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自发性高血压大鼠股骨头生长板细胞动力学的改变。

Altered cellular kinetics in the growth plate of the femoral head of spontaneously hypertensive rats.

机构信息

Department of Orthopaedic Surgery, Severance Children's Hospital, Yonsei University School of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Korea.

出版信息

Yonsei Med J. 2012 May;53(3):625-33. doi: 10.3349/ymj.2012.53.3.625.

Abstract

PURPOSE

Pathologic changes in the growth plate remain unknown in Legg-Calvé-Perthes (LCP) disease. Spontaneously hypertensive rats have proven to be a good model for studying LCP disease. This study investigated the histopathologic changes and the expression of vascular endothelial growth factor in the growth plate of spontaneously hypertensive rats (SHR).

MATERIALS AND METHODS

Sixty SHR rats were divided into two groups: those showing osteonecrosis (SHR+n group: 32), and those showing normal ossification (SHR-n group: 28). Thirty Wister Kyoto rats served as a control. For histomorphological measurement, the length of each zone of the growth plate was measured. Cell kinetics was measured by 5-bromo-2'-deoxyuridin (BrdU) immunohistochemistry and transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assays. Vascular endothelial growth factor (VEGF) immunohistochemistry was used to identify of expression of VEGF.

RESULTS

The lengths of growth plates of the SHR+n group were significantly shorter in the initial growth period than those of the other groups. The lowest proliferative rate and the highest apoptosis rate were observed in the SHR+n group at the initial growth period. The expression of VEGF in the growth plate of the SHR group was lower than the control group, and it was lower in the SHR+n group than in the SHR-n group.

CONCLUSION

The growth plate of the SHR+n group was found to be affected by disease process of ischemic necrosis of the femoral head, and this might explain the relative overgrowth of the greater trochanter in the later stages of LCP disease.

摘要

目的

莱格-卡尔弗-佩尔特斯(LCP)病的生长板的病理变化尚不清楚。自发性高血压大鼠已被证明是研究 LCP 疾病的良好模型。本研究调查了自发性高血压大鼠(SHR)生长板的组织病理学变化和血管内皮生长因子的表达。

材料和方法

60 只 SHR 大鼠分为两组:出现骨坏死(SHR+n 组:32 只)和出现正常骨化(SHR-n 组:28 只)。30 只 Wister Kyoto 大鼠作为对照。为了进行组织形态学测量,测量了生长板的每个区域的长度。通过 5-溴-2'-脱氧尿苷(BrdU)免疫组织化学和转移酶介导的脱氧尿苷三磷酸-生物素 nick 末端标记(TUNEL)测定来测量细胞动力学。血管内皮生长因子(VEGF)免疫组织化学用于鉴定 VEGF 的表达。

结果

SHR+n 组的生长板长度在初始生长期间明显短于其他组。在初始生长期间,SHR+n 组的增殖率最低,凋亡率最高。SHR 组生长板中的 VEGF 表达低于对照组,SHR+n 组低于 SHR-n 组。

结论

SHR+n 组的生长板受到股骨头缺血性坏死的疾病过程的影响,这可能解释了 LCP 疾病后期大转子相对过度生长的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3428/3343426/7ea1c2957f7a/ymj-53-625-g001.jpg

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