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@PHDTHESIS{AlAsmi:1011826,
      author       = {Al Asmi, Mohammad Nour},
      othercontributors = {Pufe, Thomas and Conrads, Georg},
      title        = {{A}ufklärung des {E}ffekts von {N}rf2 auf parodontale
                      {E}rkrankungen in vitro},
      school       = {Rheinisch-Westfälische Technische Hochschule Aachen},
      type         = {Dissertation},
      address      = {Aachen},
      reportid     = {RWTH-2025-04752},
      pages        = {VI, 74 Seiten : Illustrationen},
      year         = {2025},
      note         = {Dissertation, Rheinisch-Westfälische Technische Hochschule
                      Aachen, 2025},
      abstract     = {Periodontal diseases (PD) are among the most significant
                      health issues worldwide. They are caused by bacterial
                      infections, including Porphyromonas gingivalis (P. g.),
                      which can damage the periodontal ligament and alveolar bone,
                      leading to tooth loss and a significant reduction in quality
                      of life. Lipopolysaccharide (LPS) from P. g. is considered a
                      critical factor in the onset and development of PD, as it
                      induces the formation of intracellular reactive oxygen
                      species (ROS). The accumulation of ROS leads to oxidative
                      stress, influencing the progression of PD and degrading
                      nuclear factor erythroid-derived 2-related factor 2 (Nrf2),
                      which plays a crucial role in bone healing. This study
                      investigates the impact of LPS-P. g. as an ROS inducer and
                      methysticin as an Nrf2 activator on the proliferation and
                      mineralization of preosteoblasts from the MC3T3-E1 (subclone
                      4) cell line. Cells were cultured in α-MEM and stimulated
                      with LPS-P. g. (STD and ULT). NF-κB activity was determined
                      using a dual luciferase assay, while cell proliferation and
                      cytotoxicity were assessed using the CyQUANT® Cell Assay.
                      Mineralization was evaluated by Alizarin Red staining of
                      calcium deposits after a 28-day differentiation process, and
                      ALP activity was measured. The protein concentration of
                      IL-6, IL-1ß, VEGF, and TNF-α was determined using sandwich
                      ELISAs. Results showed weak activation of NF-κB in MC3T3-E1
                      cells compared to RAW 264.7 macrophages after stimulation
                      with 1µg/ml LPS-P. g. (STD). LPS-P. g. (STD and ULT) had no
                      inhibitory effect on cell proliferation. However, LPS P. g.
                      (STD) could inhibit the differentiation of MC3T3-E1 cells
                      and their ALP activity. Conversely, methysticin positively
                      affected ALP activity and mineralization. Injection of
                      LPS-P. g. (STD) increased IL-6 expression and decreased VEGF
                      expression. In summary, the concentration of 1µg/ml LPS-P.
                      g. (STD) used is significantly above the physiological range
                      and could cause decreased mineralization of MC3T3-E1 cells
                      due to inflammation or increased ROS formation. Methysticin,
                      due to its antioxidative properties, could potentially be
                      developed as a drug for the treatment or prevention of PD in
                      the future. However, its toxicity needs to be considered in
                      the overall assessment.},
      cin          = {511001-5 ; 921210},
      ddc          = {610},
      cid          = {$I:(DE-82)511001-5_20140620$},
      pnm          = {DFG project G:(GEPRIS)545931001 - Die oxidative
                      Stressreaktion als Angriffspunkt in nicht-kleinzelligem
                      Lungenkrebs (A06) (545931001) / TRR 387: Funktionalisierung
                      des Ubiquitin Systems gegen Krebserkrankungen - UbiQancer
                      (514894665)},
      pid          = {G:(GEPRIS)545931001 / G:(GEPRIS)514894665},
      typ          = {PUB:(DE-HGF)11},
      url          = {https://publications.rwth-aachen.de/record/1011826},
}