小檗碱
牙周炎
基质骨
化学
细胞外基质
细胞外
新陈代谢
骨重建
牙科
生物化学
内科学
解剖
医学
软骨
作者
Yujia Cui,Jing Xie,Linyi Cai,Demao Zhang,Jianxun Sun,Xuedong Zhou
出处
期刊:Oral Diseases
[Wiley]
日期:2021-12-23
卷期号:29 (3): 1184-1196
被引量:5
摘要
Abstract Objectives The objectives of this study were to explore the role and related mechanism of berberine in repairing bone destruction in apical periodontics (AP). Materials and Methods AP was established in 14 of 21 male Wistar rats (four weeks of age; 70–80 g) for 3 weeks. The canals were cleaned and administered berberine (2 mg/ml; n = 7) or calcium hydroxide (100 mg/ml; control; n = 7), followed by glass ionomer cement sealing. After 3 weeks, specimen collection followed by micro‐computed tomography (μ‐CT) and histological staining was performed, including haematoxylin and eosin staining, Masson's trichrome staining, tartrate‐resistant acid phosphatase staining, immunohistochemistry and immunofluorescence histochemistry. Results μ‐CT showed that AP lesion volume reduced in the berberine group. Histopathology showed that berberine decreased the activity and number of osteoclasts but increased the expression of proteins related to osteoblast differentiation, including alkaline phosphatase and osterix. The immune cell, T cell, dendritic cell and macrophage counts were significantly decreased in the berberine group. In the berberine group, the expression of extracellular matrix‐degraded proteases, metalloproteinases, was decreased; however, that of extracellular matrix‐stable proteases, lysyl oxidases, was increased. Conclusions Berberine controlled the inflammatory response and regulated bone metabolism in AP by reducing metalloproteinase expression and increasing lysyl oxidases expression.
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