4.6 Article

Effects of puerarin on the intervertebral disc degeneration and biological characteristics of nucleus pulposus cells

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PHARMACEUTICAL BIOLOGY
卷 61, 期 1, 页码 12-22

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TAYLOR & FRANCIS LTD
DOI: 10.1080/13880209.2022.2147548

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Apoptosis; inflammation; extracellular matrix; toll-like receptor 4/nuclear factor-?B

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Puerarin (PU) can delay the progression of intervertebral disc degeneration (IDD) by inhibiting activation of the TLR4/NF-kappa B pathway.
Context: Intervertebral disc degeneration (IDD) is the pathological basis of spinal degenerative diseases. Puerarin (PU) is an isoflavonoid with functions and medicinal properties. Objective: To explore the effect of PU on IDD and its potential mechanism of action. Materials and methods: Sprague-Dawley (SD) rats were divided into sham, IDD, low PU, and high PU groups. Rat nucleus pulposus cells (NPCs) were isolated and divided into control, IL-1 beta, 100 and 200 mu mol/mL PU, TAK-242 (TLR4 inhibitor), or 200 mu mol/mL PU + LPS (TLR4 activator) groups. The water content, inflammatory factors, proliferation activity, TLR4/NF-kappa B pathway activity, apoptosis rate, protein expression of apoptosis, and histology of the extracellular matrix (ECM) were analysed. Results: In vivo: Compared with the IDD group, disorganization of intervertebral disc tissue was significantly improved, water content (2.80 +/- 0.24 mg, 3.91 +/- 0.31 mg vs. 2.02 +/- 0.21 mg) and expression levels of collagen II and aggrecan were significantly increased, and the levels of inflammatory factors and the expression levels of TLR4, MyD88, and p-p65 were significantly decreased in IDD rats treated with PU. In vitro: Compared with the IL-1 beta group, the proliferation activity of IL-1 beta-treated NPCs and the expression of collagen II and aggrecan were significantly increased, while the apoptosis rate, levels of inflammatory factors, and the expression levels of TLR4, MyD88, and p-p65 were significantly decreased in IL-1 beta-treated NPCs treated with PU. LPS reversed the biological function changes of IL-1 beta-treated NPCs induced by PU. Conclusions: PU can delay the progression of IDD by inhibiting activation of the TLR4/NF-kappa B pathway.

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