Abstract
The treatment for intervertebral disc degeneration (IDD) has drawn great attention and recent studies have revealed that the p38 MAPK pathway is a potential therapeutic target for delaying the degeneration of intervertebral discs. In this study, we analyzed a nature-derived protein tyrosine kinase inhibitor, Genistein, and its function in delaying IDD in rats both in vitro and in vivo via the p38 MAPK pathway. Nucleus pulposus cells treated with Genistein showed better function compared with untreated cells. Further study revealed that Genistein could play a protective role in IDD by inhibiting phosphorylation of p38, consequently inhibiting the p38 pathway-mediated inflammatory response. The rat IDD model also demonstrated that Genistein could effectively delay the degeneration of intervertebral disc tissue. The current study reveals new biological functions of Genistein, further demonstrates the effects of the p38 MAPK pathway on intervertebral disc degeneration, and deepens our understanding of the treatment and prevention of IDD.
Highlights
Intervertebral disc degeneration (IDD) is the most common diagnosis in patients with lower back pain
We found that IL-1β treatment reduced the mRNA expression level of COL2A1, aggrecan, and collagen X in a dose-dependent manner (Figure 1A–1C)
The reduction in the mRNA expression of aggrecan and COL2A1 was found after treatment with IL-1β at a concentration of 1 ng/mL (p
Summary
Intervertebral disc degeneration (IDD) is the most common diagnosis in patients with lower back pain. Degenerated discs can display high levels of inflammation, which can lead to stressinduced cell senescence and increased apoptosis [2] and can play a crucial role in disrupting tissue homeostasis. It is well known that inflammatory cytokines can activate multiple intracellular signaling cascades, leading to changes in gene expression and to various corresponding biological effects. The main kinases involved in the MAPK pathway cascade are MAPK kinase kinase (MKKK), MAPK kinase (MKK), and MAPK, which includes four www.aging-us.com subtypes: ERK, p38 MAPK, c-jun-terminal kinase, and ERK5. Among these subtypes, p38 MAPK is most closely associated with the regulation of inflammatory response [4]. The p38 MAPK pathway plays a central role in the regulation of various inflammatory response
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