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本文引用的文献

1
STAT1-caspase 3 pathway in the apoptotic process associated with steroid-induced necrosis of the femoral head.与类固醇诱导的股骨头坏死相关的凋亡过程中的STAT1-半胱天冬酶3通路。
J Mol Histol. 2014 Aug;45(4):473-85. doi: 10.1007/s10735-014-9571-6. Epub 2014 Feb 20.
2
Prevention of steroid-induced osteonecrosis by intravenous administration of vitamin E in a rabbit model.在兔模型中通过静脉注射维生素E预防类固醇诱导的骨坏死
J Orthop Sci. 2010 Sep;15(5):674-7. doi: 10.1007/s00776-010-1516-7. Epub 2010 Oct 16.
3
Vitamin E prevents steroid-induced osteonecrosis in rabbits.维生素 E 可预防兔类固醇性骨坏死。
Acta Orthop. 2010 Feb;81(1):154-60. doi: 10.3109/17453671003587101.
4
Reactive oxygen species, cellular redox systems, and apoptosis.活性氧、细胞氧化还原系统与细胞凋亡。
Free Radic Biol Med. 2010 Mar 15;48(6):749-62. doi: 10.1016/j.freeradbiomed.2009.12.022. Epub 2010 Jan 4.
5
Management of avascular necrosis of femoral head at pre-collapse stage.股骨头缺血性坏死塌陷前期的治疗
Indian J Orthop. 2009 Jan;43(1):6-16. doi: 10.4103/0019-5413.45318.
6
Troglitazone, but not rosiglitazone, damages mitochondrial DNA and induces mitochondrial dysfunction and cell death in human hepatocytes.曲格列酮而非罗格列酮会损害人肝细胞中的线粒体DNA,诱导线粒体功能障碍和细胞死亡。
Toxicol Appl Pharmacol. 2009 Nov 1;240(3):348-54. doi: 10.1016/j.taap.2009.07.021. Epub 2009 Jul 24.
7
Protection of acetaminophen induced mitochondrial dysfunctions and hepatic necrosis via Akt-NF-kappaB pathway: role of a novel plant protein.通过Akt-NF-κB途径保护对乙酰氨基酚诱导的线粒体功能障碍和肝坏死:一种新型植物蛋白的作用
Chem Biol Interact. 2009 Jan 27;177(2):96-106. doi: 10.1016/j.cbi.2008.09.006. Epub 2008 Sep 12.
8
A protein from Cajanus indicus Spreng protects liver and kidney against mercuric chloride-induced oxidative stress.来自木豆的一种蛋白质可保护肝脏和肾脏免受氯化汞诱导的氧化应激。
Biol Pharm Bull. 2008 Sep;31(9):1651-8. doi: 10.1248/bpb.31.1651.
9
Altered expression of apoptosis-related genes in osteocytes exposed to high-dose steroid hormones and hypoxic stress.暴露于高剂量类固醇激素和低氧应激下的骨细胞中凋亡相关基因的表达改变。
Pathobiology. 2006;73(6):304-9. doi: 10.1159/000099125.
10
Prevention of glucocorticoid-induced apoptosis in osteocytes and osteoblasts by calbindin-D28k.钙结合蛋白-D28k对糖皮质激素诱导的骨细胞和成骨细胞凋亡的预防作用
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维生素E对大鼠早期激素性股骨头缺血性坏死的影响及机制

[Effect and mechanisms of vitamin E on early steroid-induced avascular necrosis of femoral head in rats].

作者信息

Li Mufan, Zhang Eryang, Lü Leifeng, Ban Wenrui, Dang Xiaoqian, Zhang Chen

机构信息

The First Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an Shaanxi, 710004, P.R.China.

The First Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an Shaanxi, 710004,

出版信息

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2018 Nov 1;32(11):1421-1428. doi: 10.7507/1002-1892.201801046.

DOI:10.7507/1002-1892.201801046
PMID:30417618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8414123/
Abstract

OBJECTIVE

To investigate the possibility of mitochondria-dependent apoptosis as a mechanism of early steroid-induced avascular necrosis of femoral head (SANFH) in rats and vitamin E as a possible prevention strategy.

METHODS

Seventy-two male Sprague Dawley rats were randomly divided into control group, model group, and intervention group, with 24 rats in each group. The rats in control group were not treated as normal control. The rats in model group and intervention group were established early SANFH models by lipopolysaccharide combined with methylprednisolone injection. At the same time, the rats in intervention group were injected with vitamin E (40 mg/kg) every day for 7 days. At 2, 4, and 8 weeks after the final injection, the bilateral femoral heads were harvested and observed by HE staining, TUNEL assay, immunohistochemical staining, and Western blot. The rate of empty lacunae, apoptotic index, and the expressions of Caspase-9, Caspase-3, and cytochrome-c (Cyt-c) proteins were calculated.

RESULTS

According to histological staining, there were significant differences in the rate of empty lacunae between intervention group and control group at 8 weeks ( <0.05) and between intervention group and model group at 4 and 8 weeks ( <0.05). The apoptotic index of intervention group was significantly lower than that of model group at each time point ( <0.05). And there was significant difference between the intervention group and the control group at 8 weeks ( <0.05). According to immunohistochemistry staining and Western blot, the expressions of Cyt-c, Caspase-9, and Caspase-3 all significantly decreased in intervention group than those in model group at each time point ( <0.05); and the differences were significant between intervention group and control group at 8 weeks ( <0.05).

CONCLUSION

Vitamin E can delay the progression of early SANFH by reducing mitochondrial dependent osteocyte apoptosis.

摘要

目的

探讨线粒体依赖性凋亡作为大鼠早期类固醇诱导的股骨头缺血性坏死(SANFH)机制的可能性,以及维生素E作为一种可能的预防策略。

方法

72只雄性Sprague Dawley大鼠随机分为对照组、模型组和干预组,每组24只。对照组大鼠不做处理作为正常对照。模型组和干预组大鼠通过脂多糖联合甲基强的松龙注射建立早期SANFH模型。同时,干预组大鼠每天注射维生素E(40mg/kg),共7天。在最后一次注射后2、4和8周,采集双侧股骨头,进行苏木精-伊红(HE)染色、TUNEL检测、免疫组织化学染色和蛋白质免疫印迹法检测。计算空骨陷窝率、凋亡指数以及半胱天冬酶-9(Caspase-9)、半胱天冬酶-3(Caspase-3)和细胞色素c(Cyt-c)蛋白的表达。

结果

组织学染色显示,干预组与对照组在8周时空骨陷窝率有显著差异(<0.05),干预组与模型组在4周和8周时空骨陷窝率有显著差异(<0.05)。干预组在各时间点的凋亡指数均显著低于模型组(<0.05),且干预组与对照组在8周时有显著差异(<0.05)。免疫组织化学染色和蛋白质免疫印迹法检测结果显示,干预组在各时间点Cyt-c、Caspase-9和Caspase-3的表达均显著低于模型组(<0.05);干预组与对照组在8周时有显著差异(<0.05)。

结论

维生素E可通过减少线粒体依赖性骨细胞凋亡来延缓早期SANFH的进展。