mTOR在SD大鼠TMJOA髁突软骨中表达变化的实验研究

  目的  明确mTOR在SD大鼠TMJOA髁突软骨中的表达变化。  方法   采用偏侧咀嚼的方法建立SD大鼠TMJOA模型，并设立相应假手术组。建模后2、4、8周分别取右侧髁突。使用HE染色、番红O-固绿染色进行病理学检查；通过免疫组织化学染色检测SOX9、mTOR的表达量。  结果   苏木精-伊红（HE）染色和番红O-固绿染色显示对照组标本髁突软骨结构层次清晰，表面平滑完整，蛋白多糖分布均匀。随着时间推移，实验组（TMD组）髁突软骨结构出现明显的退行性病变（P < 0.05），且病损在4周时最高。免疫组织化学染色显示，在实验组大鼠髁突软骨组织中SOX9的表达水平在2周（P < 0.01）、4周（P < 0.05）、8周（P < 0.05）依次下降且均低于对照组，mTOR的表达水平在2周（P < 0.05）、4周（P < 0.001）时下降，但在8周（P < 0.05）时相对上升。  结论   随着炎症进展，mTOR在SD大鼠TMJOA髁突软骨中呈现出早期下调，晚期上调的趋势，在将保护性自噬转变为破坏性的凋亡中发挥了关键作用。

Experimental Study on the Expression of mTOR in TMJOA Condylar Cartilage of SD Rats

  Objective   To investigate the expression of mTOR in TMJOA condylar cartilage of SD rats.   Methods   The model of TMJOA in SD rats was established by unilateral mastication, and the corresponding sham-operation group was established. TMJOA model was established by unilateral mastication.The right condyle was taken 2, 4 and 8 weeks after modeling. HE staining and safranine o-solid green staining were used for pathological examination; The expressions of Sox9 and mTOR were detected by immunohistochemical staining.   Results  Hematoxylin-eosin （HE） staining and saffron o-green staining showed that the condylar cartilage of the control group had clear structure, smooth and intact surface, and the proteoglycans were evenly distributed. In the experimental group （TMD group）, obvious degenerative changes of condylar cartilage were observed over time （P < 0.05）, and the lesions were the highest in 4 W. Immunohistochemical staining showed that the expression level of Sox9 in the condylar cartilage of the experimental group decreased successively at 2 W （P < 0.01）, 4 W （P < 0.05） and 8 W （P < 0.05）, and were lower than that of the control group. The expression level of mTOR decreased at 2 W （P < 0.05） and 4 W （P < 0.001）, but increased relatively at 8 W （P < 0.05） .  Conclusion  With the progress of inflammation, mTOR in TMJOA condylar cartilage of SD rats shows a trend of early down-regulation and late up-regulation, which plays a key role in transforming protective autophagy into destructive apoptosis.