炎症,皮质类固醇,加载都会影响肌腱愈合,他们之间的互动。然而,皮质类固醇作用背后的潜在机制以及与负荷的相互作用仍不清楚.这项研究的目的是探讨地塞米松在肌腱愈合过程中的作用,包括对腱细胞的特定作用。大鼠(n=36)被随机分配到重负荷或轻度负荷,跟腱被切断,和动物用地塞米松或生理盐水治疗。对于细胞外基质,进行了愈合肌腱的基因和蛋白质分析。炎症-,和肌腱细胞标记。我们进一步测试了地塞米松在体外对腱细胞的特定作用。地塞米松增加S100A4的mRNA水平,降低ACTA2/α-SMA的水平,无论负载水平。重负荷+地塞米松降低FN1和TenC的mRNA水平(p<0.05),而分辨率相关基因未改变(p>0.05)。相比之下,轻度负荷+地塞米松增加分辨率相关基因ANXA1,MRC1,PDPN,和PTGES(p<0.03)。在轻度负荷的肌腱中证实了蛋白质水平的改变。地塞米松体外治疗可防止肌腱结构形成,S100A4mRNA水平升高,SCX和胶原蛋白水平降低。在肌腱愈合过程中,地塞米松似乎通过促进分辨率的免疫调节起作用,而且还通过对腱细胞的影响。
Inflammation, corticosteroids, and
loading all affect tendon healing, with an interaction between them. However, underlying mechanisms behind the effect of corticosteroids and the interaction with
loading remain unclear. The aim of this study was to investigate the role of dexamethasone during tendon healing, including specific effects on tendon cells. Rats (n = 36) were randomized to heavy
loading or mild
loading, the Achilles tendon was transected, and animals were treated with dexamethasone or saline. Gene and protein analyses of the healing tendon were performed for extracellular matrix-, inflammation-, and tendon cell markers. We further tested specific effects of dexamethasone on tendon cells in vitro. Dexamethasone increased mRNA levels of S100A4 and decreased levels of ACTA2/α-SMA, irrespective of load level. Heavy
loading + dexamethasone reduced mRNA levels of FN1 and TenC (p < 0.05), while resolution-related genes were unaltered (p > 0.05). In contrast, mild loading + dexamethasone increased mRNA levels of resolution-related genes ANXA1, MRC1, PDPN, and PTGES (p < 0.03). Altered protein levels were confirmed in tendons with mild
loading. Dexamethasone treatment in vitro prevented tendon construct formation, increased mRNA levels of S100A4 and decreased levels of SCX and collagens. Dexamethasone during tendon healing appears to act through immunomodulation by promoting resolution, but also through an effect on tendon cells.