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间歇性完全鼻阻塞对幼年大鼠髁突软骨细胞凋亡影响的研究 被引量:3

Study on influence of bilateral intermittent nasal obstruction on condylar cartilage cell apoptosis in young rats
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摘要 目的研究幼年大鼠在双侧间歇性鼻阻塞情况下双侧髁突软骨细胞的凋亡情况,尝试探讨间歇性鼻阻塞对张口呼吸儿童髁突软骨发育的影响。方法将20只4周龄大鼠(Sprague-Dawley rat,SD rat)分为2组,A组:双侧鼻阻塞组,常氧条件下鼻孔双侧阻塞8 h(早晨8点至下午4点),持续35 d;B组:对照组,常氧条件下饲养。2组给予同样的饮食以及饮水,然后分别取出双侧髁突,用甲醛保存做成石蜡切片,同时进行caspase-3以及Bcl-2,Bax蛋白免疫组化染色。以观察在双侧鼻阻塞对髁突前斜面中上部软骨细胞增殖以及凋亡的影响,以及双侧间歇性鼻阻塞情况下Bcl-2基因家族的调控机制以及与下颌骨生长发育的关系。结果双侧鼻阻塞的未成年大鼠前斜面中上部髁突细胞Bcl-2蛋白以及Bax蛋白,Caspase-3,Bax蛋白表达均较对照组增加,Bcl-2蛋白表达数量实验组较对照组表达减少,髁突软骨细胞凋亡数量较对照组明显增加。结论在间歇性双侧完全鼻阻塞情况下,SD幼年大鼠双侧髁突软骨细胞凋亡较对照组明显增加。 Objective To investigate the condylar cartilage cell apoptosis in young rats with bilateral intermittent nasal obstruction to try exploring the influence of intermittent nasal obstruction on the development of condylar cartilage of children who have to breathe through mouth. Methods Twenty 4-week-old SD rats were employed and divided into two groups. Group A : 10 of them had both nos-trils occluded by nose plugs on normal oxygen conditions up to 8 hours for 35 d and group B served as the control group: 10 of them were raised under normal oxygen conditions. The same food and water were offered to the two groups and then the bilateral condylar was extracted to make parafin section for the immumohistochemical staining,including Caspase-3, Bcl-2, Bax protein. Cartilage cell prolifera- tion and apoptosis,the regulatory mechanism of Bcl-2 gene family and its correlation with maxillary growth were observed and analyzed. Results Under the circumstance of bilateral intermittent nasal obstruction,the apoptosis of condylar chondrocytes in Group A increased significantly compared with the control group. The expression of caspase-3, bcl-2, bax protein was significantly higher than the control group. Conclusions Oral breathing caused by nasal obstruction results in the apoptosis in the condyle process cells.
出处 《口腔医学》 CAS 2014年第7期492-496,共5页 Stomatology
基金 上海市科委项目(11140902001)
关键词 双侧间歇性完全鼻阻塞 下颌髁突 凋亡 大鼠 nasal obstruction condyle process apoptosis rat
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