抑制巨噬细胞对异种胰岛移植物的作用

目的　观察普伐他汀 (pravastatin)对异种胰岛移植物存活的影响。方法　将猪→小鼠胰岛移植模型分成A组 (对照组 )、B组 (CsA组 )、C组 (普伐他汀组 )、D组 (CsA +普伐他汀组 )。观察指标 :移植物存活时间、病理检查、免疫组化染色、血清NO含量及移植物IFN γmRNA的表达。结果　A、B、C和D组移植物平均存活时间分别为 (6 .2±0 .82 )d、(9.2± 1 .92 )d、(7.2± 1 .30 )d及 (1 1 .2± 1 .76)d,D组存活时间明显长于其它 3组 (P<0 .0 5) ;D组移植物浸润细胞较其它 3组少。术后第 4天 ,血清NO水平A组为 (1 0 5 .8± 1 9.3)mmol/L ,明显高于B组的 (88.2± 2 1 .4)mmol/L(P<0 .0 5)、C组的 (70 .7± 1 7.8)mmol/L(P<0 .0 1 )及D组的 (56 .3± 1 6 .4)mmol/L(P<0 .0 1 ) ,出现移植排斥时 ,C、D组的血清NO水平分别为 (83 .7± 1 0 .6)mmol/L及 (71 .3± 1 3 .8)mmol/L ,仍较A组低 (P<0 .0 5) ,B组为 (1 0 4 .7± 1 6 .3)mmol/L ,与A组比较差异无显著性意义 (P>0 .0 5)。术后第 4天血清IFN γmRNA表达 ,D组为 2 3 .5± 4 .6 ,较A组的2 8.8± 4 .8低 (P<0 .0 5) ,而B、C组与A组间差异无显著性意义 (P>0 .0 5)。结论　普伐他汀能抑制巨噬细胞活性 ,延长异种胰岛移植物存活 ,尤其与CsA联用效果更好     

腺苷与单磷酯A联合预处理对供心保存的实验研究

目的　探讨腺苷与单磷酯A联合预处理对供心保存的效果。方法　健康大白兔 39只 ,随机分为 4组。A、B组以单磷酯A预处理 2 4h后 ,制成离体心脏 ,A组再用腺苷预处理 ;C组用腺苷作经典预处理 ;D组仅注射生理盐水作对照。各组预处理后 ,用 4℃改良St.Thomas液诱导心脏停搏 ,低温保存 4h ,复灌 1h。观察心功能恢复率、心肌三磷酸腺苷 (ATP)和丙二醛 (MDA)含量、心肌磷酸肌酸激酶 (CK mb)释放量等。结果　A、B、C、D组心功能恢复率 (+dp/dtmax ,% )分别为 :70 .97± 17.92 ,6 5 .5 4± 2 2 .6 2 ,6 4 .36± 16 .10 ,39.0 7± 13.78;A组高于B、C、D组 ,并与D组的差异有显著性 (P <0 .0 1)。A、B、C、D组心肌组织ATP含量 (10 -3 μmol/g湿重 )分别为 :5 .4 6± 1.37,3.97± 1.0 4 ,4 .4 5± 1.2 9,2 .0 7± 0 .74 ;A组高于B、C、D组 ,差异有显著性 (P <0 .0 5orP <0 .0 1)。结论　用单磷酯A和腺苷联合预处理 ,对供心有一定的保护效果。     

心脏机械瓣置换后不同强度抗凝对病人凝血激活的影响

目的　探讨不同强度抗凝时 ,心脏机械瓣置换术后病人的凝血激活状态。方法　将 16 2例心脏机械瓣置换术后病人 ,根据抗凝强度 (INR)分成 4组 :A组 (<1 5 ) 2 5例 ;B组 (1 5～ <2 0 ) 4 4例 ;C组 (2 0～ <3 0 ) 6 1例 ;D组 (3 0～ <4 5 ) 32例。 2 0例正常成人为对照组。采用酶联免疫吸附法 (ELISA)测定各组血浆凝血酶原片段 1+2 (F1 + 2 )、D 二聚体浓度。结果　A、B、C、D和对照组F1 + 2 浓度分别为(2 4 8± 1 32 )、(1 2 3± 0 6 5 )、(0 81± 0 4 5 )、(0 73± 0 39)、(1 11± 0 35 )nmol L ;D 二聚体浓度分别为(0 4 5± 0 2 4 )、(0 30± 0 17)、(0 2 4± 0 10 )、(0 2 5± 0 11)、(0 2 1± 0 0 9)mg L。A组F1 + 2 和D -二聚体浓度均显著高于对照组 (P <0 0 1) ;B组F1 + 2 浓度与对照组无差异 (P >0 0 5 ) ,D 二聚体浓度显著高于对照组 (P <0 0 5 ) ;C、D组F1 + 2 浓度均显著低于对照组 (P <0 0 5 ) ,但C、D两组间差异无显著性 (P >0 0 5 ) ;C、D组D 二聚体浓度与对照组之间均差异无显著性 (P >0 0 5 )。结论　在INR 2 0～ 3 0的抗凝强度下 ,心脏机械瓣置换术后病人凝血激活受到明显抑制     

去蛋氨酸/缬氨酸空肠喂饲荷瘤大鼠对肿瘤核酸及蛋白质代谢的影响

目的　观察去蛋氨酸 /缬氨酸空肠喂饲荷瘤鼠对肿瘤核酸及蛋白质代谢的影响。方法SD大鼠空肠造瘘 ,皮下接种Walker 2 5 6癌肉瘤 ,分A、B、C、D共 4组。分别以平衡氨基酸、去蛋氨酸、平衡氨基酸、去缬氨酸空肠喂养 6d ,注入3 H 蛋氨酸 /缬氨酸 7.4× 10 5Bq 0 .5、1、2、4h后分别测定肿瘤组织RNA、DNA及蛋白质的3 H掺入率。结果　B、D组各时点蛋白质3 H掺入率分别为 (0 .5 0 0±0 .0 2 0 ) %～ (3.6 70± 0 .110 ) %及 (1.887± 0 .0 2 0 ) %～ (3.813± 0 .0 76 ) % ,分别低于A、C组 ;B组RNA和DNA的3 H掺入率分别为 (0 .2 73± 0 .0 75 ) %及 (0 .2 31± 0 .0 5 2 ) % ,低于A组的 (0 .30 7±0 .0 73) %及 (0 .30 4± 0 .0 73) % ;C、D组核酸3 H掺入率差异无显著性 (P >0 .0 5 )。结论　去蛋氨酸 /缬氨酸空肠喂饲荷瘤鼠可抑制肿瘤蛋白质合成 ,缺乏蛋氨酸还可影响核酸的合成代谢。     

关节镜下同种异体组织重建膝关节前后交叉韧带的临床研究

目的　评价关节镜下同种异体组织重建膝关节前后交叉韧带 (ACL ,PCL)的疗效。方法　回顾调查了 36例孤立性交叉韧带损伤病人 ,将其分为 2组 ,A组 :ACL损伤 2 8例 ;B组 :PCL损伤 8例。分别应用同种异体B -PT -B、半腱与股薄肌腱、胫后肌腱、跟腱 -骨和四头肌腱 -骨重建 ,平均随访 2 1 5个月。结果　Lysholm评分 :A组术前平均 6 3± 5 6 ;术后 90±5 5 ;B组术前平均 6 1± 7 6 ,术后 88± 6 0 ;两组手术前后差异显著 (P <0 0 1) ;IKDC评分 :A组A级 2例 (7% ) ,B级 16例 (5 7% ) ,C级 8例 (2 9% ) ,D级 2例 (7% ) ;B组A级 1例 (12 5 % ) ,B级 3例 (37 5 % ) ,C级 3例 (37 5 % ) ,D级 1例 (12 5 % )。KT2 0 0 0测定 :A组由术前胫骨前移平均 11 90± 0 2 7mm减少至术后 4 30± 1 4 2mm ;B组胫骨后移由术前平均 10 5± 2 5mm减少至术后 5 9± 1 5mm ,两组手术前后有显著差异 (P <0 0 1)。术后健患侧比较 :A组平均 2 3± 0 9mm ;B组 2 7± 1 3mm ;健患差异 :A组 <3mm2 3/ 2 8例 (82 % ) ,>5mm 3例 (11% ) ;B组 <3mm 5 / 8例 (6 2 5 % ) ,>5mm 2例 (2 5 % )。前后抽屉试验大部分平均恢复 1°以上 ,并呈现明显的硬终点。术后ROM ,A组 :正常 2 6 / 2 8例 (93% ) ,接近正常 2 / 2 8例 (7% ) ;B组 :     

延长大鼠异种心脏移植后存活时间的实验研究

目的　研究如何延长大鼠异种心脏移植后的存活时间。方法　实验分为A、B、C、D四组。A组 :移植术前 12、8、4、0d及 10、6、2、0d分别将脾细胞 1× 10 8个 ,抗血清 0 .2ml静脉注入受体大鼠 ;B组 :在A组的基础上 ,加用中华眼镜蛇毒 (CCV) 0 .2mg·kg-1·d-1,术前 3d至术日腹腔注射。C组 :在B组的基础上 ,加用环孢素A(CsA) 10mg·kg-1·d-1、环磷酰胺 (Cy) 2 0mg·kg-1·d-1,术前 12d开始至术日腹腔注射。D组 :在C组的基础上 ,加用抗巨噬细胞和抗自然杀伤细胞单克隆抗体 2 5 0 μg·kg-1·d-1,术前 12d开始至术日腹腔注射。结果　A、B、C、D四组移植心脏分别存活 (0 .32± 0 .12 )h ,(2 5 .6± 9.6 )h、(48.6± 10 .4)h和 (72 .4± 2 1.7)h ;术日各组IgG均下降 ,尤以C、D组下降明显 ,与A、B组比较 ,差异有显著性 (P <0 .0 5 )。结论　术前静脉注射供体脾细胞及抗血清 ,尤其与CCV、CsA、Cy合用 ,能显著抑制IgG的产生 ,延长移植心脏的存活时间。     

冲洗液温度对前列腺术后膀胱无抑制性收缩的影响

目的探讨不同温度冲洗液对前列腺切除术后膀胱无抑制性收缩的影响。方法将 180例前列腺切除术后并发膀胱无抑制性收缩的患者随机分为A、B、C、D、E、F 6组 ,各 30例 ,术后均予持续膀胱冲洗 ,冲洗液温度分别为(2 3.5 0± 1.5 0 )℃、(2 6 .5 0± 1.5 0 )℃、(2 9.5 0± 1.5 0 )℃、(32 .5 0± 1.5 0 )℃、(35 .5 0± 1.5 0 )℃、(38.5 0± 1.5 0 )℃。观察前列腺术后膀胱无抑制性收缩症状并对其评分 ,同时观察记录持续膀胱冲洗的时间。结果E组及F组症状评分显著低于A、B、C、D组 (均P <0 .0 1) ;E组膀胱持续冲洗时间明显短于A、B、C、D、F组 (均P <0 .0 1)。结论前列腺术后持续膀胱冲洗液的温度在 (35 .5 0± 1.5 0 )℃为最佳 ,其可最大限度地减轻前列腺术后膀胱无抑制性收缩 ,减少持续膀胱冲洗的时间。     

激素性股骨头坏死病程中骨形态发生蛋白-2的改变及其意义

目的　观察激素性股骨头坏死病程中骨形态发生蛋白 2 (BMP2 )的变化。方法　用醋酸氢化泼尼松诱发早期股骨头坏死动物模型 ,实验动物根据醋酸氢化泼尼松用量分为A组 (对照组 )、B组 (4mg/kg体重 )、C组 (8mg/kg体重 )、D组 (16mg/kg体重 ) ,肌注给药 ,每周 1次。取股(肱 )骨头标本行免疫组织化学染色。采用图像分析技术 ,测得平均染色面积百分比和平均吸光度。结果　A、B、C、D组阳性染色区染色强度依次减弱 ,平均吸光度值依次降低 ,且A组和D组间差异有非常显著性 (P <0 .0 1)。A组平均染色面积百分比 (股骨头 2 5 .5 8± 7.76、肱骨头 2 4.98± 8.2 3)明显高于D组 (股骨头 12 .30± 6 .6 0、肱骨头 12 .5 0± 8.0 3,P <0 .0 1)。各实验组平均吸光度和平均染色面积百分比随用药时间延长而降低。结论　在激素性股骨头坏死病程中 ,BMP2表达受抑制 ,抑制程度与用药时间和用药剂量正相关。     

1,25-(OH)_2D_3对小鼠皮肤移植后脾T细胞亚群、MLR及NK细胞活性的影响

目的　探讨 1,2 5 二羟维生素D3 [1,2 5 (OH) 2 D3 ]抑制机体免疫功能的机理 ,为用于临床抗排斥治疗提供实验依据。方法　建立不同系小鼠间皮肤移植的动物模型。术日将实验小鼠随机分为四组 ,均用小鼠灌胃器给药。对照组 :每日 2 0ml/kg生理盐水 ;维生素D3 (VD3 )组 :单独应用 1,2 5 (OH) 2 D3 2 .5 μg·kg-1·d-1;环孢素A(CsA)组 :单独应用CsA 2 5mg·kg-1·d-1;VD3 +CsA组 :联合应用VD3 +CsA ,按VD3 组和CsA组用药剂量给药。术后 10d ,测定小鼠脾的T细胞亚群、单向混合淋巴细胞反应 (MLR)、自然杀伤细胞 (NK)活性。结果　VD3 组的移植皮片存活时间 (13.13±1.13)d ,明显长于对照组的 (9.75± 0 .89)d ;CD3+ 、CD4 + T细胞百分率 4 0 .19%± 4 .2 5 %、2 4 .6 5 %±3.4 7%均明显低于对照组 4 8.70 %± 7.19%、 33.5 5 %± 4 .34% ,P <0 .0 1;对BALB/C鼠的MLR(0 .95± 0 .12 )明显低于对照组 (1.19± 0 .2 2 ) ,P <0 .0 5 ;NK细胞的活性与对照组小鼠比较 ,差异无显著性。结论　 1,2 5 (OH) 2 D3 能延长小鼠皮肤移植的存活时间 ,其抑制机体免疫功能的作用是通过减少CD3+ 、CD4 + T细胞的数量及抑制T细胞功能而发挥的 ,对NK细胞活性无明显影响。     

血管襻骨膜内腓骨组合移植修复负重长段骨缺损的实验研究

目的　研究血管袢骨膜内腓骨组合移植修复负重长段粗骨缺损临床应用可行性。　方法　健康新西兰大白兔 72 只,随机分为 3 组。A组:单腓移植组;B组:骨膜外双腓骨组合移植组;C组:骨膜内双腓骨组合移植组。制成胫骨中上段骨缺损 10 0 mm,采用 3 种手术方式,术后 2、4、8、12、16周分别拍X线片及测定血清碱性磷酸酶、骨钙素、骨密度及组织学、生物力学检查。　结果　X线结果显示,C组较A、B组骨痂增加明显,骨小梁排列整齐,移植腓骨明显增粗。术后 4 周血清 ALP:A组 (91 .6±9. 2)、B组 (11.4 9±5 .1)、C组 (136 6±3 9);血清 BGP:A组(3. 90±1. 02)、B组 (4. 69±0. 58)、C组 (5 .84±0. 98);骨密度:A组 (0. 179±0 .03)、B组(0. 286±0 .04)、C组 (0. 301±0. 07),C组较A组、B组差异均有统计学意义(P<0 01)。组织学检查C组较A、B组骨痂形成早、成熟早,骨小梁排列整齐,两腓骨形成一体,髓腔再通。成骨量:A组 (398±4 0)、B组 (41. 7±2 .3)、C组(49. 2±5 .7),C组与A、B组比较,P<0. 05。生物力学测试,移植骨平均最大载荷、最大扭距及剪切应力,C组均大于A、B组。　结论　血管袢骨膜内腓骨组合移植是治疗负重长段粗骨缺损较为理想的手术方式。     

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.