Evaluating the Effect of Low-Level Laser Therapy on Healing of Tentomized Achilles Tendon in Streptozotocin-Induced Diabetic Rats by Light Microscopical and Gene Expression Examinations Publisher Pubmed



Aliodoust M¹ ; Bayat M² ; Jalili MR¹ ; Sharifian Z³ ; Dadpay M⁴ ; Akbari M⁵ ; Bayat M² ; Khoshvaghti A⁴ ; Bayat H⁷
Source: Lasers in Medical Science Published:2014

Abstract

Tendon healing is impaired in individuals diagnosed with diabetes mellitus (DM). According to research, there is considerable improvement in the healing of surgically tenotomized Achilles tendons following low-level laser therapy (LLLT) in non-diabetic, healthy animals. This study uses light microscopic (LM) and semi-quantitative reverse transcription PCR (RT-PCR) analyses to evaluate the ability of LLLT in healing Achilles tendons from streptozotocin-induced diabetic (STZ-D) rats. A total of 88 rats were randomly divided into two groups, non-diabetic and diabetic. DM was induced in the rats by injections of STZ. The right Achilles tendons of all rats were tenotomized 1 month after administration of STZ. Laser-treated rats were treated with a helium-neon (He-Ne) laser that had a 632.8-nm wavelength and 7.2-mW average power. Experimental group rats received a daily dose of 0.014 J (energy density, 2.9 J/cm2). Control rats did not receive LLLT. Animals were sacrificed on days 5, 10, and 15 post-operatively for semi-quantitative LM and semi-quantitative RT-PCR examinations of transforming growth factor-beta1 (TGF-β1) gene expression. The chi-square test showed that LLLT significantly reduced inflammation in non-diabetic rats compared with their non-diabetic controls (p = 0.02). LLLT significantly decreased inflammation in diabetic rats on days 5 (p = 0.03) and 10 (p = 0.02) compared to the corresponding control diabetic rats. According to the student's t test, LLLT significantly increased TGF-β1 gene expression in healthy (p = 0.000) and diabetic (p = 0.000) rats compared to their relevant controls. The He-Ne laser was effective in altering the inflammatory reaction and increasing TGF-β1 gene production. © 2014 Springer-Verlag.