mTOR自噬通路在染氟大鼠软骨关节损伤中的作用  

Role of m TOR autophagy signaling in rats cartilages with fluorosis-caused damage

作　　者：陈荣[1] 于燕妮[1] 徐淋[1] 邓超男[1] 

机构地区：[1]贵州医科大学病理教研室,贵州贵阳550004

出　　处：《中国地方病防治》2017年第1期18-19,共2页Chinese Journal of Control of Endemic Diseases

基　　金：国家自然科学基金(81260419);教育部博士点教育基金(博导类)(20125215110001):博士启动基金(YJ2015-14)

摘　　要：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 explore the relationship of the related molecules among autophagy and apoptosis in cartilage with chronic fluorosis. Methods Healthy SD rats were selected and fluorosis model was duplicated; Dental fluorosis was observed. Results The detection rate was 66.7% and 83.3% in the low fluorine group rats and high fluoride group,respectively. The articular cartilage tissues were obviously thinning and disordered arrangement with the increase of fluorine contents in the low and high fluoride group. Conclusion Excessive fluoride can inhibit the m TOR signaling pathway and apoptosis to activate autophagy,and indicates that m TOR signaling pathway and apoptosis simultaneously participate in the mechanism of cartilage damage in the fluoride poisoning.

关 键 词：氟中毒 软骨 自噬 凋亡 

分 类 号：R114[医药卫生—卫生毒理学]