密骨片对破骨细胞基质金属蛋白酶-9mRNA表达的影响  被引量:1

Effects of Migu Tablet on Expression of Matrix Metailoproteinase-9 mRNA in Osteoclasts

在线阅读下载全文

作  者:沈霖[1] 杜靖远[1] 赵海波 

机构地区:[1]华中科技大学同济医学院附属协和医院,武汉430022

出  处:《中国中西医结合杂志》2001年第S1期135-137,共3页Chinese Journal of Integrated Traditional and Western Medicine

基  金:卫生部科学研究基金(No.96-1-153)

摘  要:目的:探讨白细胞介素-1(IL-1)诱导的破骨细胞性骨吸收过程中基质金属蛋白酶-9(MMP-9)mRNA 的表达及补肾中药密骨片的调控作用。方法:从出生24 h 的乳鼠长骨中分离破骨细胞,从1月龄大鼠长骨中分离骨髓基质细胞,建立破骨细胞培养和骨髓基质细胞、破骨细胞培养系。在重组 IL-1α(rhIL-α)作用的同时,加入不同剂量的密骨片药液,分别与牛骨片共同培养20 h,计数骨吸收陷窝数及测算陷窝面积;并采用原位杂交技术研究破骨细胞 MMP-9 mRNA 的表达。结果:在基质细胞存在的条件下,IL-1可使骨吸收活性提高2~4倍,MMP-9 mRNA 呈高表达;而用密骨片药液处理后,MMP-9 mRNA 表达下降,作用呈量效关系。结论:密骨片可对抗 IL-1对基质细胞的影响,抑制破骨细胞重要的蛋白分解酶 MMP-9的表达而减少骨吸收。To investigate the expression of matrix metalloproteinase-9(MMP-9)mRNA in the course of osteoclastic bone resorption induced by interleukin-1(IL-1)and the regulation of Migu Tablet(MGT)on it.Methods:Osteoclasts were isolated from 1 day old neona- tal rat long bones and bone marrow stroma cells(BMSCs)were isolated from 1 month old Wistar rats long bones.Osteoclasts culture and osteoclasts,BMSCs co-culture system were established.The number of resorption lacunae on each slice and the plane surface area were measured after incubation on bone slice for 20 hrs in the presence of rhlL-1α and MGT of various dosages.Using in situ hybridization on cultured cell,the expression of MMP-9 mRNA in osteoclasts were studied.Results:In the presence of BMSCs,IL-I caused 2 to 4 fold enhancement of bone resorption and the high level of MMP-9 mRNA expression in osteoclasts.After treatment with MGT,MMP-9 ex- pression was declined in dose dependent manner.Conclusion:The role of MGT could resist the effects of IL-1 on BMSCs,decrease the bone resorption by inhibiting the MMP-9 expression,one of the key proteolytic enzymes in osteoclasts.

关 键 词:密骨片 基质金属蛋白酶-9 破骨细胞 骨吸收 

分 类 号:R285.5[医药卫生—中药学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象