efficacy.},
      cin          = {510000-1},
      ddc          = {610},
      cid          = {$I:(DE-82)510000-1_20140620$},
      typ          = {PUB:(DE-HGF)11},
      urn          = {urn:nbn:de:hbz:82-opus-2860},
      url          = {https://publications.rwth-aachen.de/record/56880},
}