辛伐他汀促进成骨细胞在牵张应力作用下产生增殖、抗凋亡等反应及其机制

应力转导异常所造成的骨科临床众多疾病，如骨质疏松等，给社会带来沉重经济负担，患者带来极大的痛苦。雌激素受体ERα在骨组织应力转导中起重要作用，ERα减少可以造成骨组织对于应力反应减低，导致骨质疏松。我们前期试验发现，辛伐他汀在体内、体外可以诱导骨组织表达ERα，那么，辛伐他汀是否可以因此促进ERα参与的应力转导呢？我们体外培养成骨细胞，检测辛伐他汀对于应力作用下成骨细胞增殖、抗凋亡等反应的影响，以及对ERα相关信号通路重要因子表达情况。体内试验通过MicroCT、检测骨密度、病理等手段检测辛伐他汀和应力共同作用于大鼠胫骨的成骨效果。通过这些研究，初步探索辛伐他汀对于成骨细胞受到应力后各种反应的影响，为临床治疗和组织工程提供实验依据和理论支持。

Mechanical stress is transducted into biochemical signals in bone and many other tissues.The abnormal mechanotransduction is an important part in many diseases, such as osteoporosis.These diseases bring heavy ecnomic burden to the society and great suffering to patients. We found in articles that estrogen receptor alpha(ERα) is a key factor in mechanotransduction of bone. The deficience of ERα leads to low response of bone to mechanical stress, which ultimately results in osteoporosis.In our previous studies, simvastatin induced ERα expression in bone tissue. We thus assume that simvastatin can promote the mechanotransduction process which involves ERα. We use western blot and RT-PCR to explore whether simvastatin promotes the effect that mechanical stress enhance proliferation, differentiation, and antiapoptosis of osteoblast and the signal pathway involved ERα, in vitro. And in vivo, we examine the BMD and HE slides to identify simvastatin and mechanical stress' effect. In this research, we fundmentally explore the effect of simvastatin in mechanical response of osteoblasts. The research may shed lights on the clinical therapy of osteoporosis and bioengineering.