sIL-13Rα2-Fc 对大鼠尾椎间盘退变进展的影响。
Effect of sIL-13Rα2-Fc on the progression of rat tail intervertebral disc degeneration.
机构信息
Department of Orthopedics, First Clinical Medical College of Lanzhou University, The First Hospital of Lanzhou University, Lanzhou, 730000, Gansu, China.
Changzheng Orthopedics Hospital, Second Military Medical University, Shanghai, 200003, China.
出版信息
J Orthop Surg Res. 2019 Nov 27;14(1):386. doi: 10.1186/s13018-019-1361-0.
BACKGROUND
The incidence of degenerative disc disease caused by intervertebral disc injury is increasing annually, seriously affecting the quality of life of patients and increasing the disease burden on society. The mechanisms of intervertebral disc degeneration include changes in extracellular matrix (ECM) deposition and tissue fibrosis. sIL-13Rα2-Fc potently inhibits interleukin (IL)-13, as well as blocks related cell signaling pathways and inhibits fibrosis in certain tissues. However, it is unknown whether sIL-13Rα2-Fc inhibits fibrosis in injured intervertebral discs and slows the process of degeneration. We hypothesized that sIL-13Rα2-Fc delays the progression of intervertebral disc degeneration by inhibiting intervertebral disc fibrosis and improving ECM deposition.
METHODS
A rat tail intervertebral disc degeneration model was established. Pathological changes in rat intervertebral disc tissue were observed by hematoxylin and eosin staining and Masson staining. Glycosaminoglycan (GAG), chondroitin sulfate (CS), keratan sulfate (KS), and hyaluronic acid (HA) contents were quantitatively analyzed by enzyme-linked immunosorbent assay. Type I and type II collagen expression levels were analyzed by reverse transcription-PCR and western blotting.
RESULTS
Hematoxylin and eosin staining and Masson staining revealed annulus fibrosus rupture, disordered arrangement, decreased nucleus pulposus tissue, and decreased collagen fiber in the rat intervertebral disc tissue. Following treatment with sIL-13Rα2-Fc, pathological changes in the rat intervertebral disc were reduced. Rat intervertebral disc tissue showed decreased GAG, CS-KS, and (HA) contents, increased type I collagen levels, and decreased type II collagen levels in degenerated intervertebral discs. sIL-13Rα2-Fc intervention increased the contents of GAG, CS, KS, and HA; inhibited the expression of type I collagen; and promoted the expression of type II collagen.
CONCLUSION
These results demonstrate that intervertebral disc degeneration is associated with tissue fibrosis. sIL-13Rα2-Fc can regulate type I and type II collagen expression levels by increasing GAG, CS, KS, and HA contents, thereby slowing the progression of intervertebral disc degeneration.
背景
由椎间盘损伤引起的退行性椎间盘疾病的发病率逐年增加，严重影响患者的生活质量，并增加了社会的疾病负担。椎间盘退变的机制包括细胞外基质（ECM）沉积和组织纤维化的变化。sIL-13Rα2-Fc 能强有力地抑制白细胞介素（IL）-13，阻断相关细胞信号通路，并抑制某些组织的纤维化。然而，sIL-13Rα2-Fc 是否抑制损伤的椎间盘纤维化并减缓退变过程尚不清楚。我们假设 sIL-13Rα2-Fc 通过抑制椎间盘纤维化和改善 ECM 沉积来延缓椎间盘退变的进展。
方法
建立大鼠尾椎间盘退变模型。通过苏木精和伊红染色和 Masson 染色观察大鼠椎间盘组织的病理变化。通过酶联免疫吸附试验定量分析糖胺聚糖（GAG）、软骨素硫酸盐（CS）、硫酸角质素（KS）和透明质酸（HA）含量。通过逆转录-PCR 和 Western blot 分析 I 型和 II 型胶原表达水平。
结果
苏木精和伊红染色和 Masson 染色显示纤维环破裂、排列紊乱、髓核组织减少、胶原纤维减少。sIL-13Rα2-Fc 治疗后，大鼠椎间盘的病理变化减轻。退变的大鼠椎间盘组织中 GAG、CS-KS 和（HA）含量降低，I 型胶原水平升高，II 型胶原水平降低。sIL-13Rα2-Fc 干预增加了 GAG、CS、KS 和 HA 的含量；抑制 I 型胶原的表达；并促进 II 型胶原的表达。
结论
这些结果表明椎间盘退变与组织纤维化有关。sIL-13Rα2-Fc 通过增加 GAG、CS、KS 和 HA 的含量来调节 I 型和 II 型胶原的表达水平，从而减缓椎间盘退变的进展。
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