海藻酸钠-成年软骨细胞培养移植修复成年兔关节软骨缺损的研究

目的 利用海藻酸纳-成年软骨细胞复合构建工程化软骨,并观察应用该工程软骨移植修复成年兔关节软骨缺损的长期效果。方法 取34周龄成年新西兰兔双膝关节软骨,分离软骨细胞.与海藻酸钠混合,细胞密度为4×10~6/ml,通过硅胶模型制成圆形柱状海藻酸纳-软骨细胞盘(20μl/个),体外培养。分别于2、4、6、8、10周取细胞盘,行苏木素-伊红(HE)、AB-PAS染色、免疫组织化学分析。同时选用成年新西兰兔28只,两侧股骨内髁造成全层软骨缺损模型,缺损处随机植入体外培养4周的海藻酸钠一软骨细胞盘(实验组)及无细胞的海藻酸钠载体(对照组),分别于术后6、12、24、48周取材,观察软骨缺损修复情况。结果 成年软骨细胞在海藻酸钠中呈丛状或球状增殖,4周时达增殖高峰,培养期内软骨细胞始终呈圆形或椭圆形,免疫组织化学显示盘中Ⅱ型胶原含量丰富,无Ⅰ型胶原产生。动物实验实验组软骨缺损以透明样软骨修复为主,对照组则以纤维组织填充为主,48周时两组修复组织均有一定程度退变。结论 成年软骨细胞在海藻酸钠中体外培养可维持良好的细胞表型,并形成工程化软骨。用此工程化软骨修复关节软骨损伤经48周观察有透明样软骨修复。     

兔关节软骨细胞体外培养的生物学特性及中药黄芪对其的影响

目的:研究兔关节软骨细胞与海藻酸钠复合体外培养的生物学特性及中药黄芪对其的影响。方法:取5个月龄兔膝关节软骨分离成软骨细胞悬液分组培养,A组只用培养液培养,B组用含2%黄芪注射液的培养液培养。分别于第2、4、6、8周进行细胞组织形态学、糖胺多糖(GAG)含量的测定及Ⅱ型胶原蛋白表达的观察。结果:①两组于第4～6周体外培养的软骨细胞合成糖胺多糖的能力及Ⅱ型胶原蛋白的表达均达高峰,6周后逐渐下降;②B组软骨细胞合成糖胺多糖及Ⅱ型胶原蛋白的能力均比同期A组增强,具有显著统计学意义(P<0.05)。结论:软骨细胞与海藻酸钠复合培养,可保持软骨细胞的表型,用其构建组织工程化软骨是可行的。黄芪有促进软骨细胞合成Ⅱ型胶原和GAG的作用。     

同种异体软骨细胞移植术后关节软骨蛋白多糖的测定

目的 应用Pluronic F-127负载同种异体软骨细胞移植修复兔全厚关节软骨损伤,对于新生的修复组织进行基质蛋白多糖含量测定,以探讨此方法修复全厚关节软骨损伤的可行性.方法 取3个月龄新西兰大白兔关节软骨细胞体外培养扩增,与20%Plurortic F-127凝胶混合.选27只健康同种成年大白兔,人为造成双侧膝关节软骨缺损.实验组软骨缺损处植入培养的软骨细胞/Pluronic F-127混合物,对照组缺损处单纯注入Pluronic F-127凝胶和空白对照.然后,对修复组织进行大体观察及蛋白多糖含量测定.结果 移植的软骨细胞-载体复合物中的软骨细胞能良好地生长,12周时再生组织与周围正常软骨组织外观相似,界限模糊.实验组与对照组各时期蛋白多糖含量均有非常显著性差异,实验组不同时期的蛋白多糖含量之间均有显著性差异,实验组12周时蛋白多糖含量与正常软骨组织无显著性差异.结论 Pluronic F-127负载同种异体软骨细胞移植是治疗关节软骨缺损的有效方法.     

软骨脱细胞基质对软骨细胞生物学功能的影响

目的 检测软骨脱细胞基质(ACM)对软骨细胞的生物学作用,探讨其作为软骨组织工程支架的可行性.方法 切取健康的雄性日本大耳白兔膝关节的软骨,经低温粉碎成软骨颗粒,通过多步骤酶方法将软骨颗粒行脱细胞处理,并用含20%胎牛血清的DMEM研磨制成ACM液.再切取兔膝关节的软骨,制成碎屑后分离培养软骨细胞.取培养第2、3代的软骨细胞,分成对照A组和B、C、D3个实验组(分别加入0.5、1.0、5.0ms/ml的ACM液).采用MTT法检测软骨细胞的活力,测定糖胺多糖的含量,以及H-胸腺嘧啶(3H-TdR)和3H-脯氨酸(3H-Pro)掺人法测定软骨细胞的增殖情况和胶原的合成能力.结果 ACM扫描电镜观察软骨巢内软骨细胞消失.软骨细胞在ACM液中生长良好,形态正常.B、C、D与A组相比,软骨细胞的生长活力分别增加了7.73%、13.50%、16.5%(P<0.05或P<0.01).糖胺多糖的含量在B组与A组相比其差异无统计学意义(P>0.05);而C、D组比A组增加了51.15%、62.68%(P<0.05或P<0.01).软骨细胞3H-TdR和3H-Pro掺入后,在B、C、D组中细胞的增殖及合成的胶原与A组相比,其差异均有统计学意义(P<0.01).结论 ACM能够提高软骨细胞的生长活力,增加糖胺多精的含量,刺激软骨细胞的增殖和胶原的合成,是可供选择的组织工程支架材料之一.     

骺板软骨细胞复合三维支架体外构建组织工程软骨的研究

目的探讨将骺板软骨细胞复合三维支架经体外培养,构建组织工程软骨的效果及其生物学特点. 方法将3周龄幼兔第1代骺板软骨细胞与液态的生物凝胶混合,接种于聚磷酸钙纤维/L-聚乳酸(CPPF/PLLA)三维支架材料,构建组织工程软骨组织块,连续培养4周.行大体、倒置显微镜及组织学、Ⅰ型和Ⅱ型胶原免疫组织化学光镜观察,定量检测硫酸糖胺多糖(GAG)含量. 结果构建的组织工程软骨块在培养过程中能保持其初始外形,种子细胞呈稳定的三维均相分布,外观逐渐呈乳白色、半透明,硬度亦不断增加.培养1周有软骨细胞陷窝形成,2周后形成富含Ⅱ型胶原和蛋白聚糖、具有典型软骨组织结构的工程化软骨,且Ⅰ型胶原逐渐转为阴性.4周时构建软骨的组织结构与天然骺板软骨相类似,硫酸GAG含量平均为天然骺板软骨的34%以上. 结论骺板软骨细胞复合三维支架体外培养可生成典型软骨,且可形成类似天然骺板软骨的组织结构,能满足修复骺板缺损的基本要求.体外培养1～2周可能是植入体内修复骺板缺损的较佳时机.     

关节软骨细胞三维支架双相接种体外生成软骨组织的观察

目的联合应用自制生物凝胶和三维支架材料,建立组织工程种子细胞的三维支架双相接种技术,并对其构建生成组织工程关节软骨的效果进行初步观察。方法酶消化法分离幼兔关节软骨细胞,于培养瓶中接种、培养,收集第1代软骨细胞,以2.5×107/ml加入液态的自制生物凝胶液中充分混均,制成细胞-凝胶混悬液,接种于CPPf/PLLA(caliumpolyphosphatefiber/poly-L-lacticacid)三维支架材料中,经固化后形成工程化组织块,体外连续培养4周。行大体、倒置显微镜以及组织学、Ⅰ型和Ⅱ型胶原免疫组化光镜观察,二甲基亚甲蓝显色法定量检测硫酸糖胺多糖含量。结果(1)细胞-凝胶混悬液接种后完全充满CPPf/PLLA支架的孔隙,固化后三者很好地形成一个工程化组织整体。构建的工程化组织块在培养过程中不仅能够保持其初始外形,而且能保持种子细胞稳定的三维均相分布,无细胞脱落现象。同时,硬度亦不断增加,有弹性,表面湿润、光滑。(2)随着培养时间的延长,软骨组织的形成是由外周向中心进行。培养2周后,逐渐形成富含Ⅱ型胶原和蛋白聚糖、具有典型软骨组织结构的成熟工程化软骨。同时,Ⅰ型胶原逐渐转为阴性,支架材料亦不断降解。4周时硫酸糖胺多糖含量平均为(15.70±2.00)mg/g(湿重),为天然关节软骨的30%以上。结论种子细胞的三维支架双相     

同种异体软骨细胞移植术后关节软骨蛋白多糖的测定

目的应用Pluronic F-127负载同种异体软骨细胞移植修复兔全厚关节软骨损伤，对于新生的修复组织进行基质蛋白多糖含量测定，以探讨此方法修复全厚关节软骨损伤的可行性。方法取3个月龄新西兰大白兔关节软骨细胞体外培养扩增，与20％Pluronic F-127凝胶混合。选27只健康同种成年大白兔，人为造成双侧膝关节软骨缺损。实验组软骨缺损处植入培养的软骨细胞／Pluronic F-127混合物，对照组缺损处单纯注入Pluronic F-127凝胶和空白对照。然后，对修复组织进行大体观察及蛋白多糖含量测定。结果移植的软骨细胞-载体复合物中的软骨细胞能良好地生长，12周时再生组织与周围正常软骨组织外观相似，界限模糊。实验组与对照组各时期蛋白多糖含量均有非常显著性差异，实验组不同时期的蛋白多糖含量之间均有显著性差异，实验组12周时蛋白多糖含量与正常软骨组织无显著性差异。结论Pluronic F-127负载同种异体软骨细胞移植是治疗关节软骨缺损的有效方法。     

双相支架负载软骨细胞修复兔关节软骨缺损

目的研究自固化磷酸钙/纤维蛋白凝胶(CPC/FG)双相支架负载软骨细胞修复兔关节软骨缺损的可行性和有效性.方法将分离培养的第3代软骨细胞包埋在CPC/FG双相支架的FG中,体外培养1周后,将软骨细胞-支架复合体移植修复兔膝关节股骨髁的软骨缺损(φ4 mm,深3.5 mm,达软骨下骨质).然后对软骨缺损的修复情况进行大体、光镜和电镜观察.同时对移植后第12周的修复软骨进行胶原含量测定,并与正常的关节软骨细胞胶原含量进行比较.结果移植的软骨细胞能在双相支架上良好地生长,软骨缺损以透明软骨的形式被修复,而对照组为纤维组织修复.多孔自固化磷酸钙在软骨修复过程中能起软骨下骨的临时替代作用.胶原含量测定显示:移植术后12周的修复软骨胶原含量为(43.25±0.85)%;正常的关节软骨胶原含量为(55.69±0.76)%,两者差异有显著性(P<0.01).结论 CPC/FG双相支架负载软骨细胞能以透明软骨的形式修复兔关节软骨缺损.新环境中移植的软骨细胞生长的不适应和FG降解过快,可能是导致新生修复软骨与自身正常关节软骨胶原含量有差异的原因.     

组织工程软骨的体外实验研究

目的 :研究软骨细胞在纤维胶内体外生成组织工程化软骨的可行性。方法 :将 4 - 10× 10 7cells/mL细胞 /毫升的软骨细胞植入纤维胶 ,在体外培养 2个月后进行组织学、免疫组织化学分析。结果 :细胞在纤维胶内产生大量的软骨特异性Ⅱ型胶原和蛋白多糖。结论 :纤维胶内的软骨细胞可在体外培养的环境下生成大量透明软骨基质。     

兔阴囊原位构建组织工程化睾丸假体的实验研究

目的探讨以HDPE-PGA复合支架接种兔耳软骨细胞后,于兔阴囊原位内构建组织工程化睾丸假体的可能性。方法取成年兔耳软骨分离培养软骨细胞,制备HDPE-PGA复合支架,细胞-支架复合物体外培养2w。摘除单侧兔睾丸后即时将经体外培养的细胞-支架复合物植入阴囊原位,术后3m将兔处死取材。单纯支架植入为对照组。标本行大体观察、组织学、组织化学、免疫组化、GAG含量检测。结果实验组取材标本经检测具有预制形态与体积,有新生软骨组织产生,软骨组织呈岛状分布,其间有不同程度的纤维组织长入及炎性细胞浸润。对照组无软骨形成。结论兔阴囊原位内构建组织工程化睾丸假体具有预制形态与体积、结构与组织学形态良好。     

杭州健康女性定量骨超声测定原发性骨质疏松

目的 评价杭州健康女性骨超声速度(SOS)值随增龄减少和骨质疏松患病率，建立杭州地区女性骨超声速度值参考数据库。方法 定量超声法测定1208例杭州地区健康女性桡骨远端(RAD)，第3指骨近节(PLX)，第V跖骨(MTR)和胫骨中段(TIB)的超声速度值。结果 RAD、PLX、MTR和TIBSOS峰值(Peak of SOS)均出现在40-45岁，TJB的SOS峰值出现在35—40岁，此后随年龄增长而下降。绝经后妇女在绝经后早期和晚期各有1个SOS快速减少期，前见于桡骨近端，平均年减少率为2．4％，后见于胫骨中段，平均年减少率为1．8％。各部位骨SOS累积减少率随年龄增长而增加，到85岁4部位累积减少为13％-18％。60岁以后骨质疏松性症(OP)检出率为45％-70％，OP检出率以桡骨远端最高，60-70岁平均为67％，第3指骨近端次之约50％，胫骨中段最低为36％；75岁以后分别为70％，65％和45％。结论 全身各部位骨超声速度值到达峰值的年龄不同，峰值也各有差异。绝经后妇女骨超声速度值随年龄增加减少较快，应予激素和补钙治疗，桡骨远端为本地区SOS检测和OP检出的敏感部位。     

Importance of echocardiography in prognosis of surgical outcomes in cholecystitis in elderly patients

The authors propose to use more often echocardiography (EchoCG) in examination of elderly (over 60 years) of age patients with cholecystitis that permits to increase surgical activity to 92.4%. Left ventricular ejection fraction is the most informative. When this fraction is lower than 45% surgery must be recommended on vital indications only. EchoCG was used in 155 patients with cholecystitis, 131 of them were operated. 2 (1.52%) patients died due to acute cardio-vascular insufficiency and pulmonary artery thromboembolism.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8～10周,体重18～22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7～11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.