摘要
目的观察失重下骨碎补总黄酮对成骨细胞增殖的作用及JNK通路变化,确定骨碎补总黄酮促成骨细胞增殖的机制。方法提取大鼠成骨细胞,体外培养,建立失重模型,加高、中、低骨碎补血清培养液,观察细胞形态学变化,MTT检测增殖情况,PNPP测定ALP活性,PCR测定JNK通路。结果与空白对照组和小剂量组相比,中、大剂量组细胞增殖能力及ALP活性值均明显升高,且具有统计学意义(P<0.05),与阳性对照组接近。JNK通路表达明显降低。结论骨碎补可促进模拟失重状态下成骨细胞的增殖,其作用机制可能是通过抑制JNK通路实现。
Objective To observe the role of JNK pathway in the process total flavonoidsin drynaria fortunei （TFDF） affect onosteoblastin in weightlessness. Methods Rat bone osteoblast were cultured in weightlessness, the different dose of TFDF were added, the changes of cell morphology were observed, increasing of cell was tested by MTT, ALP was tested by PNPP, JNK pathway was tested by PCR. Results Osteoblast and ALP were significantly increased （P 〈0. 05）, in TFDF group, JNK pathway was inhibited by TFDF statistically significant compared with other groups （P 〈 0. 05 ）. Conclusion TFDF can inhibit JNK pathway to increase osteoblast.
出处
《哈尔滨医科大学学报》
CAS
2016年第5期403-406,共4页
Journal of Harbin Medical University
基金
国家自然科学基金面上项目(81374070)
关键词
失重
骨碎补总黄酮
JNK
成骨细胞
weightlessness
total flavonoidsin drynaria fortunei
JNK
osteoblast
