Abstract

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-β/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-β1 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.

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