[1]石磊,张兵①,夏春*.股骨头坏死组织中半胱氨酰天冬氨酸蛋白酶（Caspase）-3与细胞凋亡的关系[J].中国微创外科杂志,2009,09(8):737-746.
　Shi Lei*,Zhang Bing,Xia Chun*..Relationship between Caspase3 and Apoptosis in Aseptic Necrosis of Femoral Head[J].Chinese Journal of Minimally Invasive Surgery,2009,09(8):737-746.
点击复制

股骨头坏死组织中半胱氨酰天冬氨酸蛋白酶（Caspase）-3与细胞凋亡的关系()
分享到：

《中国微创外科杂志》[ISSN:1009-6604/CN:11-4526/R]

卷:
09
期数:
2009年8期
页码:
737-746
栏目:
基础研究
出版日期:
2009-08-31

文章信息/Info

Title:
Relationship between Caspase3 and Apoptosis in Aseptic Necrosis of Femoral Head
作者:
石磊; 张兵①; 夏春*
厦门大学附属中山医院骨科，厦门361004
Author(s):
Shi Lei*; Zhang Bing; Xia Chun*.
*Department of Orthopaedics, Zhongshan Hospital Affiliated to Xiamen University Medical Institute, Xiamen University,Xiamen 361004, China
关键词:
股骨头坏死; 半胱氨酰天冬氨酸蛋白酶-3; 细胞凋亡
Keywords:
Avascular necrosis of femoral head; Caspase3; Apoptosis
分类号:
R681.8
文献标志码:
A
摘要:
目的探讨半胱氨酰天冬氨酸蛋白酶（Caspase）-3在无菌性股骨头坏死（avascular/aseptic necrosis of femoral head，ANFH）进展过程中的表达及意义。方法21例（22髋）ANFH取股骨头病灶周围骨松质，其中早期ANFH组（6髋），中期ANFH组（8髋），晚期ANFH组（8髋）；另取19例（19髋）新鲜股骨颈骨折的股骨头对应部位骨松质为对照组。采用原位末端标记（TUNEL）法、空骨陷窝计数法检测细胞凋亡水平，比色法检测股骨头组织Caspase3活性。结果骨陷窝空虚百分率(F=45.43，P=0.000)、成骨细胞凋亡率(F=120.86，P=0.000)等凋亡指标均随ANFH临床分期进展而显著升高，ANFH早、中期组显著高于对照组（q=18.899，P<0.05；q=6.398，P<0.05），但并不随着ANFH病变进展而增强，而呈现进行性下降；ANFH晚期组Caspase-3活性与对照组Caspase-3活性无统计学差异（q=2.021，P>0.05）。Caspase3活性与细胞凋亡率统计学相关性不显著（r=0.126，P=0.425）。结论在ANFH进展过程中，Caspase3可能不是细胞凋亡的主要执行分子；Caspase3在ANFH进展中可能发挥非凋亡作用。
Abstract:
ObjectiveTo investigate the expression and role of Caspase3 during the development of nontraumatic avascular/aseptic necrosis of femoral head(ANFH). MethodsTissue samples were obtained from 22 femoral heads of 21 patients with ANFH. The samples were divided into three groups: early stage (6 cases), middle stage (8 cases) and late stage (8 cases) groups according to the progress of the disease. Meanwhile, 19 tissue samples of 19 femoral heads were obtained from 19 cases of acute femoral neck fracture and set as a control group. The level of apoptosis of each group was compared in terms of the percentages of TUNEL positive osteocytes and empty osteocyte lacuna, and then the activity of Caspase3 was detected by colorimetric method.ResultsBoth the pecentages of empty osteocyte lacunae (F=45.43, P=0.000) and the TUNEL positive osteocytes (F=120.86, P=0.000) increased significantly with the progress of ANFH. The two indexes in the early and middle stage groups were significantly higher than those in the control (q=18.899, P<0.05 and q=6.398, P<0.05, respectively) but decreased instead of increasing along with the progress of pathology. In the late stage group, the indexes were not significantly different from the control (q=2.021, P>0.05). Caspase3 activity was not significantly related to the capacity of osteogenesis (r=0126, P=0425).ConclusionsCaspase3 is not the major executor of apoptosis in ANFH. It is very likely that it does not play a nonapoptotic role in the progress of the diseases.

参考文献/References:

[1]何宇, 杨述华,梁袁昕. 创伤性股骨头坏死中骨细胞凋亡初探. 中国矫形外科杂志, 2005, 13(16):1238-1240.
[2]Weinstein RS, Nicholas RW,Manolagas SC. Apoptosis of osteocytes in glucocorticoidinduced osteonecrosis of the hip. J Clin Endocrinol Metab, 2000, 85(8):2907-2912.
[3]熊明月, 王坤正,党晓谦. 早期激素性股骨头坏死骨细胞凋亡的实验研究. 中国修复重建外科杂志, 2007, 21(3):262-265.
[4]郭坤亮, 安洪, 蒋电明, 等. 早期酒精性股骨头缺血坏死骨细胞凋亡的实验研究. 重庆医科大学学报, 2003, 28(3):313-315.
[5]Fernando P, Kelly JF, Balazsi K, et al. Caspase 3 activity is required for skeletal muscle differentiation. PNAS, 2002, 99(17):11025-11030.
[6]Okuyama R, Nguyen BC, Talora C, et al. High commitment of embryonic keratinocytes to terminal differentiation through a Notch1caspase 3 regulatory mechanism. Dev Cell, 2004, 6(4):551-562.
[7]Oomman S, Strahlendorf H, Dertien J, et al. Bergmann glia utilize active caspase3 for differentiation. Brain Res, 2006, 1078(1):19-34.
[8]Mogi M,Togari A.Activation of caspases is required for osteoblastic differentiation. J Biol Chem, 2003, 278(48):47477-47482.
[9]Miura M, Chen XD, Allen MR, et al. A crucial role of Caspase3 in osteogenic differentiation of bone marrow stromal stem cells. J Clin Invest, 2004, 114(12):1704-1713.
[10]Ashkenazi A,Dixit VM. Death Receptors: Signaling and Modulation. Science 1998, 281(5381):1305-1308.
[11]Luo X, Budihardjo I, Zou H, et al. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Cell, 1998, 94(4):481-490.
[12]蒋杞英, 胡艳秋, 程相树, 等. 孕期酒精接触对子鼠视皮质神经元凋亡的影响. 解剖学报, 2007, 38(4):400-404.
[13]金武丕, 权修权, 孟繁平, 等. 大鼠酒精性肝病细胞凋亡与细胞色素P4502E1和氧化应激的关系.世界华人消化杂志,2007, 15(20):2181-2185.
[14]包倪荣, 赵建宁, 王与荣, 等. 地塞米松诱导成骨细胞凋亡. 南京医科大学学报（英文版）, 2004, 18(5):256-261.
[15]Chua CC, Chua BH, Chen Z, et al. Dexamethasone induces caspase activation in murine osteoblastic MC3T3-E1 cells. Biochim Biophys Acta, 2003, 1642(1-2):79-85.
[16]Liu Y, Porta A, Peng X, et al. Prevention of glucocorticoidinduced apoptosis in osteocytes and osteoblasts by calbindinD28k. 2004, 19(3):479-490.
[17]景淑英，赵庆国，毕黎琦.激素性股骨头坏死早期细胞凋亡相关基因表达及阿仑磷酸钠的干预.中国组织工程研究与临床康复，2008，12（46）：9095-9099.
[18]Shintani T, Klionsky DJ.Autophagy in health and disease: A doubleedged sword. Science, 2004, 306(5698):990-995.
[19]张军,胡大海.AIF诱导细胞凋亡. 医学分子生物学杂志, 2008, 5(1):87-90.
[20]Sperandio S, Poksay K, de Belle I, et al. Paraptosis: mediation by MAP kinases and inhibition by AIP1/Alix. Cell Death Differ, 2004, 11(10):1066-1075.
[21]Castedo M, Perfettini JL, Roumier T, et al. Cell death by mitotic catastrophe: a molecular definition. Oncogene, 2004, 23(16):2825-2837.

备注/Memo

备注/Memo:
①（厦门大学医学院形态学教研室，厦门361004）*通讯作者
更新日期/Last Update: 2013-09-17