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Carthamin yellow inhibits matrix degradation and inflammation induced by LPS in the intervertebral disc via suppression of MAPK pathway activation.

ABSTRACT: Carthamin yellow (CY), which is a flavonoid compound isolated from safflower, has various pharmacological effects including promoting blood circulation to remove blood stasis and alleviating pain. CY is a herb used in Chinese traditional medicines. Intervertebral disc degeneration (IDD) is a common spinal disorder and degeneration of nucleus pulposus (NP) cells and inflammation are significant parts of the pathological cascade. The curative effect of CY on NP cells in association with degeneration and inflammation remains to be elucidated. In the present study, rat NP cells were isolated, cultured and used to detect the suppressive effects of CY on lipopolysaccharide (LPS)-induced genetic expression variation and the expression of matrix degradation enzymes, including matrix metallopeptidase-3, ADAM metallopeptidase with thrombospondin type 1 motif (ADAMTS)-4 and ADAMTS-5. A protective effect of CY on NP cells was observed against LPS-induced matrix degradation and inflammation. Western blotting results demonstrated that pretreatment with CY significantly suppressed the LPS-induced activation of the mitogen activated protein kinase (MAPK) pathway. The results of the present study suggested that CY exerted anti-degenerative and anti-inflammatory effects on NP cells via inhibition of MAPK pathway activation. Therefore, CY may be a potential therapeutic drug for the treatment of IDD in the future.

SUBMITTER: Chen B

PROVIDER: S-EPMC5525633 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:Transient receptor potential (TRP) channels have emerged as potential sensors and transducers of inflammatory pain. The aims of this study were to investigate (1) the expression of TRP channels in intervertebral disc (IVD) cells in normal and inflammatory conditions and (2) the function of Transient receptor potential ankyrin 1 (TRPA1) and Transient receptor potential vanilloid 1 (TRPV1) in IVD inflammation and matrix homeostasis. RT-qPCR was used to analyze human fetal, healthy, and degenerated IVD tissues for the gene expression of TRPA1 and TRPV1. The primary IVD cell cultures were stimulated with either interleukin-1 beta (IL-1?) or tumor necrosis factor alpha (TNF-?) alone or in combination with TRPA1/V1 agonist allyl isothiocyanate (AITC, 3 and 10 µM), followed by analysis of calcium flux and the expression of inflammation mediators (RT-qPCR/ELISA) and matrix constituents (RT-qPCR). The matrix structure and composition in caudal motion segments from TRPA1 and TRPV1 wild-type (WT) and knock-out (KO) mice was visualized by FAST staining. Gene expression of other TRP channels (A1, C1, C3, C6, V1, V2, V4, V6, M2, M7, M8) was also tested in cytokine-treated cells. TRPA1 was expressed in fetal IVD cells, 20% of degenerated IVDs, but not in healthy mature IVDs. TRPA1 expression was not detectable in untreated cells and it increased upon cytokine treatment, while TRPV1 was expressed and concomitantly reduced. In inflamed IVD cells, 10 µM AITC activated calcium flux, induced gene expression of IL-8, and reduced disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and collagen 1A1, possibly via upregulated TRPA1. TRPA1 KO in mice was associated with signs of degeneration in the nucleus pulposus and the vertebral growth plate, whereas TRPV1 KO did not show profound changes. Cytokine treatment also affected the gene expression of TRPV2 (increase), TRPV4 (increase), and TRPC6 (decrease). TRPA1 might be expressed in developing IVD, downregulated during its maturation, and upregulated again in degenerative disc disease, participating in matrix homeostasis. However, follow-up studies with larger sample sizes are needed to fully elucidate the role of TRPA1 and other TRP channels in degenerative disc disease.

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Carthamin yellow inhibits matrix degradation and inflammation induced by LPS in the intervertebral disc via suppression of MAPK pathway activation.

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