This study was conducted to investigate the correlation between lipid-lowering and bone-protective effects of eicosapentaenoic acid on steroid-induced bone changes in rats. Twenty-one male 10-week-old Wistar rats were divided into 3 groups (n = 7 each) and treated with 0.9% NaCl SC (group 1) or methylprednisolone 7 mg/kg SC once a week (group 2) or methylprednisolone 7 mg/kg SC once a week + eicosapentaenoic acid 160 mg/kg, PO daily (group 3), for 6 weeks. At the end of the experiment, serum total cholesterol and triglycerides concentrations were determined using enzymatic colorimetric assays and bone histomorphometric analyses were performed on cancellous bone of femoral epiphysis and metaphysis using a photomicroscope and a digital camera. Histomorphometric parameters demonstrated a significant bone loss due to methylprednisolone administration, which was partly restored by eicosapentaenoic acid. A strong inverse correlation was observed between the serum total cholesterol concentration and epiphyseal trabecular width and metaphyseal trabecular osteoid width (R = -0.82, P = 0.04 and R = -0.86, P = 0.01, respectively). Serum triglycerides concentration was also strongly and inversely correlated with the above mentioned parameters (R = -0.88, P = 0.02 for epiphyseal trabecular width and R = -0.81, P = 0.02 for metaphyseal trabecular osteoid width). The correlation between the lipid-lowering and bone-protective effects of eicosapentaenoic acid may be helpful in the clarification of its effects on bone and lipid metabolism.

Background: Radiation-induced hematopoietic suppression and myelotoxicity can occur due to the nuclear accidents, occupational irradiation and therapeutic interventions. Bone marrow dysfunction has always been one of the most important causes of morbidity and mortality after ionizing irradiation. Objective: This study aims to investigate the protective effect of telmisartan against radiation-induced bone marrow injuries in a Balb/c mouse model. Material and Methods: In this experimental study, male Balb/c mice were divided into four groups as follow: group 1: mice received phosphate buffered saline (PBS) without irradiation, group 2: mice received a solution of telmisartan in PBS without irradiation, group 3: mice received PBS with irradiation, and group 4: mice received a solution of telmisartan in PBS with irradiation. A solution of telmisartan was prepared and administered orally at 12 mg/kg body weight for seven consecutive days prior to whole body exposing to a single sub-lethal dose of 5 Gy X-rays. Protection of bone marrow against radiation induced damage was investigated by Hematoxylin-Eosin (HE) staining assay at 3, 9, 15 and 30 days after irradiation. Results: Histopathological analysis indicated that administration of telmisartan reduced X-radiation-induced damage and improved bone marrow histology. The number of different cell types in bone marrow, including polymorphonuclear /mononuclear cells and megakaryocytes significantly increased in telmisartan treated group compared to the only irradiated group at all-time points. Conclusion: The results of the present study demonstrated an efficient radioprotective effect of telmisartan in mouse bone marrow against sub-lethal X-irradiation.

Background: Introduction: Oxytocin (OT) has been proposed to assist in the regulation of bone remodeling and to exert an antiosteoporotic effect. We evaluated the possible protective effect of OT against bone degeneration in ovariectomized (OVX) rats. Methods: The study was performed on three groups of adult female rats,group I was subjected to sham operation, group II was subjected to ovariectomy, and group III was subjected to ovariectomy and intraperitoneal injection with OT for eight successive weeks. At the end of the study, bone mass density (BMD) was measured,then the rats were euthanized and their blood and bone tissues were examined. Results: The group II rats had significantly less BMD and greater serum bone-specific alkaline phosphatase (bALP), osteocalcin (OC), and tartrate-resistant acid phosphatase (TRAP) levels than the group I rats. Furthermore, group II rats had fewer osteocytes and osteoblasts, and less OPG/RANKL mRNA expression than group I rats. The groups I and III and rats showed no significant differences in BMD, bALP, OC, TRAP, OPG/RANKL mRNA expression, or osteocyte and osteoblast numbers. Conclusions: Oxytocin may have an antiosteoporotic effect in OVX rats.

Objective(s): This study aimed to determine the therapeutic effect of equol (EQ) on osteoporotic osteoarthritis (OP OA). Materials and Methods: Thirty-six 12-week-old female Sprague-Dawley rats were randomly divided into sham group, OP OA group, and EQ group (n=12). OP OA was induced by anterior cruciate ligament transection (ACLT) combined with ovariectomy (OVX). EQ was orally administrated (10 μ, g/g/day) after the operation for 12 weeks. The efficacy was evaluated by gross pathology and histopathologic evaluation. The underlying mechanism was investigated by immunohistochemical analysis, micro-computed tomography (micro-CT) scanning, and tartrate-resistant acid phosphatase (TRAP) staining. Results: EQ effectively retarded cartilage degeneration, decreased the levels of matrix metalloproteinases-13 (MMP-13), a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5), nuclear factor-kappa B P65 (NF-κ, B P65) and caspase-3, and increased the levels of collagen type II (Col-II), Col-I, aggrecan (AGG), and inhibitor of NF-κ, B α,(Iκ, Bα, ) in the cartilage. In addition, EQ increased bone mineral density, improved the microstructural parameters of the subchondral bone (SB), and decreased the number of osteoclasts. Conclusion: EQ exerted a chondroprotective effect on OP OA in rats, associated with inhibition of the NF-κ, B signaling pathway and chondrocyte apoptosis. Furthermore, EQ showed an osteoprotective effect on SB via inhibiting osteoclastic activities.