Abstract

Burns are serious life-threatening health problems. This study was performed to determine the effect of educated platelets on burn wound healing process. 28 female wistar albino 200-220 gr rats were randomly divided into four groups. Group A1 rats(n:7) were the first-line burnt group from which blood samples are extracted to develop platelet-rich plasma(PRP) with the educated platelets that have a response to burn injury. Group B1 rats(n:7) were the unburnt group with ordinary platelets. Group A2 rats(n:8) were the second-line burnt group which was given PRP with educated platelets. Group B2 rats(n:6), as control group, were the second-line burnt group which was given PRP with ordinary platelets. Photos of rats' dorsum were taken by digital camera on the first day and 21st day of the study. Wound healing was determined by scar surface area. In the study group (Group A2) mean wound area was 53±37 mm², in the control group (Group B2) mean wound area was 114±55 mm² on the last day of the experiment. The sizes of the wounded areas were significantly lower in the study group compared with the control group (p: 0.039). Educated platelets seem to facilitate the recovery period of burn wound healing in rats.

Highlights

  • Platelets are small, nucleated, discoid cells with a diameter of 2-4 microns

  • In the light of this, we investigate if there is a relationship between acceleration of burn wound healing and educated platelets which are produced as a response to burn trauma

  • Group A1 rats(n:7) were the first line burnt group from which blood samples are extracted for platelet rich plasma (PRP) with the educated platelets that are response to the burn injury

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Summary

Introduction

Platelets are small, nucleated, discoid cells with a diameter of 2-4 microns They are produced from megakaryocytes which are precursor cells found in the bone marrow or intravascular regions of the lungs. Their prominent functions are blood coagulation and wound healing. Tumor educated platelets are the cells that enhance tumor cell proliferation and metastasis by several patophysiological pathways [3,4]. One of these is altered RNA profiles in TEPs that conduct different protein synthesis.

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