Osteoporosis, a skeletal disorder characterized by low bone mass associated with destruction of trabecular structure, threatens bone health of women in the world. The major contributing factors of osteoporosis are withdrawal of ovarian oestrogen production in postmenopausal women. 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), an endogenous ligand for peroxisome proliferator-activated receptor gamma (PPARγ), is one of the terminal products of the cyclooxygenase 2-catalysed reactions. 15d-PGJ2 has been known to exert various biological actions, such as anti-inflammatory, anti-viral, anti-tumour, and apoptotic activities. Previous several studies also demonstrated that 15d-PGJ2, as PPARγ agonist, ameliorated rheumatoid arthritis and suppressed RANKL or TNF-α-mediated osteoclast differentiation. This study investigated the activity of 15d-PGJ2 on bone loss of postmenopausal oestrogen deficiency in ovariectomised (OVX) mice. The OVX mice causing oestrogen deprivation led to a gain of body weight, changes of bone turnover markers in blood serum, and significant destruction in femoral bone, compared with sham-operated mice. However, 15d-PGJ2 treatment inhibited the increase of body weight, and almost recovered the serum levels of TRAP, CTX, ALP, osteocalcin and calcium in OVX mice. 15d-PGJ2 also reduced levels of pro-inflammatory cytokines, including TNF-α and IL-1β, increased by ovariectomy. Histomorphometric and histological analysis supported that 15d-PGJ2 blocked the damage of femur trabecular architecture in OVX mice. In particular, anti-osteoporotic effect of 15d-PGJ2 at high dosage is similar to that of 17β-oestradiol. Taken together, these results propose that 15d-PGJ2 may inhibit trabecular bone loss by oestrogen deficiency.
Disclosure: The authors declared no competing interests.