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treadmill 训练通过抑制 PPARγ 的表达而不是促进 Runx2 的表达来预防去卵巢大鼠的骨丢失。

Treadmill training prevents bone loss by inhibition of PPARγ expression but not promoting of Runx2 expression in ovariectomized rats.

机构信息

Capital Institute of Physical Education, 11# Beisanhuan Xi Lu, HaiDian, Beijing, 100088, People's Republic of China.

出版信息

Eur J Appl Physiol. 2011 Aug;111(8):1759-67. doi: 10.1007/s00421-010-1820-0. Epub 2011 Jan 9.

DOI:10.1007/s00421-010-1820-0
PMID:21221986
Abstract

Exercise training has been reported to prevent bone loss in ovariectomized (OVX) rats and postmenopausal women. We hypothesized that treadmill training inhibited adipogenesis and enhanced osteogenesis through the regulation of adipocyte differentiation factor peroxisome proliferators-activated receptor gamma (PPARγ) and the osteogenic factor runt-related transcription factor 2 (Runx2) in a model of OVX-induced osteoporosis. To test this hypothesis, 3-month-old female Sprague-Dawley rats were divided randomly into the following groups: Sham, OVX, OVX exercised (EX), and OVX estrogen replacement (E(2)). At the end of the experiment, the bone mineral density (BMD) was detected using DEXA and the morphology change of bone tissues and uterus was observed by HE staining. The protein expression for PPARγ and Runx2 were measured by immunohistochemistry and western blot and the bone triacylglycerol (TG) was extracted by methanol/chloroform. OVX dramatically increased the number of fat vacuoles, protein levels for PPARγ and Runx2 as well as the TG level in tibiae and lumbar vertebrate. In contrast, the serum level of E(2), the lumbar vertebrate BMD as well as the proximal and distal femur BMD was significantly decreased in the OVX group. All changes induced by OVX were significantly reversed by exercise treatment except for the protein expression level of Runx2. Moreover, exercise treatment produced no estrogenic effects on uterus as evidenced by the uterus wet weight and histology. Treadmill training could prevent bone loss induced by OVX through the inhibition of adipocyte differentiation factor PPARγ rather than promoting osteogenic factor Runx2.

摘要

运动训练已被报道可预防去卵巢(OVX)大鼠和绝经后妇女的骨丢失。我们假设,在 OVX 诱导的骨质疏松模型中,通过调节脂肪细胞分化因子过氧化物酶体增殖物激活受体 γ(PPARγ)和成骨因子 runt 相关转录因子 2(Runx2),跑步机训练可以抑制脂肪生成并增强成骨作用。为了验证这一假设,将 3 月龄雌性 Sprague-Dawley 大鼠随机分为以下几组:假手术组(Sham)、OVX 组、OVX 运动组(EX)和 OVX 雌激素替代组(E(2))。实验结束时,使用 DEXA 检测骨密度(BMD),通过 HE 染色观察骨组织和子宫的形态变化。通过免疫组织化学和 Western blot 检测 PPARγ和 Runx2 的蛋白表达,并用甲醇/氯仿提取骨三酰甘油(TG)。OVX 显著增加了脂肪空泡数量、PPARγ 和 Runx2 的蛋白水平以及胫骨和腰椎的 TG 水平。相比之下,OVX 组血清 E(2)水平、腰椎 BMD 以及股骨近端和远端 BMD 显著降低。除了 Runx2 的蛋白表达水平外,运动治疗显著逆转了 OVX 引起的所有变化。此外,运动治疗对子宫没有雌激素作用,这可以从子宫湿重和组织学上得到证明。跑步机训练可以通过抑制脂肪细胞分化因子 PPARγ来预防 OVX 引起的骨丢失,而不是促进成骨因子 Runx2。

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