- 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.
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.
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/cm(2)). 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.