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作 者:林一峰[1] 张震[2] 刘海全[1] 原超[1] 唐汉武[1] 宋振杰[1] 王利仁[1]
机构地区:[1]广州中医药大学第三附属医院,广东广州510240 [2]广州中医药大学
出 处:《中医临床研究》2016年第13期16-18,共3页Clinical Journal Of Chinese Medicine
基 金:广东省科技计划项目(编号:2011B031800047);国家自然科学基金资助项目(编号:81574000)
摘 要:目的:观察补肾壮督方对大鼠腰椎间盘退变的病理及对椎间盘三磷酸腺苷(ATP)酶和肿瘤坏死因子-α(TNF-α)的影响。方法:利用针刺纤维环的方法建立大鼠椎间盘退变模型,造模成功后,随机分为空白组、模型组、补肾壮督方组、塞来昔布组,在模型建立8周后检测椎间盘组织超微量ATP酶活性和TNF-α含量,电镜扫描椎间盘胶原纤维及成纤维细胞超微结构的变化。结果:1与空白组相比,补肾壮督方组、塞来昔布组、模型组均出现明显的病理退变;与模型组相比,补肾壮督方组的病理退变较轻。2与空白组相比,模型组腰椎间盘的ATP酶活性降低,TNF-α含量升高,差异有显著的统计学意义(P<0.01);与模型组相比,补肾壮督方组腰椎间盘的ATP酶活性升高,差异有统计学意义(P<0.05),补肾壮督方组椎间盘的TNF-α含量降低,有显著的统计学差异(P<0.01)。结论:补肾壮督方具有抑制椎间盘退变作用,其机制可能与提高椎间盘组织ATP酶活性和降低TNF-α表达有关。Objective: To investigate clinical effects of Bushen Zhuangdu San on ATP enzyme and TNF-α in rats with lumbar disc degeneration- Methods: The lumbar disc degeneration models were established by annulus puncture-The rats were divided into 4 groups randomly after successful modeling, namely: the blank control group, the model group, the Bushen Zhuangdu San group and the celecoxib capsules group- In 8 weeks, the content of ATP enzyme and TNF-α were detected; the changes of intervertebral disc collagen fibers and fibroblasts ultrastructure were scanned by electron microscopy- Results: 1 Compared with the blank control group, lumbar degeneration disces in rats in others groups were obvious- Compared with the model group, the changes of lunbar degeneration disces in the Bushen Zhuangdu San group were slighter- 2 Compared with the blank control group, the expression of ATP enzyme in the model group was reduced; the expression of TNF-α was increased in the model group; the differences were very significant(P〈0-01)- Compared with the model group, the expression of ATP enzyme was increased in the Bushen Zhuangdu San group; and the differences were very significant(P〈0-05); the expression of TNF-α was reduced in the Bushen Zhuangdu San group; and the differences were very significant(P〈0-01)-Conclusion: Bushen Zhuangdu San can improve disc tissue ATP enzyme activity and reduce the expression of TNF-α,which may explain the mechanism of protective effect on intervertebral disc degeneration.
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