Background: Muscle injury is the most frequent event among sportsmen of various modalities, reaching 55% of injury’s cases in athletes and occurs in both recreational and competitive
activities. Recent studies involving athletes from professional football revealed about 4483 injuries could occur after 500,000 hours of gameplay, being 35.2% muscle injuries reaching an average of 2
injuries per season for each player. The re-injury of the hind limbs is responsible for 27% of absences competition and basically occurs by inefficient healing. The muscle tissue remodeling after
injury is a very complex and dynamic process and the role of kinin receptors in this process is very little explored.
Methods: To understand the role of these receptors in the healing process, one muscle injury model was previously established in C57Bl6 mice. After injury, WT (wild-type) and knockout
mice with the same genetic background (B1KO mice, B2KO mice and B1B2KO mice) were analyzed in the following times: 0, 4, 8, 15 and 30 days. (All the procedures were reviewed and approved by the
Research Ethics Committee of UNIFESP-EPM).
Results: Injured B1KO mice showed a slow progress of the injury area with around 2.5 times smaller than WT injury. B1B2KO showed an injury area 3.5 and 2.8 times smaller than WT on
the 4th and 8th day, respectively. About the tissue regenerative potential, B1KO showed large amount of the centrally nucleated fiber on the 8th, 15th and 30th day post-injury compared with WT (75%,
39% and 29% versus 58.7%, 9.21% and 4.5%, respectively), as well as B2KO mice on the 15th and 30th day (41.2% and 20.7% respectively). B1B2KO showed a small area of regeneration on the 4th day (2.7%),
with a significant percentage on the 30th day post-injury (20%), compared with WT mice. However, all KO mice showed a significant increase in the fibrosis tissue compared with WT, especially in the
B1B2KO which showed an accelerated fibrosis and collagen deposition on the 4th and 8th day. The groups showed a different inflammatory cell profile. WT mice showed an inflammatory burst in the 4th day
(1068± 278.3 cell/HPF) followed by a decrease on the 8th day until 601± 164 cell/HPF. In contrast, B1KO showed an increase of 425± 233.5 (4th day) to 1015± 292.6 (8th day) cell/HPF, maintaining a
small population of the 221± 128.6 cell/HPF in the 15th day post-injury. B1B2KO showed a similar profile of inflammation compared with B1KO. B2KO showed a similar profile of inflammation compared with
WT, but with an 44% and 55% increase in the 4th and 8th day, respectively.
Conclusions: These results show that kinin B1 and B2 receptors can regulate the healing process during the repair of injured skeletal muscle and show the potential of this molecular
manipulation in clinical research studies, especially in rehabilitation treatments.