Impact of Preconditioned Diabetic Stem Cells and Photobiomodulation on Quantity and Degranulation of Mast Cells in a Delayed Healing Wound Simulation in Type One Diabetic Rats Publisher Pubmed



Ahmadi H¹ ; Bayat M^{1, 9} ; Amini A¹ ; Mostafavinia A² ; Ebrahimpourmalekshah R¹ ; Gazor R³ ; Asadi R⁴ ; Gachkar L⁵ ; Rezaei F⁶ ; Shafikhani SH⁷ ; Ghoreishi SK⁸ ; Chien S⁹
Source: Lasers in Medical Science Published:2022

Abstract

Herein, we report the influence of administering different protocols of preconditioned diabetic adipose-derived mesenchymal stem cells (ADSs) with photobiomodulation in vitro, and photobiomodulation in vivo on the number of mast cells (MCs), their degranulation, and wound strength in the maturation step of a Methicillin-resistant Staphylococcus aureus (MRSA)-infectious wound model in rats with type one diabetes. An MRSA-infectious wound model was generated on diabetic animals, and they were arbitrarily assigned into five groups (G). G1 were control rats. In G2, diabetic ADS were engrafted into the wounds. In G3, diabetic ADS were engrafted into the wound, and the wound was exposed to photobiomodulation (890 nm, 890 ± 10 nm, 80 Hz, 0.2 J/cm2) in vivo. In G4, preconditioned diabetic ADS with photobiomodulation (630 and 810 nm; each 3 times with 1.2 J/cm2) in vitro were engrafted into the wound. In G5, preconditioned diabetic ADS with photobiomodulation were engrafted into the wound, and the wound was exposed to photobiomodulation in vivo. The results showed that, the maximum force in all treatment groups was remarkably greater compared to the control group (all, p = 0.000). Maximum force in G4 and G5 were superior than that other treated groups (both p = 0.000). Moreover, G3, G4, and G5 showed remarkable decreases in completely released MC granules and total numbers of MC compared to G1 and G2 (all, p = 0.000). We concluded that diabetic rats in group 5 showed significantly better results in terms of accelerated wound healing and MC count of an ischemic infected delayed healing wound model. © 2021, The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature.