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作 者:姜月艳[1] 方剑利[1] 毛强[1] 童培建[2]
机构地区:[1]浙江中医药大学,杭州310053 [2]浙江省中医院,杭州310000
出 处:《医学研究杂志》2011年第11期35-38,共4页Journal of Medical Research
基 金:国家自然科学基金资助项目(30672702)
摘 要:目的通过基因芯片技术研究右归饮对激素性股骨头坏死(SINFH)氧化应激途径相关基因表达的影响,筛选出右归饮抗氧化应激的可能作用位点,为中药防治SINFH的研究奠定基础。方法取健康成年Wistar大鼠20只,随机分为模型对照组和右归饮治疗组,每组各10只。两组大鼠均以腹腔注射大肠杆菌内毒素后,于左侧臀肌注射大剂量甲泼尼龙的方法建立激素性股骨头坏死模型。模型对照组予以蒸馏水灌胃,右归饮治疗组给予右归饮灌胃,每天1次。6周后取两组大鼠的左侧股骨头标本进行组织病理学观察和基因芯片检测。结果组织病理学观察可见模型组大鼠出现骨细胞坏死,骨小梁紊乱、变细,空骨陷窝率增加;右归饮治疗组骨小梁板层样结构稀疏但较为整齐,骨小梁边缘成骨细胞多见,软骨下血管丰富,偶见少量空骨陷窝。基因芯片检测发现氧化应激途径(oxidative stress)活性下降,代表性基因为Gclc、SOD3和COX6A2。结论右归饮可影响大鼠激素性股骨头坏死组织中氧化应激相关基因的表达,代表性基因为Gclc、SOD3和COX6A2。Objective To identify the effect of You gui yin on oxidative stress(OS) - related gene expression in SINFH rats by using gene chip technique, then to detect the possible correspondent binding sites of You gui yin in OS - related genes,with the hope of building a foundation for further studies of TCM treatment on SINFH. Methods Totally 20 healthy matured Wistar rats were divided into controlled group and You gui yin group randomly. There were 10 rats within each group. The SINFH rat model of both groups was built by in- traperitoneal injection of Escherichia coli endotoxin combined with high - dosage Methylprednisolone injection in left hip muscle. Controlled group was given distilled water. You gui yin group was given You gui yin, fed through gastric tube once a day for 6 weeks. Then the left femur head was harvested for gene chip detection and histopathological observation. Results Histopathological observation showed that controlled group had lots of bone cell necrosis, bone trabecula structural disorder and increased bone lacuna rate; while You gui yin group presented relatively organized bone trabecula with active osteoblast cells by the edge, rich vessels beneath cartilage and rare bone lacuna. Gene chip detection found OS pathway activity downward modulation, especially in 3 prominent gene sites (Gclc, SOD3 and COX6A2). Conclusion You gui yin can influence OS - related gene expression in SINFH, especially in Gclc,SOD3 and COX6A2 gene sites.
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