补肾壮筋汤介导内质网应激延缓毒胡萝卜素诱导大鼠椎间盘软骨细胞的退变

目的:观察补肾壮筋汤(BZD)对毒胡萝卜素(TG)诱导大鼠椎间盘软骨细胞内质网应激反应的影响。方法:①RT-PCR法检测经TG(2μmol·L-1)诱导大鼠椎间盘软骨细胞中蛋白激酶样内质网激酶(PERK)、真核翻译起始因子(Eif2α)、激活转录因子4(ATF4)、生长阻滞和DNA损伤诱导基因153(GADD153)mRNA表达;②Western Blot法检测经TG诱导大鼠椎间盘软骨细胞PERK、Eif2α、ATF4、GADD153蛋白含量表达。结果:①RT-PCR结果显示,与模型对照组比较,补肾壮筋汤200,400,600μg·mL^-1组的PERK、Eif2α、ATF4、GADD153mRNA含量表达均呈降低趋势;②Western Blot结果显示,与模型对照组比较,补肾壮筋汤200,400,600μg·mL^-1组的PERK、Eif2α、ATF4、GADD153蛋白含量表达显著降低,尤其400μg·mL^-1组降低更显著(P<0.01)。结论:补肾壮筋汤可通过下调TG诱导大鼠椎间盘软骨细胞中与内质网应激反应相关的PERK、Eif2α、ATF4、GADD153 mRNA与蛋白含量表达,进而延缓大鼠椎间盘软骨细胞退变。

The relationship between cartilage end-plate calcification and disc degeneration: an experimental study

Objective To study the relationship between cartilage end plate calcification and intervertebral disc degeneration Methods An experimental model of cervical disc degeneration in rabbits was established by resection of the cervical supraspinous and interspinous ligaments and detachment of the posterior paravertebral muscles from the cervical vertebrae Mechanical instability in the cervical spine elicited by this surgical intervention accelerated the process of intervertebral disc degeneration The extent of intervertebral disc degeneration was graded in morphologically, and the thicknesses of the calcified layer and the uncalcified layer of the cartilage end plate were measured in each degenerated cervical disc Results In less severely degenerative cervical discs, the morphology of the cartilage end plate showed nearly normal construction, and the tidemark was clear In severely degenerative discs, the matrix and cells showed fibrosis, the tidemark advanced, and the calcified cartilage thickened There exists a positive correlation between the thickness of the calcified layer of the cartilage end plate and the degree of cervical disc degeneration Conclusion The calcification of the cartilage end plate is the key factor that initiates and promotes cervical disc degeneration