Cargando…
Hydroxysafflor Yellow A (HSYA) Protects Endplate Chondrocytes Against IL-1β-Induced Injury Through Promoting Autophagy
BACKGROUND: Intervertebral disc degeneration (IDD) refers to intractable pain in patients' waist and legs, which is caused by internal structural disorder and degeneration of intervertebral. This disease severely affects the quality-of-life of people. It has been reported that hydroxysafflor ye...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9273358/ https://www.ncbi.nlm.nih.gov/pubmed/35832517 http://dx.doi.org/10.1155/2022/6326677 |
Sumario: | BACKGROUND: Intervertebral disc degeneration (IDD) refers to intractable pain in patients' waist and legs, which is caused by internal structural disorder and degeneration of intervertebral. This disease severely affects the quality-of-life of people. It has been reported that hydroxysafflor yellow A (HSYA), the active ingredient in safflower extract, could inhibit IL-1β-induced apoptosis of endplate chondrocytes. However, the mechanism by which HSYA regulates the occurrence and progression of IDD remains unclear. METHODS: Rat endplate chondrocytes were isolated from the intervertebral disc. Next, toluidine blue staining and collagen II immunofluorescence staining were used to identify endplate chondrocytes. Then, MDC staining was used to detect the autophagy of endplate chondrocytes. In addition, Western blot was used to measure the expression of cleaved caspase 3, LC-3I/II and ATG7 in endplate chondrocytes. RESULTS: IL-1β obviously inhibited the viability and proliferation of endplate chondrocytes, while these phenomena were notably reversed by HSYA. Additionally, HSYA was able to inhibit IL-1β-induced apoptosis of endplate chondrocytes. Moreover, HSYA protected endplate chondrocytes against IL-1β-induced inflammation via inducing autophagy. CONCLUSION: HSYA protected rat endplate chondrocytes against IL-1β-induced injury via promoting autophagy. Therefore, the present study might provide some theoretical basis for exploring novel and effective methods for patients with IDD. |
---|