Link protein N-terminal peptide and fullerol promote matrix production and decrease degradation enzymes in rabbit annulus cells.
Link protein N-terminal peptide and fullerol promote matrix production and decrease degradation enzymes in rabbit annulus cells.
复制标题
连接蛋白 N 端肽和富勒醇可促进兔环状细胞中的基质生成并减少降解酶。
DOI：
10.1080/03008207.2017.1330333
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发表时间：
2018
影响因子：
2.9
通讯作者：
Li,Xudong
中科院分区：
文献类型：
--
作者：
Yeh,Ching-Hua;Chen,Dennis;Aghdasi,Bayan;Xiao,Li;Ding,Mengmeng;Jin,Li;Li,Xudong
目的：腰椎间盘退变是引起腰背痛的主要原因。需要预防或逆转椎间盘退变的新疗法。材料和方法：在3D培养模型中评价连接蛋白N端肽(LN)和富勒醇对纤维环细胞的联合再生能力。结果：富勒醇(IL-1α，IL-1α)诱导的纤维环细胞变性可被富勒醇、富勒醇和富勒醇+LN拮抗，其中富勒醇+LN对基质生成的影响最大。IL-1α诱导的促炎介质(IL-6和环氧合酶-2)和基质金属蛋白酶(MMP1、-2、-9和-13)的增加也可被富勒醇和LN所拮抗。结论：LN和富勒醇单独及联合应用可促进房颤细胞产生基质，并具有抗炎和抗分解代谢作用。
Purpose: Intervertebral disc degeneration is a major cause of back pain. Novel therapies for prevention or reversal of disc degeneration are needed. It is desirable for potential therapies to target both inflammation and matrix degeneration.Materials and Methods: The combined regenerative potential of link protein N-terminal peptide (LN) and fullerol on annulus fibrosus (AF) cells was evaluated in a 3D culture model.Results: Interleukin-1α (IL-1α)-induced AF cell degeneration was counteracted by fullerol, LN, and fullerol + LN, with the latter having the greatest effect on matrix production as evaluated by real-time polymerase chain reaction and glycosaminoglycan assay. IL-1α-induced increases in pro-inflammatory mediators (interleukin-6 and cyclooxygenase-2) and matrix metalloproteinases (MMP-1, -2, -9, and -13) were also counteracted by fullerol and LN.Conclusion: Our data demonstrate that LN and fullerol individually, and in combination, promote matrix production and have anti-inflammatory and anti-catabolic effects on AF cells.