本文關(guān)鍵詞： 去卵巢骨質(zhì)疏松 大鼠 成骨細胞 脂肪細胞 骨髓間充質(zhì)干細胞　出處：《四川大學》2005年碩士論文　論文類型：學位論文

【摘要】：絕經(jīng)后骨質(zhì)疏松癥是一種中老年婦女最常見的全身性骨骼系統(tǒng)疾病。其特點為骨量減少,骨組織微觀結(jié)構(gòu)退化,致使骨脆性增加,易于發(fā)生骨折。該病嚴重威脅著絕經(jīng)后婦女的健康和生命,給家庭和社會帶來了巨大的人力和經(jīng)濟負擔,已成為當前世界性的主要公共健康問題。目前,關(guān)于絕經(jīng)后骨質(zhì)疏松癥的病因仍不十分清楚。有研究發(fā)現(xiàn)絕經(jīng)后骨質(zhì)疏松癥引起的骨量減少往往與骨髓中的脂肪組織增多相伴行,但是有關(guān)其細胞學機制還不清楚。學者認為這種骨量減少與脂肪增多是由于成骨細胞和脂肪細胞的前體細胞-骨髓間充質(zhì)干細胞(Mesenchymal stem cells,MSCs)向兩者分化的交互關(guān)系發(fā)生了改變。在體內(nèi)一定條件下,MSCs 可以向成骨細胞、脂肪細胞和軟骨細胞等不同的細胞系分化。生理或病理條件下,如果MSCs 生長增殖能力和分化特性發(fā)生改變而影響其向成骨細胞系和脂肪細胞系分化的能力,造成骨形成過程和骨髓脂質(zhì)代謝異常,從而將打破骨形成與骨吸收之間的動態(tài)平衡,導(dǎo)致骨質(zhì)疏松癥等疾病。本研究的目的是在建立去卵巢骨質(zhì)疏松大鼠動物模型的基礎(chǔ)上,模擬絕經(jīng)后骨質(zhì)疏松的病理變化,探討體外培養(yǎng)去卵巢骨質(zhì)疏松大鼠MSCs 細胞增殖能力的改變;MSCs向成骨細胞和脂肪細胞分化能力的改變。以期揭示絕經(jīng)后骨質(zhì)疏松癥發(fā)生的相關(guān)細胞分子機制,為絕經(jīng)后骨質(zhì)疏松癥的診斷與防治提供新思路。 選用健康3 月齡和6 月齡雌性Sprague-Dawley(SD)大鼠,采用雙側(cè)卵巢切除術(shù),建立去卵巢骨質(zhì)疏松動物模型。動物實驗分成4 組:
[Abstract]:Postmenopausal osteoporosis is one of the most common systemic bone system diseases in middle-aged and elderly women. It is characterized by reduced bone mass and degeneration of bone microstructure, resulting in increased bone brittleness. The disease is a serious threat to the health and life of postmenopausal women and brings a huge human and economic burden to the family and society. It has become a major public health problem worldwide. The etiology of postmenopausal osteoporosis is still unclear. Some studies have found that bone loss caused by postmenopausal osteoporosis is often associated with increased adipose tissue in bone marrow. However, the cytological mechanism is not clear. Scholars believe that this decline in bone mass and fat increase is due to osteoblasts and adipocytes precursor cells-bone marrow mesenchymal stem cells (BMSCs). Mesenchymal stem cells. The interaction between MSCs and osteoblasts has changed. Under certain conditions in vivo, MSCs can be transformed into osteoblasts. Different cell lines such as adipocytes and chondrocytes are differentiated under physiological or pathological conditions. The ability of MSCs to differentiate into osteoblast and adipocyte is affected by the change of growth and proliferation ability and differentiation characteristic of MSCs, and the process of bone formation and lipid metabolism of bone marrow are abnormal. Thus, the dynamic balance between bone formation and bone resorption will be broken, resulting in osteoporosis and other diseases. The purpose of this study is to establish an animal model of ovariectomized osteoporosis in rats. To investigate the proliferation of MSCs cells in ovariectomized osteoporosis rats by simulating the pathological changes of postmenopausal osteoporosis. The change of differentiation ability of MSCs into osteoblasts and adipocytes in order to reveal the cellular molecular mechanism of postmenopausal osteoporosis and to provide a new idea for the diagnosis and prevention of postmenopausal osteoporosis. Female Sprague-Dawley SD rats aged 3 and 6 months were selected and bilateral ovariectomy was used to establish ovariectomized osteoporosis animal model.
【學位授予單位】：四川大學
【學位級別】：碩士
【學位授予年份】：2005
【分類號】：R361

【引證文獻】

相關(guān)碩士學位論文 前1條

1 陳晚嬌;蛇床子素對大鼠骨髓間充質(zhì)干細胞增殖和脂向分化的影響[D];暨南大學;2007年

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