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- 2016
慢性不可预见性心理应激致大鼠颞下颌关节损伤髁突组织中TNF-α和Caspase-3蛋白的表达*
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Abstract:
目的:通过慢性不可预见性心理应激建立大鼠颞下颌关节损伤模型,探讨髁突的病理性改变和可能的作用机制。方法:选取7周龄雄性SD大鼠64只,分为空白对照(CON)组及心理应激(PS)组。PS组予以慢性不可预见性心理应激,建立大鼠颞下颌关节损伤模型。各组于实验1、3、5、7周各处死8只大鼠,测定大鼠体重,并通过HE染色了解髁突的组织形态学改变,采用免疫组化PV染色法了解髁突组织中TNF-α和Caspase-3蛋白的表达情况。结果:与CON组相比,PS组大鼠体重增长较慢,5、7周时体重下降明显(P<0.05)。此外,PS组大鼠髁突出现了胶原松解、水肿等病理性改变,其中3周时损伤最为严重,表现为细胞胶原纤维松解、断裂,形成大小不一的裂隙; 5周时髁突表层纤维松解的情况较3周有所减轻,但细胞层次略紊乱; 7周时髁突内部细胞数目减少,出现了无细胞空白区域。PS组大鼠髁突组织中TNF-α、Caspase-3蛋白的表达均较CON组升高(P<0.05)。结论:慢性心理应激可致大鼠体重及颞下颌关节髁突组织结构改变,可能是通过上调炎症因子及凋亡相关蛋白的表达,促进髁突软骨细胞凋亡来实现的。
Aim: To observe the structure changes and possible mechanism of the temporomandibular joint(TMJ)condylar cartilage damage induced by chronic unpredicted mild stress(CUMS)in rats.Methods: Totally 64 male SD rats aged 7-weeks were randomly allocated into 8 groups, which were blank control group(1,3,5,7 weeks)and psychological stress(PS)group(1,3,5,7 weeks),and the rats were treated by CUMS except those in blank control group. After corresponding weeks CUMS treatment, the body weight was measured and the HE staining was used to research the condylar morphology change, the immunohistochemical staining was applied to detect the expressions of TNF-α and Caspase-3 proteins in condylar.Results: The rats inPS group grew slowly in weight, which showed significant differences from the fifth week(P<0.01). Besides, edema and releases of collagen fiber in the condylar surface were observed. The most serious damage of condylar surface was formed in the 3rd week in the PS group, characterized by loosen collagen fiber, and fracture of cracks. In the 5th week, the damage of condylar surface in PS group was alleviated, but the layers of cells was slightly disordered. In the 7th week, the cells in condylar decreased significantly, appearing the blank area without cells. At the same time, the immunohistochemical staining showed the higher expression of TNF-α and Caspase-3 in the PS group than those in the blank control group(P<0.05).Conclusion: CUMS can lead to changes in body weight and structure of TMJ, by up-regulating the expression of TNF-α and Caspase-3 in condylar cartilage of TMJ and induce cell apoptosis