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作 者:张铁军[1] 张伟[2] 边立功[1] 刘世昌[1] 闫甲[1] 宗一[1] 桂莉 陆地[1]
机构地区:[1]昆明医学院人体解剖学教研室,昆明650500 [2]昆明医学院第一附属医院神经内科,昆明650011 [3]云南省第三人民医院内分泌科,昆明650011
出 处:《解剖学报》2012年第5期679-684,共6页Acta Anatomica Sinica
基 金:云南省应用基础研究重点基金资助项目(2008CC007);云南省中青年学术和技术带头人后备人才培养基金资助项目(2009CI033)
摘 要:目的探讨白藜芦醇(RES)对去卵巢大鼠骨质疏松动物模型的保护作用及其分子机制。方法72只清洁级SD大鼠,按随机对照分组原则分为正常对照组、骨质疏松模型组、雌激素治疗组、RES低、中、高剂量治疗组,每组12只。除正常对照组外,双侧卵巢摘除术后1周,给予雌激素、RES治疗。12周后检测相关血清生化指标,光镜下观察骨组织形态学变化,双能X线吸收法测定其骨密度,RT-PCR检测骨组织中抗氧化酶(gpx1、trx1和γ-gt)mRNA的表达情况。结果血生化指标显示,骨质疏松模型组除血清雌激素水平明显低于其他各组外,其余指标均显著升高;骨组织形态学观察和骨密度检测提示,骨质疏松模型组骨组织呈现典型骨质疏松改变,骨组织中抗氧化酶表达降低;而雌激素治疗组和不同剂量RES治疗组血生化指标、骨组织形态学、骨密度和骨组织中抗氧化酶表达与正常对照组差异不明显。结论 RES具有类似于雌激素的维持骨形成和骨吸收平衡,拮抗骨质疏松症发生的作用,该作用与骨组织中抗氧化酶的表达量及活性相关。Objective To investigate the protective effect and its mechanism of resveratrol (RES) on rats with osteoporosis. Methods A total of 72 clean grade female SD rats were randomly divided into six cohorts: control cohort, osteoporosis model cohort, estrogen pretreated cohort, low, median and high dosage RES pretreated cohorts. Except for rats in the control cohort, rats in other cohorts were treated by bilateral oophorectomy and pretreated with 17β-E2 and different dosage of resveratrol respectively, ranging from 1 to 12 weeks after operation. The blood parameters associating with osteoporosis were tested. Morphological observation of bone tissue was performed by HE staining under a microscope. Bone mineral density was measured by a dual-energy X-ray absorptiometry. The mRNA expression level of antioxidant enzymes (gpxl , trxl and γ-gt) were assayed by RT-PCR. Results Serum calcium, serum phosphate, ALP and TRAP increased obviously, but estrogen and calcium level in serum decreased sharply in the animal model. The bone tissue of the model manifested typical osteoporosis characteristics, and the expression of antioxidant enzymes was at a low level. After treated with estrogen or different dosages of resveratrol, the parameters and phenotypes mentioned above were almost close to the control cohort. Conclusion Resveratrol, likely estrogen, can maintain a balance of bone formation and absorbance, which is critical to the homeostasis of bone, antagonizing the osteoporosis pathology progression. This protective mechanism is associated with the expression and activity of antioxidant enzymes in bone tissue.
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