Infection and Drug Resistance (Jan 2019)
Platelet-rich plasma plays an antibacterial, anti-inflammatory and cell proliferation-promoting role in an in vitro model for diabetic infected wounds
Abstract
Tao Li,1 Yu Ma,2 Min Wang,1 Tao Wang,3 Jing Wei,4 Rui Ren,1 Min He,1 Guixue Wang,2 Johnson Boey,5 David G Armstrong,6 Wuquan Deng,2 Bing Chen1 1Department of Endocrinology, Southwest Hospital, Army Medical University, Chongqing, People’s Republic of China; 2Department of Endocrinology and Nephrology, Key Laboratory for Biorheological Science and Technology of Ministry of Education, Chongqing University, Affiliated Central Hospital of Chongqing University, Chongqing, People’s Republic of China; 3Institute of Combined Injury, State Key Laboratory of Trauma, Burn and Combined Injury, Army Medical University, Chongqing, People’s Republic of China; 4Department of Endocrinology, General Hospital of Xinjiang Military Region, The Chinese People’s Liberation Army, Urumqi, People’s Republic of China; 5Department of Podiatry, Singapore General Hospital, Singapore; 6Southwestern Academic Limb Salvage Alliance (SALSA), Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA Aim: This study was designed to examine the potential mechanism underlying these roles of platelet-rich plasma in treating diabetic foot ulcers (DFUs). Methods: Staphylococcus aureus and HaCaT were co-cultured under high glucose conditions to serve as an in vitro model for infected cells in DFUs. Platelet-rich gel (PRG) or extract liquid of platelet-rich gel (EPG) were used to interfere with the model to observe the growth of HaCaT cells and S. aureus, and the effect of miR-21 changes in HaCaT cells on PDCD4, NF-κB activity and related inflammatory factors. Results: Incubation of HaCaT cells with S. aureus promoted the decline of cell proliferation. Under this condition, the level of PDCD4 and the activity of NF-κB were increased in HaCaT cells with concomitant increased of IL-6, TNF-α and decreased IL-10, TGF-β1 in cultured supernatant. Both of PRG and EPG exhibited specific anti-S. aureus activity where they protect HaCaT cells from bacterial damage and promote cell proliferation. Meanwhile, EPG was observed to increase intracellular miRNA-21 while reduce PDCD4 expression and inhibit NF-κB activity to suppress the inflammation in HaCaT cells. Conclusion: This in vitro model provides a valuable tool for study of wound healing in the treatment of DFUs. Our results suggest that miRNA-21 may regulate the expression of NF-κB through PDCD4 where it plays an anti-inflammatory role and promote proliferation in infected DFUs treated by PRP. These findings could provide novel therapeutic targets for refractory wounds. Keywords: platelet-rich plasma, antibacterial, anti-inflammatory, cell proliferation-promoting, diabetic infected wound
