Abstract
BackgroundThe 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.MethodsA 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.ResultsHematoxylin 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.ConclusionThese 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.
Highlights
Degeneration of intervertebral disc tissue may occur after injury, causing neurological disorders including low back pain
The number of nucleus pulposus (NP) cells in the intervertebral disc tissue of the model group and sIL-13Rα2Fc intervention group was decreased, the arrangement of the annulus fibrous (AF) was more disordered and exhibited ruptures, and the intervertebral disc tissue showed varying degrees of degeneration compared to the sham operation group
Compared to the model group, sIL-13Rα2-Fc significantly slowed intervertebral disc degeneration in rats, which was characterized by uniform arrangement of the AF, reduction of the rupture site, and an increased number of NP cells
Summary
Degeneration of intervertebral disc tissue may occur after injury, causing neurological disorders including low back pain. This condition affects approximately 5.4 million people worldwide, seriously decreasing their quality of life and increasing the disease burden on society [1]. The intervertebral disc is a cartilaginous joint between adjacent vertebral bodies and a complex structural tissue with multiple components It is composed of annulus fibrous (AF) and nucleus pulposus (NP) tissue, and nutrients diffuse to the intervertebral disc through the cartilage endplates (CEP). SIL-13Rα2Fc potently inhibits interleukin (IL)-13, as well as blocks related cell signaling pathways and inhibits fibrosis in certain tissues. We hypothesized that sIL-13Rα2-Fc delays the progression of intervertebral disc degeneration by inhibiting intervertebral disc fibrosis and improving ECM deposition
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