Chinese Journal of Tissue Engineering Research ›› 2018, Vol. 22 ›› Issue (6): 921-926.doi: 10.3969/j.issn.2095-4344.0069

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Autologous platelet-rich plasma in combination with tendon stem cells to treat tendinopathy in a rabbit model: histomorphological changes of the tendon tissue and matrix metalloproteinase 1 expression

Xian Jie, He Ben-xiang, Wu Xiao, Tan Ya-jun
  

  1. Chengdu Sport Institute, Chengdu 610041, Sichuan Province, China
  • Received:2017-09-08 Online:2018-02-28 Published:2018-02-28
  • Contact: He Ben-xiang, M.D., Chief physician, Doctoral supervisor, Chengdu Sport Institute, Chengdu 610041, Sichuan Province, China
  • About author:Xian Jie, Master, Chengdu Sport Institute, Chengdu 610041, Sichuan Province, China
  • Supported by:
    the Key Project of Science and Technology Department of Sichuan Province, No. 2016JY0052; Science and Technology Support Project of Science and Technology Department of Sichuan Province, No. 2014SZ0003; the Master Project of Chengdu Sport Institute, No. 16SSZX01

Abstract:

BACKGROUND: The research and application of platelet-rich plasma in tissue regeneration and restoration have always been an issue of concern in the medicine and bioengineering fields.
OBJECTIVE: To analyze the effects of platelet-rich plasma in combination with tendon stem cells on histomorphology change and matrix metalloproteinase 1 expression of the tendon tissues in a rabbit model of Achilles tendinopathy.
METHODS: Forty New Zealand white rabbits were randomly divided into model group (n=32) and blank control group (n=8). In the model group, the animals were injected about 2 cm distant to the attachment point of the left calcaneus with prostaglandin E2 (once a week, for totally 4 weeks) to make the animal model of tendinopathy. The rabbits in the blank control group were injected the equal amount of normal saline. After 4 weeks, model rabbits were randomly divided into four subgroups: combination group, tendon stem cell group, platelet-rich plasma group and model control group, with eight rabbits in each group. Platelet-rich plasma and tendon stem cells, alone or in combination, and normal saline were injected into the corresponding group, twice with an interval of 3 weeks. At 6 weeks after injection, the tendon tissue was collected and stained for histological examination and detection of matrix metalloproteinase 1 expression.
RESULTS AND CONCLUSION: (1) Hematoxylin-eosin staining: the tendon fibers in the combinationgroup were intact and arranged orderly; in the tendon stem cell group, the tendon fibers were almost arranged orderly despite some fractured fibers; in the platelet-rich plasma group, fiber breakage and loose fiber structure were observed; in the model control group, there were no intact tendon fibers, with the presence of inflammatory cell filtration. (2) Masson staining: The tendon fibers in the combination group had slight wave-shaped changes but the fibers were not cut off; in the tendon stem cell group, the tendon fibers were slightly in disorder, but with the intact structure, and obvious inflammatory cell filtration was observed; in the platelet-rich plasma group, fiber breakage, reduced collagen fibers and inflammatory cell filtration were obviously observed; in the model control group, there were no intact tendon fibers, and inflammatory cell filtration was clearly visible. (3) The expression of matrix metalloproteinase 1: Compared with the blank control group, the expression of matrix metalloproteinase 1 was significantly higher in the other groups except the combination group (P < 0.05). There was no significant difference in the expression of matrix metalloproteinase 1 between the combination group and blank control group (P > 0.05). To conclude, the combination of platelet-rich plasma and tendon stem cells can inhibit the vicious cycle of degeneration of collagen and extracellular matrix, reduce the expression of matrix metalloproteinase 1 in tenocytes, and delay inflammation responses and degeneration due to tendinopathy.

Key words: Platelet-Rich Plasma, Stem Cells, Tendinopathy, Metalloproteases, Tissue Engineering

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