Effects of Emodin on Alveolar Bone Resorption via the IL-23/Th17 Inflammatory Axis in Rats with Periodontitis

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  • Wang Chunfeng
    Department of Stomatology, Hunan University of Medicine
  • Li Yuxian
    Teaching and Research Office of Diagnostics, Medical College, Hunan University of Medicine
  • Hou Yepo
    Department of Stomatology, Hunan University of Medicine
  • Jin Ling
    Teaching and Research Office of Diagnostics, Medical College, Hunan University of Medicine
  • Chen Minmin
    Department of Endodontics, Xiangya Stomatological Hospital & Xiangya School of Stomatology, Central South University & Hunan Key Laboratory of Oral Health Research

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<p>This study aimed to analyze the effect of emodin on alveolar bone resorption in rats with periodontitis through the interleukin-23 (IL-23)/T helper 17 (Th17) cells inflammatory axis. Twenty-four male Sprague Dawley rats were randomly divided into the following three groups of eight rats each: the control group (group N), periodontitis group (group P), and periodontitis + emodin intervention group (group E). After 2 weeks of continuous emodin intervention, alveolar bone loss (ABL) was evaluated by morphological analysis. Tartrate-resistant acid phosphatase staining was performed to determine the number of osteoclasts (OCs) in periodontal tissue. The ABL and trabecular separation were greater and the number of OCs and the G1/G0 and G2/M phase ratios were higher in group P than those in groups N and E (P < 0.05). In contrast, the trabecular number and thickness were decreased and the S and G2+S phase ratios were lower in group P than those in groups N and E (P < 0.05). However, these indices did not differ significantly between groups E and N. The IL-23, IL-17, RANKL, RANK, RANKL/OPG, IL-2, IL-6, IL-1β, and TNF-α levels across the three groups were in the order of group P > group E > group N and the OPG levels were in the order of group P < group E < group N (P < 0.05). Emodin may decrease the expression of RANKL and RANK proteins and levels of inflammatory factors; increase OPG, PPAR-γ, and NF-κB protein expression levels; and decrease the number of OCs through the IL-23/Th17 inflammatory axis, thus inhibiting ABL and bone resorption in rats with periodontitis and promoting the proliferation of periodontal ligament cells and alveolar bone repair.</p>

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