Abstract
Osteoporosis is a common disease causing fracture in older populations. Abnormal apoptosis of osteoblasts contributes to the genesis of osteoporosis. Inhibiting apoptosis of osteoblasts provides a promising strategy to prevent osteoporosis. The proliferation of osteoblasts isolated from osteoporotic patients or healthy subjects was determined by MTT assay. Apoptosis was determined by Annexin V/PI assay. Protein expression was measured by western blot. The proliferation of osteoblasts isolated from osteoporotic patients was inhibited and the apoptosis level of these cells was higher than the osteoblasts from healthy subjects. Incubation with psoralen or estradiol significantly enhanced the proliferation and decreased the apoptosis level of osteoporotic osteoblasts. Western blot demonstrated that psoralen or estradiol treatment downregulated the expression of IRE1, p-ASK, p-JNK, and Bax. Meanwhile, expression of Bcl-2 was upregulated. Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts. Psoralen inhibited apoptosis of osteoporotic osteoblasts by regulating IRE1-ASK1-JNK pathway.
Highlights
Osteoporosis is a disease which was characterized by low bone mass and increased susceptibility to fracture [1]
Our results demonstrated that psoralen enhanced the proliferation of osteoblast and blocked the apoptosis of osteoblast by modulating inositol-requiring enzyme 1 (IRE1)/apoptosis signaling kinase 1 (ASK1)/c-jun N-terminal kinase (JNK) pathway
There was report indicating that idiopathic osteoporotic and normal cells had no differences in their growth rate [14], more studies supported our results that osteoporotic osteoblasts exhibited inhibitory cell growth compared with normal cell
Summary
Osteoporosis is a disease which was characterized by low bone mass and increased susceptibility to fracture [1]. It is a major reason for fracture among older people [2]. Agerelated sex hormone deficiency and other factors result in the increased bone resorption but reduced the bone formation by decreasing the number and quality of osteoclasts. Insufficient bone formation relative to bone resorption plays an important role in mediating bone loss accompanied with aging and sex hormone deficiency [5]. Current evidence suggested that estrogen prevents bone loss owing to its antiapoptosis effects in osteoblasts, but the mechanism has not been fully investigated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
