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目的通过检测自噬通路中m TOR、Beclin1、LC3及抗凋亡基因Bcl-2在慢性氟中毒软骨组织中的表达情况,探讨自噬通路在慢性氟中毒软骨损害中的作用及其与凋亡的关系。方法选择健康SD大鼠,建立氟中毒模型,观察大鼠氟斑牙情况。结果低氟组大鼠氟斑牙检出率为66.7%,高氟组为83.3%;光镜观察软骨组织形态学表现为各染氟组软骨细胞柱排列紊乱;随染氟浓度的增加软骨组织的厚度变薄,细胞数减少。结论过量氟能抑制m TOR信号通路及凋亡相关分子以及上调自噬相关分子,参与氟中毒软骨组织损伤的发生。
Objective To detect the expression of mTOR, Beclin1, LC3 and anti-apoptotic gene Bcl-2 in chronic fluorosis cartilage in autophagy pathway and to explore the role of autophagy pathway in the damage of chronic fluorosis cartilage and its relationship with apoptosis Relationship. Methods Healthy Sprague-Dawley rats were selected to establish fluorosis model and to observe the dental fluorosis in rats. Results The detection rate of dental fluorosis was 66.7% in low-fluoride group and 83.3% in high-fluoride group. The chondrocyte column was disordered in each fluorine group by light microscopy. With the increase of fluoride concentration, the cartilage tissue The thickness of the thinning, reducing the number of cells. Conclusion Excessive fluoride can inhibit mTOR signaling pathway and apoptosis related molecules and up-regulate autophagy-related molecules, and participate in the occurrence of cartilage tissue damage induced by fluorosis.