中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2015年
4期
353-359
,共7页
管大凡%刘洪美%张聪%李庆伟%陈国武%梁啸%孟纯阳
管大凡%劉洪美%張聰%李慶偉%陳國武%樑嘯%孟純暘
관대범%류홍미%장총%리경위%진국무%량소%맹순양
骨形态发生蛋白质类%血管内皮生长因子类%骨缺损
骨形態髮生蛋白質類%血管內皮生長因子類%骨缺損
골형태발생단백질류%혈관내피생장인자류%골결손
Bone morphogenetic proteins%Vascular endothelial growth factors%Bone defect
目的 评估骨形态发生蛋白2/血管内皮生长因子165(hBMP2/hVEGF165)双基因腺病毒转染骨髓间充质干细胞(BMSCs)复合多孔纳米羟基磷灰石/聚酰胺66(n-HA/PA66)对骨缺损的修复作用.方法 选取60只成年雄性新西兰大白兔,制作15 mm双侧桡骨中段骨缺损模型.按完全随机法分为3组,各组20只,根据双侧桡骨制作骨缺损模型,各大组分2小组,共6组.A1组:左桡骨缺损处不植入任何材料为空白对照组;A2组:右桡骨缺损处单纯植入n-HA/PA66人工骨材料;B1组:左桡骨缺损处植入hVEGF165/BMSCs/n-HA/PA66人工骨材料;B2组:右桡骨缺损处植入BMP2/BMSCs/n-HA/PA66人工骨材料;C1组:左桡骨缺损处植入BMSCs/n-HA/PA66人工骨材料;C2组:右桡骨缺损处植入hBMP2/hVEGF165/BMSCs/n-HA/PA66人工骨材料.分别于2,4,8,12周行X线片、HE和Masson染色观察桡骨缺损修复情况.结果 C2组术后8周X线片、HE和Masson染色显示移植部位有大量软骨形成,且在边缘有大量骨组织生成,术后12周可见组织材料被外层骨组织包裹,骨缺损修复效果优于其他组(P<0.05);且术后各时相点C2组血管数目均优于其他组(P<0.05),B1组各时相点血管数均多于B2组(P<0.05),且两组明显多于A2、C1组(P <0.05);A2与C1组间差异无统计学意义(P>0.05).结论 hBMP2/hVEGF165双基因转染BMSCs复合多孔n-HA/PA66具有明显提高修复兔桡骨干缺损的作用.
目的 評估骨形態髮生蛋白2/血管內皮生長因子165(hBMP2/hVEGF165)雙基因腺病毒轉染骨髓間充質榦細胞(BMSCs)複閤多孔納米羥基燐灰石/聚酰胺66(n-HA/PA66)對骨缺損的脩複作用.方法 選取60隻成年雄性新西蘭大白兔,製作15 mm雙側橈骨中段骨缺損模型.按完全隨機法分為3組,各組20隻,根據雙側橈骨製作骨缺損模型,各大組分2小組,共6組.A1組:左橈骨缺損處不植入任何材料為空白對照組;A2組:右橈骨缺損處單純植入n-HA/PA66人工骨材料;B1組:左橈骨缺損處植入hVEGF165/BMSCs/n-HA/PA66人工骨材料;B2組:右橈骨缺損處植入BMP2/BMSCs/n-HA/PA66人工骨材料;C1組:左橈骨缺損處植入BMSCs/n-HA/PA66人工骨材料;C2組:右橈骨缺損處植入hBMP2/hVEGF165/BMSCs/n-HA/PA66人工骨材料.分彆于2,4,8,12週行X線片、HE和Masson染色觀察橈骨缺損脩複情況.結果 C2組術後8週X線片、HE和Masson染色顯示移植部位有大量軟骨形成,且在邊緣有大量骨組織生成,術後12週可見組織材料被外層骨組織包裹,骨缺損脩複效果優于其他組(P<0.05);且術後各時相點C2組血管數目均優于其他組(P<0.05),B1組各時相點血管數均多于B2組(P<0.05),且兩組明顯多于A2、C1組(P <0.05);A2與C1組間差異無統計學意義(P>0.05).結論 hBMP2/hVEGF165雙基因轉染BMSCs複閤多孔n-HA/PA66具有明顯提高脩複兔橈骨榦缺損的作用.
목적 평고골형태발생단백2/혈관내피생장인자165(hBMP2/hVEGF165)쌍기인선병독전염골수간충질간세포(BMSCs)복합다공납미간기린회석/취선알66(n-HA/PA66)대골결손적수복작용.방법 선취60지성년웅성신서란대백토,제작15 mm쌍측뇨골중단골결손모형.안완전수궤법분위3조,각조20지,근거쌍측뇨골제작골결손모형,각대조분2소조,공6조.A1조:좌뇨골결손처불식입임하재료위공백대조조;A2조:우뇨골결손처단순식입n-HA/PA66인공골재료;B1조:좌뇨골결손처식입hVEGF165/BMSCs/n-HA/PA66인공골재료;B2조:우뇨골결손처식입BMP2/BMSCs/n-HA/PA66인공골재료;C1조:좌뇨골결손처식입BMSCs/n-HA/PA66인공골재료;C2조:우뇨골결손처식입hBMP2/hVEGF165/BMSCs/n-HA/PA66인공골재료.분별우2,4,8,12주행X선편、HE화Masson염색관찰뇨골결손수복정황.결과 C2조술후8주X선편、HE화Masson염색현시이식부위유대량연골형성,차재변연유대량골조직생성,술후12주가견조직재료피외층골조직포과,골결손수복효과우우기타조(P<0.05);차술후각시상점C2조혈관수목균우우기타조(P<0.05),B1조각시상점혈관수균다우B2조(P<0.05),차량조명현다우A2、C1조(P <0.05);A2여C1조간차이무통계학의의(P>0.05).결론 hBMP2/hVEGF165쌍기인전염BMSCs복합다공n-HA/PA66구유명현제고수복토뇨골간결손적작용.
Objective To assess the effect of bone defect repair using the recombinant of adenovirus-mediated hBMP2 and hVEGF165 genes transfer of BMSCs with porous nano-hydroxyapatite/polyamide 66 (n-HA/PA66).Methods Sixty male adult New Zealand rabbits were assigned to groups A,B and C according the completely random design,with 20 rabbits per group.Bone defect of 15 mm in length was made in the middle segment of bilateral radii in rabbits.In Group A,the defects were filled with nothing on the left side in blank controls (Group A1) and with n-HA/PA66 material alone on the right side (Group A2).In Group B,the defects were filled with hVEGF165/BMSCs/n-HA/PA66 on the left side (Group B1) and hBMP2/BMSCs/n-HA/PA66 on the right side (Group B2).In Group C,the defects were filled with BMSCs/n-HA/PA66 on the left side (Group C1) and hBMP2/hVEGF165/BMSCs/n-HA/PA66 on the right side (Group C2).Radiological analysis,HE staining,and Masson coloration were performed 2,4,8 and 12 weeks after operation.Results Radiographs,HE staining and Masson staining taken 8 weeks after cell transplantation showed large amount of new cartilage grown into the defect area and massive bony tissue formation around the margin in Group C2.At postoperative 12 weeks,Group C2 showed transplants were surrounded by outer bone tissues with superior bone repair effect to other groups (P < 0.05).Number of vessels in Group C2 increased compared with that in other groups (P < 0.05).Number of vessels was greater in Group B1 than in Group B2 (P < 0.05),and both were greater than those in Groups A2 and C1 (P < 0.05).Moreover there was no significant difference between Groups A2 and C1 (P >0.05).Conclusion hBMP2/hVEGF165 genes transferred BMSCs seeded on porous n-HA/PA66 can contribute to osteogenesis during the repair of rabbit radius defect.