背景：有研究表明双膦酸盐可抑制破骨细胞的骨吸收功能，但对其骨吸收功能关键细胞因子组织蛋白酶K是否产生作用，至今少有报道。目的：观察双膦酸盐对破骨细胞分化中组织蛋白酶K及骨吸收功能影响。方法：用小鼠单核巨噬细胞RAW264.7诱导培养破骨细胞。实验分2组：对照组加入质量浓度100μg/L核因子κB受体活化因子配体进行诱导至收获细胞，双膦酸盐组在对照组的基础上加入10-7 mol/L阿仑膦酸盐处理至收获细胞。培养第7天检测各组破骨细胞生成和骨吸收功能，培养72 h免疫荧光检测两组组织蛋白酶K表达差异，Western blot检测组织蛋白酶K蛋白表达情况。结果与结论：两组均有抗酒石酸酸性磷酸酶阳性多核破骨细胞生成，并在牙本质磨片上形成吸收陷窝；但对照组抗酒石酸酸性磷酸酶阳性多核细胞数目、吸收陷窝数目及陷窝面积均大于双膦酸盐组（P〈0.01）。免疫荧光检测组织蛋白酶K表达对照组强于双膦酸盐组（P〈0.01）；Western blot检测组织蛋白酶K表达双膦酸盐组低于对照组（P〈0.01）。结果证实，双膦酸盐通过抑制组织蛋白酶K因子的表达，阻碍破骨细胞的骨吸收功能。

BACKGROUND:Studies have shown that bisphosphonates inhibit osteoclast resorption, but whether cathepsin K, a key cytokine of bone resorption, plays an effect has rarely been reported. OBJECTIVE:To study the effect of bisphosphonate on capthesin K and bone resorption function during osteoclast differentiation. METHODS:Osteoclasts were cultured by mouse monocyte-macrophage cellline-RAW264.7. The cells were divided into two groups:control group, treated with 100μg/L receptor activator of nuclear factorκB ligand factor;alendronate group, treated with 100μg/L receptor activator of nuclear factorκB ligand factor+10-7 mol/L alendronate. Osteoclastogenesis and resorption function of osteoclasts were examined at 7 days of culture and gene expression of capthesin K was detected by immunofluorescence method at 72 hours of culture. Western blot assay was used to detect capthesin K protein expression at 72 hours of culture. RESULTS AND CONCLUSION:Tartrate-resistant acid phosphatase po

目的：观察基底细胞样乳腺癌（BLBC）组织中凋亡蛋白酶活化因子1（Apaf-1）、细胞凋亡蛋白酶9（Caspase-9）的表达变化，并探讨其意义。方法采用免疫组化法检测43例BLBC（A组）、57例non-BLBC（B组）和60例癌旁正常乳腺组织（C组）Apaf-1、Caspase-9的表达，分析两指标间及与BLBC临床病理参数的关系。结果A、B、C组Apaf-1阳性率分别为23．3％（10/43）、49．1％（28/57）、75％（45/60），两两比较，P均＜0．01；Caspase-9阳性率分别为27．9％（12/43）、54．4％（31/57）、85％（51/60），两两比较，P均＜0．01。Apaf-1表达与BLBC肿瘤直径、淋巴结转移、临床分期有关（P均＜0．05），Caspase-9表达与BLBC淋巴结转移、临床分期有关（P均＜0．05）。BLBC组织Apaf-1与Caspase-9阳性表达呈正相关（r＝0．639，P＜0．01）。结论BLBC组织Apaf-1、Caspase-9表达降低，两者异常表达可能与BLBC的发生、发展密切相关。

Objective To observe the changes of Apaf-1, Caspase-9 expression in the basal-like breast cancer ( BLBC) tissues and explore its clinical significance.Methods The expressions of Apaf-1 and Caspase-9 were detected in 43 cases of BLBC( group A) , 57 cases of non-BLBC( group B) and 60 cases of normal breast tissue( group C) by immuno-histochemistry.The relationship between Apaf-1, Caspase-9 expression and clinicopathological features were analyzed.The correlation between Apaf-1 and Caspase-9 expression was analyzed.Results The positive expression rate of Apaf-1 in group A, B, C was 23.3%(10/43), 49.1%(28/57), 75%(45/60) respectively.The difference between each group was significant(all P<0.01).The positive expression rate of Caspase-9 in group A, B, C was 27.9%(12/43), 54.4%(31/57), 85%(51/60) respectively.The difference between each group was all significant(all P<0.01).The expres-sion of Apaf-1 was significantly correlated with the size of tumor, lymph nodes metastasis and the

背景：课题组以往研究证实，氧浓度过低乃至处于低氧时(体积分数2%O2的分化和功能都受到抑制，但体外培养的破骨细胞在不同氧环境下的基因表达未见有相关报道。 目的：实验拟观察不同氧环境下破骨细胞各特异性基因的表达规律，探寻氧环境改变影响破骨细胞分化的表达机制。 方法：将破骨前体细胞株经质量浓度均为10μg/L的核因子κB受体活化因子配体和巨噬细胞集落刺激因子联合诱导成为成熟的破骨细胞，然后分别置于常氧、组织氧、低氧(体积分数20%，7%，2%)条件下培养，用抗酒石酸酸性磷酸酶染色检测破骨细胞形成的变化，并分别在培养第1-7天收集细胞，通过定量PCR方法检测核因子κB受体活化因子，肿瘤坏死因子受体相关因子6，抗酒石酸酸性磷酸酶，组织蛋白酶K基因mRNA的表达。 结果与结论：低氧条件下抗酒石酸酸性磷酸酶阳性的破骨细胞数显著低于组织氧和常氧培养时形成的抗酒石酸酸性磷酸酶阳性细胞数(P<0.05)。不同氧环境下，破骨细胞中核因子κB受体活化因子mRNA的表达无明显改变，组织氧和常氧培养下肿瘤坏死因子受体相关因子6 mRNA的表达在培养第5天最高(P<0.05)。随着氧浓度的降低，抗酒石酸酸性磷酸酶和组织蛋白酶K mRNA表达时间延后，组织氧培养条件下此2者

BACKGROUND:Preliminary studies of our research group have confirmed that the proliferation of preosteoclasts and the differentiation and function of osteoclasts could be inhibited when they were cultured in lower oxygen tension even hypoxia (2%O 2 ), but the gene expression of osteoclasts cultured in vitro have not been reported. OBJECTIVE:To examine the effect of oxygen tension on specific gene expression of osteoclasts in vitro and explore the mechanism of osteoclast differentiation influenced by oxygen tension. METHODS:The preosteoclasts were induced with 10μg/L macrophage colony stimulating facto and 10μg/L soluble receptor activator of nuclear factor-κB ligand into mature osteoclasts. Then the osteoclasts were culturedin normoxia, tissue oxygen and hypoxia (20%, 7%, 2%O 2 ) respectively. cells were then stained for tartarate-resistant acid phosphatase to assess osteoclastic formation. cells were col ected at 1, 2, 3, 4, 5, 6, 7 days after culture respectively. The sol

目的：探讨银柴胡提取物对兔脊髓慢性渐进性压迫后基质金属蛋白酶2、12（MMP-2、12）表达及神经功能的影响。方法：家兔随机分为脊髓损伤后应用生理盐水对照组（A组）和银柴胡提取物干预治疗组（B组）,损伤后不同时间取材,HE染色观察损伤脊髓组织病理变化;免疫组化染色检测MMP-2及Real-Time PCR检测MMP-12的表达变化;采用Tarlov评分评价神经功能。结果：HE染色镜检发现脊髓组织病理学改变B组明显轻于A组。2组均发现MMP-2、12的表达,MMP-2、12表达A组〉B组（P〈0.05）。B组神经功能改善优于A组。结论：银柴胡提取物可有效抑制家兔脊髓慢性渐进性压迫后MMP-2、12表达,促进神经功能恢复。

Objective:To discuss the influence of YinChaiHu (Radix Stellariae) extracts on neurological func-tion, the expressions of matrix metalloproteinase-2, 12 (MMP-2, 12) of the rabbits suffering from chronic progressive oppressive spinal cord injury. Methods: The rabbits were randomized into the control group (group A) receiving physiological saline and the treatment group (group B) intervened by YinChaiHu extracts after spinal cord injury, the tissue was cut at different times, pathological changes of damaged spinal cord were observed by HE staining;the ex-pressions of MMP-12 by Real-Time PCR and MMP-2 by immuohistochemical staining; neurological function as-sessed by Tarlov scaling. Results:HE staining microscopy revealed that group B was lighter than group A obviously in histopathology of spinal cord. The expressions of MMP-2, 12 were found in both groups, group A was more than group B in the expressions of MMP-2, 12(P<0.05). Group B was superior to group A in the improvements

二膦酸盐与骨组织有着高度的亲和力,对骨组织的药理作用取决其与骨组织的亲和力和对破骨细胞的抑制作用,各代二膦酸盐的性能差别使其临床疗效存有差异。一定剂量的二膦酸盐可防止牙槽骨密度降低,且对牙槽嵴高度降低有一定的预防作用,可促进炎性根尖周组织的血管重建和骨缺损修复。含氮二膦酸盐通过抑制法尼基焦膦酸合成酶的活性抑制破骨细胞的破骨作用。核因子-κB受体活化因子配体(RANKL)和骨保护蛋白(OPG)的相对比值决定着骨代谢的方向和骨吸收的程度,两者比值上升则骨吸收增加,反之则骨吸收抑制。二膦酸盐可致RANKL与OPG的比值明显降低。二膦酸盐可竞争性地抑制基质金属蛋白酶活化,减少活性基质金属蛋白酶造成的局部细胞外基质破坏。骨特异性碱性磷酸酶(BAKP)水平降低可造成牙槽骨高度降低,而二膦酸盐可防止BAKP水平的降低,有效地降低炎性反应,降低牙槽骨高度降低速率。

Bisphosphonates?can?bind?to?hydroxyapatite?crystals?in?a?mineralized?bone?matrix?and?increase?bone?resistance?against?osteoclasts.?The?relative?contributions?of?these?properties?differ?among?individual?bisphosphonates,?and?can?help?determine?their?clinical?behavior?and?effectiveness.?Appropriate?doses?of?bisphosphonates?appear?to?prevent?the?loss?of?alveolar?bone?on?density?and?height,?and?promote?angiogenesis?and?bone?tissue?repair.?The?anti-resorptive?effects?of?nitrogen-containing?bisphosphonates?on?osteoclasts?appear?to?result?from?their?properties?as?potent?inhibitors?of?farnesyl?pyrophosphate synthase. Bisphosphonates can decrease the relative ratio of the receptor activator of nuclear factor-κB ligand/osteoprotegerin,?which?determines?the?progress?of?bone?metabolism?and?degree?of?bone?resorption.?Some?studies?have?shown?that?bisphosphonates?can?decrease?matrix?metalloproteinase?expression?in?the?periapical?area,?and?inhibit?bone?resorption.?Other?studies?demonstrated?