【摘要】：婦女絕經(jīng)后因卵巢功能下降、雌激素水平驟降,體內(nèi)骨轉(zhuǎn)換率顯著加快,骨吸收的速度超過骨形成的速度,導(dǎo)致骨量丟失、骨密度下降、骨骼脆性增加引起的骨質(zhì)疏松癥稱為絕經(jīng)后骨質(zhì)疏松癥(postmenopausal osteoporosis,PMOP)。婦女絕經(jīng)后雌激素分泌銳減,加速骨質(zhì)的流失,PMOP儼然成為一種嚴(yán)重危害社會公共健康的高發(fā)性疾病,也是國際骨病研究中的熱點(diǎn)和難點(diǎn)。本研究通過觀察雌二醇對絕經(jīng)后骨質(zhì)疏松大鼠骨組織、子宮、陰道結(jié)構(gòu)損傷的影響,以及雌二醇對骨質(zhì)疏松大鼠骨組織肥大細(xì)胞增生的影響,探討雌二醇對骨質(zhì)疏松大鼠骨組織和生殖系統(tǒng)損傷的修復(fù)作用及肥大細(xì)胞作為絕經(jīng)后骨質(zhì)疏松癥診斷和治療依據(jù)的可能性。本研究以3月齡SD大鼠構(gòu)建絕經(jīng)后骨質(zhì)疏松大鼠模型,然后通過腹腔注射雌二醇進(jìn)行治療性給藥。給藥結(jié)束后頸椎脫臼處死大鼠,計(jì)算各臟器指數(shù),采用火焰原子吸收法檢測血清鈣(Ca)含量,ELISA法檢測血清中的雌二醇(E2)和堿性磷酸酶(ALP)水平;股骨、脛骨、股骨頭組織固定和脫鈣后制作石蠟切片,進(jìn)行HE染色和甲苯胺藍(lán)染色,應(yīng)用Image-Pro Plus圖像分析系統(tǒng)進(jìn)行形態(tài)計(jì)量學(xué)分析,顯微計(jì)數(shù)骨組織肥大細(xì)胞數(shù)量;取子宮和陰道組織常規(guī)石蠟切片后HE染色,顯微觀察子宮、陰道的組織病理學(xué)變化,并進(jìn)行形態(tài)計(jì)量學(xué)分析。研究結(jié)果表明:去卵巢組大鼠較假手術(shù)組血清Ca顯著降低(P0.05)、血清E2顯著降低(P0.01)、血清ALP顯著升高(P0.01),子宮指數(shù)顯著降低(P0.01);去卵巢組大鼠股骨干骺端和股骨頭的骨小梁面積百分率和骨小梁厚度較假手術(shù)組顯著降低(P0.01),骨小梁間距增大(P0.01);去卵巢組股骨和股骨頭橫斷面全層的肥大細(xì)胞數(shù)量較假手術(shù)組顯著增多(P0.01);子宮管徑厚度降低(P0.01)、子宮黏膜上皮厚度和子宮腺體數(shù)量降低(P0.05);陰道黏膜上皮厚度和肌層血管數(shù)量降低(P0.01),固有層血管數(shù)量減少(P0.05),而給藥雌二醇治療后以上癥狀均得到緩解。由研究結(jié)果得到以下結(jié)論:3月齡SD大鼠去除卵巢后3個(gè)月可成功建立絕經(jīng)后骨質(zhì)疏松疾病模型;間歇性腹腔注射雌二醇可有效改善去卵巢骨質(zhì)疏松大鼠的骨代謝生化指標(biāo)以及骨組織微結(jié)構(gòu),具有防治絕經(jīng)后骨質(zhì)疏松癥的作用;雌二醇可有效抑制去卵巢骨質(zhì)疏松大鼠的骨肥大細(xì)胞增生,骨肥大細(xì)胞有望成為絕經(jīng)后骨質(zhì)疏松癥診斷和治療的依據(jù);雌二醇可有效緩解去卵巢骨質(zhì)疏松大鼠子宮和陰道的萎縮,對絕經(jīng)后骨質(zhì)疏松大鼠生殖系統(tǒng)損傷具有修復(fù)作用。
[Abstract]:In postmenopausal women, due to the decrease of ovarian function, the level of estrogen plummeted, the bone turnover rate in vivo was significantly accelerated, the rate of bone resorption exceeded the rate of bone formation, resulting in bone mass loss and decreased bone mineral density. Osteoporosis caused by increased bone fragility is called postmenopausal osteoporosis (postmenopausal osteoporosis,PMOP). With the sharp decrease of estrogen secretion and accelerated bone loss in postmenopausal women, PMOP has become a high incidence disease which seriously endangers social and public health, and is also a hot and difficult point in international bone disease research. The purpose of this study was to observe the effects of estrogen on bone tissue, uterus and vaginal structure injury in postmenopausal osteoporosis rats, and the effect of estrogen on mastocyte proliferation in bone tissue of osteoporotic rats. To investigate the repair effect of estrogen on bone tissue and reproductive system injury in osteoporotic rats and the possibility of mast cells as the basis for the diagnosis and treatment of postmenopausal osteoporosis. In this study, 3-month-old SD rats were used to establish the rat model of postmenopausal osteoporosis, and then Estradiol was injected intraperitoneally for therapeutic administration. After administration, the rats were killed after cervical dislocated. The indexes of each organ were calculated. The content of serum calcium (Ca) was measured by flame atomic absorption spectrometry, and the levels of estrogen (E2) and alkaline phosphatase (ALP) in serum were measured by ELISA method. Paraffin sections were made after fixation and decalcification of femur, tibia and femoral head. HE staining and toluidine blue staining were performed. Morphometric analysis was carried out by Image-Pro Plus image analysis system, and the number of mastocytes in bone tissue was counted microscopically. The pathological changes of uterus and vagina were observed by HE staining after routine paraffin sections of uterus and vagina, and morphometric analysis was carried out. The results showed that serum Ca, E2, ALP and uterine index in ovariectomy group were significantly lower than those in pseudo-operation group (P 0.05), P < 0.01, P 0.01, P < 0.01, respectively. The percentage of bone trabecular area and the thickness of bone cerebellum in ovariectomy group were significantly lower than those in false operation group (P 0.01), and the distance between bone trabeculae was increased (P 0.01). Compared with the pseudo-operation group, the number of mastocytes in the cross section of the femur and femoral head in the ovariectomy group was significantly increased (P 0.01), the thickness of uterine canal diameter was decreased (P 0.01), the thickness of uterine mucous membrane and the number of uterine gland were decreased (P 0.05), and the thickness of uterine canal diameter was decreased (P < 0.01). The thickness of vaginal mucosa and the number of vessels in muscle layer decreased (P 0.01), the number of vessels in lamina propria decreased (P 0.05), and the above symptoms were relieved after treatment with estridiol. The conclusions are as follows: 3 months old SD rats can successfully establish postmenopausal osteoporosis model 3 months after ovariectomy. Intermittent intraperitoneal injection of estrogen can effectively improve the biochemical indexes of bone metabolism and bone tissue microstructure in ovariectomy osteoporosis rats, and has the effect of preventing and treating postmenopausal osteoporosis. Estradiol can effectively inhibit the proliferation of bone hypertrophic cells in ovariectomy osteoporosis rats, and bone hypertrophic cells are expected to be the basis for the diagnosis and treatment of postmenopausal osteoporosis. Estradiol can effectively alleviate the atrophy of uterus and vagina in ovariectomy osteoporosis rats and repair the reproductive system injury in postmenopausal osteoporosis rats.
【學(xué)位授予單位】：陜西理工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R580

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