Ann Plast Surg. 2025 Dec 19. doi: 10.1097/SAP.0000000000004598. Online ahead of print.
ABSTRACT
BACKGROUND: The bradykinin B2 receptor (B2R), a type of G protein-coupled receptor, exerts several beneficial biological effects on flaps. Accordingly, we investigated the role of the bradykinin B2R in the survival of perforator flaps.
METHODS: In this study, a total of 50 male Sprague-Dawley rats were allocated equally into 2 groups: one receiving a bradykinin B2R blocker and the other serving as a control, with both groups undergoing flap procedures. Flap viability was assessed 7 days postoperatively by quantifying the surviving flap area. Blood perfusion within the flap was evaluated using laser Doppler imaging. The levels of Beclin-1, p62, and LC3-II/I were used to assess autophagy. The extent of flap angiogenesis was evaluated using immunohistochemistry and hematoxylin and eosin staining. Western blotting revealed the expression levels of vascular endothelial growth factor (VEGF) and the apoptotic index. Moreover, superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were used to evaluate oxidative stress. This study used a nitric oxide (NO) assay kit to determine NO production.
RESULTS: The bradykinin B2R blocker group exhibited significantly reduced flap survival areas (blocker group: 64.7 ± 3.36%; control group: 85.6 ± 3.35%; P < 0.01), diminished blood perfusion (blocker group: 389.8 ± 7.92; control group: 491.8 ± 5.81; P < 0.05), and decreased neovascularization (blocker group: 20.13 ± 1.58; control group: 52.17 ± 1.49; P < 0.05). Compared to the control group, the bradykinin B2R blocker group also demonstrated lower SOD activity, NO content, and VEGF expression, and increased MDA levels (all P < 0.05). Rats treated with the bradykinin B2R blocker exhibited higher levels of autophagy and apoptosis than those observed in the control group.
CONCLUSION: According to our research, the bradykinin B2R protects multiterritory perforator flaps through diverse molecular pathways, which involve inhibiting apoptosis, combating oxidation, modulating autophagy, and fostering angiogenesis to improve the blood supply to the flap.
PMID:41418072 | DOI:10.1097/SAP.0000000000004598