Platelet-rich plasma plays an antibacterial, anti-inflammatory and cell proliferation-promoting role in an in vitro model for diabetic infected wounds
Received 6 September 2018
Accepted for publication 27 December 2018
Published 29 January 2019 Volume 2019:12 Pages 297—309
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Eric Nulens
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
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