Otrocka-Domagała Iwona, Paździor-Czapula Katarzyna, Gesek Michał
Department of Pathological Anatomy, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowskiego Street 13, 10-719, Olsztyn, Poland.
BMC Vet Res. 2019 Feb 11;15(1):56. doi: 10.1186/s12917-019-1804-1.
Due to the routine use of dexamethasone (DEX) in veterinary and human medicine and its negative impact on the rate of wound healing and skeletal muscle condition, we decided to investigate the effect of DEX on the inflammatory and repair phases of skeletal muscle regeneration. In this study, a porcine skeletal muscle injury model was used. The animals were divided into non-treated and DEX-treated (0.2 mg/kg/day) groups. On the 15th day of DEX administration, bupivacaine hydrochloride-induced muscle injury was performed, and the animals were sacrificed in subsequent days. Regeneration was assessed by histopathology and immunohistochemistry. In the inflammatory phase, the presence and degree of extravasation, necrosis and inflammation were evaluated, while in the repair phase, the numbers of muscle precursor cells (MPCs), myotubes and young myofibres were estimated.
In the inflammatory phase, DEX increased the severity and prolonged extravasation, prolonged necrosis and inflammation at the site of the muscle injury. In the repair phase, DEX delayed and prolonged MPC presence, impaired and prolonged myotube formation, and delayed young myofibre formation. Furthermore, DEX markedly affected the kinetics of the parameters of the inflammatory phase of the skeletal muscle regeneration more than that of the repair phase.
DEX impairment of the inflammatory and repair phases of the skeletal muscle regeneration was proven for the first time. The drug appears to affect the inflammatory phase more than the repair phase of regeneration. In light of our results, the possibility of reduction of the regenerative capacity of skeletal muscles should be considered during DEX therapy, and its use should be based on risk-benefit assessment.
由于地塞米松（DEX）在兽医学和人类医学中的常规使用及其对伤口愈合速度和骨骼肌状况的负面影响，我们决定研究DEX对骨骼肌再生的炎症和修复阶段的影响。在本研究中，使用了猪骨骼肌损伤模型。动物被分为未治疗组和DEX治疗组（0.2毫克/千克/天）。在给予DEX的第15天，进行盐酸布比卡因诱导的肌肉损伤，并在随后的几天内处死动物。通过组织病理学和免疫组织化学评估再生情况。在炎症阶段，评估血管外渗、坏死和炎症的存在及程度，而在修复阶段，估计肌肉前体细胞（MPC）、肌管和年轻肌纤维的数量。
在炎症阶段，DEX增加了肌肉损伤部位的严重程度，延长了血管外渗、坏死和炎症的时间。在修复阶段，DEX延迟并延长了MPC的存在时间，损害并延长了肌管形成时间，延迟了年轻肌纤维的形成。此外，DEX对骨骼肌再生炎症阶段参数动力学的影响明显大于修复阶段。
首次证实DEX对骨骼肌再生的炎症和修复阶段有损害作用。该药物对再生炎症阶段的影响似乎大于修复阶段。根据我们的研究结果，在DEX治疗期间应考虑骨骼肌再生能力降低的可能性，其使用应基于风险效益评估。
