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Tanshinone IIA Prevent Tendon Adhesion in the Rat Achilles Tendon Model

机译:丹参酮IIA预防大鼠跟腱肌腱模型中的肌腱粘连

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Background: Tendon adhesion between the sheath and tendon surface is a common clinical problem. Orthopedist makes the improvement of repair techniques and rehabilitation to treat tendon adhesion, but it fails to cure completely. TSA was one of the major active phytochemicals because of its anti-inflammatory activity. We used tanshinone IIA (TSA) for the prevention of tendon adhesion in the rat Achilles tendon model and investigated the possible mechanisms, including microRNAs (miRNAs) and protein expression via TGF-beta/Smad signaling pathway. Method: Sprague-Dawley (SD) rat Achilles tendons were half partial lacerated and sutured by a modified Kessler's technique, with TSA and normal saline for control. Macroscopic and histological evaluations were applied to examine the injured tendon six weeks after surgery. We evaluated the degree of adhesion in Gross observation and the remodeling of collagen fibers by observing microscopically and determining the amount of scar formation. The expression of microRNAs (miRNAs) was quantified by real-time PCR detection and protein expression were quantified by western blotting detection. Results: In gross evaluation of tendon adhesion, the TSA group had less adhesion appeared. No evidences of tendon rupture or local infection were observed. The content of collagen fibers in tendon tissue was decreased in TSA group compared with the control group, it indicated a significant difference from the control group, P = 0.0004. The expression of miRNAs including miR-155, miR-29b, miR21, miR-133b and let7 were detected in the repaired tendon tissue, and only miR-29b treated with TSA was observed significantly higher than control group, P < 0.0001. The protein expression of TGF-beta 1 and p-Smad3 treated with TSA was lower than control group. Conclusions: The usage of TSA may be an efficient approach for preventing tendon adhesion.
机译:背景:鞘和肌腱表面之间的肌腱粘连是常见的临床问题。骨科医生对修复肌腱粘连的修复技术和康复进行了改进,但无法完全治愈。由于其抗炎活性,TSA是主要的活性植物化学物质之一。我们使用丹参酮IIA(TSA)预防大鼠跟腱模型中的肌腱粘连,并研究了可能的机制,包括通过TGF-beta / Smad信号通路的microRNA(miRNA)和蛋白质表达。方法:用改良的Kessler技术将Sprague-Dawley(SD)大鼠跟腱部分撕裂并缝合,用TSA和生理盐水进行控制。术后六周进行肉眼和组织学评估以检查受伤的肌腱。我们通过肉眼观察并确定疤痕形成的数量,评估了肉眼观察的粘附程度和胶原纤维的重塑。通过实时PCR检测定量microRNA(miRNA)的表达,通过蛋白质印迹检测定量蛋白质的表达。结果:在对肌腱粘连的总体评估中,TSA组出现的粘连较少。没有观察到肌腱破裂或局部感染的迹象。与对照组相比,TSA组肌腱组织胶原纤维含量降低,与对照组相比差异有统计学意义,P = 0.004。在修复的肌腱组织中检测到miRNA的表达,包括miR-155,miR-29b,miR21,miR-133b和let7,只有经TSA处理的miR-29b显着高于对照组,P <0.0001。 TSA处理的TGF-β1和p-Smad3的蛋白表达低于对照组。结论:TSA的使用可能是预防肌腱粘连的有效方法。

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