Department of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, 377-2 Ohnohigashi, Osakasayama, Osaka, 589-8511, Japan.
Life Science Research Institute, Kindai University Faculty of Medicine, 377-2 Ohnohigashi, Osakasayama, Osaka, 589-8511, Japan.
J Bone Miner Metab. 2022 Sep;40(5):735-747. doi: 10.1007/s00774-022-01353-3. Epub 2022 Aug 4.
Irisin is a proteolytic product of fibronectin type II domain-containing 5, which is related to the improvement in glucose metabolism. Numerous studies have suggested that irisin is a crucial myokine linking muscle to bone in physiological and pathophysiological states.
We examined the effects of local irisin administration with gelatin hydrogel sheets and intraperitoneal injection of irisin on the delayed femoral bone repair caused by streptozotocin (STZ)-induced diabetes in female mice. We analyzed the femurs of mice using quantitative computed tomography and histological analyses and then measured the mRNA levels in the damaged mouse tissues.
Local irisin administration significantly blunted the delayed bone repair induced by STZ 10 days after a femoral bone defect was generated. Local irisin administration significantly blunted the number of Osterix-positive cells that were suppressed by STZ at the damaged site 4 days after a femoral bone defect was generated, although it did not affect the mRNA levels of chondrogenic and adipogenic genes 4 days after bone injury in the presence or absence of diabetes. On the other hand, intraperitoneal injection of irisin did not affect delayed bone repair induced by STZ 10 days after bone injury. Irisin significantly blunted the decrease in Osterix mRNA levels induced by advanced glycation end products or high-glucose conditions in ST2 cells in the presence of bone morphogenetic protein-2.
We first showed that local irisin administration with gelatin hydrogel sheets improves the delayed bone repair induced by diabetic state partially by enhancing osteoblastic differentiation.
鸢尾素是纤维连接蛋白 II 型结构域包含 5 的蛋白水解产物，与葡萄糖代谢的改善有关。大量研究表明，鸢尾素是一种关键的肌因子，将肌肉与生理和病理状态下的骨骼联系起来。
我们检查了局部给予明胶水凝胶片和腹腔内注射鸢尾素对链脲佐菌素（STZ）诱导的糖尿病雌性小鼠延迟性股骨骨修复的影响。我们使用定量计算机断层扫描和组织学分析分析了小鼠的股骨，然后测量了受损小鼠组织中的 mRNA 水平。
局部给予鸢尾素可显著减轻 STZ 诱导的骨修复延迟，在股骨骨缺损形成 10 天后。局部给予鸢尾素可显著减少 STZ 在股骨骨缺损形成 4 天后受损部位的 Osterix 阳性细胞数量，尽管它不影响糖尿病存在或不存在时骨损伤后 4 天软骨和成脂基因的 mRNA 水平。另一方面，腹腔内注射鸢尾素不能影响 STZ 诱导的骨损伤 10 天后的延迟性骨修复。鸢尾素在骨形态发生蛋白-2 存在下显著减弱了 ST2 细胞中晚期糖基化终产物或高葡萄糖条件下 Osterix mRNA 水平的降低。
我们首次表明，局部给予明胶水凝胶片的鸢尾素可通过增强成骨细胞分化，部分改善糖尿病状态引起的延迟性骨修复。
