Effect of Running with Different Intensities on Lubricin Expression of Achilles Tendon in a Rat Model

Abstract

Background: Lubricin is well known to facilitate the movement of tendon fascicles gliding and recoil against the surrounding tissues in tendons. However, little is known about its response under various mechanical loading conditions. This study was aimed to understand the effect of treadmill running with different exercise intensities on the alternations of lubricin content in rat Achilles tendon.Methods: In this study, eighteen rats were randomly divided into three groups, strenuous treadmill running (STR), moderate treadmill running (MTR), and control (CON). Rats in two running groups were subjected to treadmill running (8 weeks) protocol. Histological observation and biochemical analysis were conducted using the collected Achilles tendons.Results: After 8 weeks, the morphologies of collagen fibers are relatively parallel, crimping and elastic in the CON and MTR groups, but more ruptured in the STR group. The cell density in Achilles tendon sections markedly increased in MTR group than CON group, whereas considerably decreased in STR group than CON or MTR group. Additionally, compared to the CON group, the content of lubricin was dramatically increased in MTR group. However, the lubricin content in STR group was markedly decreased compared with that in CON or MTR group. Moreover, the TGF-β1 expression was upregulated in MTR group in contrast to CON group, while significantly downregulated in STR group than that in CON or MTR group. Conversely, the expression of IL-1 was statistically downregulated in MTR group compared with CON group, but statistically upregulated in STR group than that in CON or MTR group. Conclusions: These results suggest that moderate treadmill running might induce the increase of lubricin by the up-regulation of TGF-β1 expression to improved lubrication, and enhance the loading transmission efficiency. Whereas, strenuous treadmill running could result in the decrease of lubricin as a result of the dramatically increased expression of IL-1 to enhance interfascicular tribology, and predispose to tendinopathy even tendon rupture.