目的 評估腺苷受體A2A抑制劑ZM241385對骨折愈合生物力學(xué)的影響。方法 采用溫敏水凝膠聚乙交酯丙交酯（PLGA）-聚乙二醇（PEG）-聚乙交酯丙交酯（PLGA）溶解ZM241385制備緩釋系統(tǒng)。取20只大鼠隨機(jī)分為腺苷受體A2A抑制劑組與對照組，每組10只。制備大鼠股骨干骨折模型，造模時骨折局部應(yīng)用ZM241385緩釋系統(tǒng)，造模后每24 h骨折局部im相應(yīng)藥物，持續(xù)7 d。造模后第14、28天對大鼠骨折局部進(jìn)行micro-CT掃描，測量骨折局部總體積、骨體積、骨痂體積。通過Ansys Workbench 2017軟件進(jìn)行仿真分析，對大鼠骨折局部施加軸向以及旋轉(zhuǎn)應(yīng)力評估骨折生物力學(xué)強(qiáng)度。結(jié)果 腺苷受體A2A抑制劑組大鼠造模后14 d總體積、骨體積、骨痂體積均顯著低于對照組，差異有統(tǒng)計(jì)學(xué)意義（P＜0.05、0.01）。造模后28 d，腺苷受體A2A抑制劑組大鼠總體積、骨痂體積均超過對照組，差異具有統(tǒng)計(jì)學(xué)意義（P＜0.01），骨體積無統(tǒng)計(jì)學(xué)差異。當(dāng)軸向應(yīng)力為1、5、10 N或者旋轉(zhuǎn)應(yīng)力為0.5 N·m時，腺苷受體A2A抑制劑組造模后14、28 d最大應(yīng)力、最大應(yīng)變、平均位移均顯著高于對照組，差異具有統(tǒng)計(jì)學(xué)意義（P＜0.001）。結(jié)論 腺苷受體A2A抑制劑明顯抑制骨愈合，降低骨折局部軸向和旋轉(zhuǎn)的力學(xué)強(qiáng)度，腺苷受體A2A可能是發(fā)生二次骨折或骨不連的關(guān)鍵受體。

Objective To evaluate the effects of adenosine receptor A2A inhibitor on biomechanics strength of fracture healing. Methods PLGA-PEG-PLGA was used to dissolve receptor inhibitor to make drug delivery system. 20 rats were randomly divided into inhibitor group and control group with 10 rats in each group. The femoral shaft fracture rat model was made, and the drug release system was applied to the fracture site. Rats were received the corresponding drugs every 24h during seven days after modeling by fracture site injection. On the 14th and 28th day after modeling, micro CT scanning was performed to measure the total volume, bone volume and callus volume. Through the simulation analysis of ANASYS workbench 2017 software, the axial and rotational stresses were applied to evaluate the biomechanical strength of the fracture. Results The total fracture volume, bone volume and callus volume of the inhibitor group were significantly lower than those of the control group at 14 d after model (P < 0.05 and 0.01). At 28 d after modeling, the total volume and callus volume in adenosine receptor A2A inhibitor group were higher than those in control group, the differences were statistically significant (P < 0.05), but there was no significant difference in bone volume. When the axial stress was 1, 5, 10 N or the rotational stress was 0.5 N·m, the maximum stress, maximum strain and average displacement of the inhibitor group were significantly higher than those of the control group at 14 and 28 d after model (P < 0.001). Conclusion adenosine receptor A2A inhibitor inhibits bone healing and is closely related to bone biomechanical strength. After inhibiting the receptor, the axial and rotational mechanical strength of fracture decreased significantly, and secondary fracture or nonunion were prone to occur

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