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溶髓方对大鼠椎间盘退变中软骨终板IL-1β的影响 被引量:7

Influence of Rongsui Formula on IL-1β in Cartilage Endplate of Rats with Intervertebral Disc Degeneration
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摘要 目的:观察溶髓方对大鼠椎间盘退变中软骨终板IL-1β的影响。方法:选取36只wista大鼠,鼠龄6周,体重为(100±20)g,随机分成假手术组、模型对照组、溶髓方实验组,每组12只。建立大鼠颈椎动力平衡失调模型,诱导椎间盘退变(假手术组仅作颈背后正中皮切开缝合),造模1周后实验组予以溶髓方中药灌胃1月,假手术组和模型对照组喂等量生理盐水。在术后9周、18周、36周处死每组四只动物,用酶联免疫吸附试验(Elisa)检测椎间盘中白介素-1β含量,并在形态学上评定椎间盘退变程度。结果:对照组中椎间盘中白介素-1β含量明显升高,椎间盘细胞数量减少、细胞形态变化明显,细胞外基质中胶原水平减少,并出现大量裂隙,溶髓方可部分延缓这一过程:溶髓方可以部分抑制椎间盘细胞减少,随着培养时间延长,对照组各组椎间盘软骨终板的白介素-1β含量明显增加,溶髓方则可抑制IL-1β含量的增加。结论:溶髓方可抑制炎性因子白介素-1β含量的增加,阻止椎间盘细胞数量的凋亡,对椎间盘具有保护作用。 Objective: To observe the effects of Rongsui Formula on IL-1β level in the cartilage endplate for the rats with intervertebral disc degeneration. Methods: Thirty-six Wistar rats were randomly divided into 3 groups: the sham-operation group,the model group( control group) and Rongsui Formula group( experimental group),12 rats in each group. The rat model of power imbalance that induced cervical intervertebral discs degeneration was established. One week after the model accomplished,rats of experimental group took Rongsui Formula drugs by intragastric administration a month,and meantime,rats of sham-operation group and model control group were fed with isodose normal saline respectively. Four animals were sacrificed in each group at the end of week 9,18,36,respectively. IL-1β level in the cartilage endplate was tested simultaneously and the cell morphology changes of the endplate cartilage degeneration were assessed. Results: Prolonged incubation and extensive culturing lowered the IL-1βlevel of discs and inhibited the decrease of intervertebral discs cells significantly in the experimental group. Conclusion: Rongsui Formula may have the protective effects of intervertebral discs by lowering the IL-1β level in the intervertebral discs.
出处 《辽宁中医杂志》 CAS 2014年第6期1284-1287,共4页 Liaoning Journal of Traditional Chinese Medicine
基金 2011年度广西壮族自治区中医药管理局中医药科技专项课题(GZKZ1128)
关键词 椎间盘 软骨终板 溶髓方 白介素-1Β intervertebral discs cartilage endplate Rongsui Formula IL-1β
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参考文献11

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