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Nutgall Experimental study of the anti-inflammatory mechanism of periodontal inflammation

Author: WangZhiLiang
Tutor: TangRongYin
School: Fourth Military Medical University
Course: Clinical Stomatology
Keywords: Nutgall Periodontitis Endotoxin Cytokines Mediated Suppression
CLC: R781.4
Type: Master's thesis
Year: 2003
Downloads: 127
Quote: 8
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Abstract


In the inflammatory periodontal disease, bacteria directly damaging effects on periodontal tissue is limited, and the host response to excitation by bacterial products is the main cause of periodontal tissue destruction. Periodontal advantage of lipopolysaccharide (LPS) is recognized as the inflammatory initiation factor, more and more important role in the pathogenesis of periodontitis. Periodontal advantage of lipopolysaccharide (LPS) acting on the monocyte-macrophage cells, induced by a variety of cytokines and inflammatory mediators involved in periodontal disease inflammatory activation and tissue trauma. The strength of the LPS pathogenic role, in a sense, reflected in its ability to stimulate the body to produce endogenous cytokines. The purpose of this study is to investigate the impact of the nutgall inflammatory process of periodontal disease periodontal advantage of lipopolysaccharide (LPS) and LPS-mediated generation of cytokines and inflammatory mediators, as nutgall for the prevention and treatment of periodontal disease provide experimental basis. 1 nutgall Pg-LPS activity EDS-99 bacterial LPS detection system kinetic turbidimetric method, the study nutgall PG-LPS activity observed gall water extraction in the degradation of Pg- the timeliness of LPS, dose-effect relationship. The study shows that 5 concentrations Nutgall extracts were able to significantly inhibit the activity of PG-of LPS and its degradation in a concentration-dependent manner within a certain range, while having a time-dependent manner. The 2 nutgall PG-LPS structure observed by transmission electron microscopy nutgall PG-LPS structure, electron microscopy by nutgall role after PG-LPS has lost its normal structure , was the scattered distribution Broken mesh or short ribbon. Description nutgall inhibition of PG-LPS activity is not a temporary suppression, but by the destruction of Pg-LPS structure play an antagonistic role. 3 nutgall Pg-LPS-mediated IL-1beta activity of radioimmunoassay (RIA), to explore nutgall PG-LPS-mediated human peripheral blood mononuclear cells secrete IL-1beta activity affected. The results showed that the five concentration nutgall can significantly inhibit the activity of PG-LPS-mediated single the nuclear cells secrete IL-1beta, and its inhibition in a dose-dependent manner. The mechanism of prompt nutgall anti-inflammatory effect is achieved by inhibiting the activity of the PG-LPS-mediated induction of IL-1beta. Journal of the Fourth Military Medical University, nutgall human PDLC PGEz and LTB. Synthesis of ELISA and high performance liquid chromatography to observe the nutgall PDLC PGE. And LTB. , And to explore the mechanism of nutgall anti-inflammatory effects. The results show that the water of gall extract has anti-inflammatory effects, can significantly reduce the PGEz and LTB. Synthesis and release, and having a concentration-dependent manner. Show that nutgall anti-inflammatory effects may be related to inhibition of cyclooxygenase, lipoxygenase. But the five concentration nutgall suppression effect are lower than indomethacin of 100ng plus l. 5, nutgall periodontal inflammation collagenase application hydroxyproline assay explore nutgall collagenase periodontal inflammation. The experiments showed that nutgall could significantly inhibit the activity of collagenase, and its role in a concentration-dependent manner. Description nutgall blocking collagenase role in the destruction of connective tissue, inhibiting or slowing the progression of periodontitis. However, the concentrations of less than less than sug plus doxycycline the 100ug plus its inhibitory effect.

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