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Porcine placenta hydrolysates enhance osteoblast differentiation through their antioxidant activity and effects on ER stress

Hwa-Young Lee, Han-Jung Chae, Sun-Young Park, Jong-Hyun Kim
BMC complementary and alternative medicine 2016 v.16 no.1 pp. 291
NAD(P)H oxidase (H2O2-forming), RNA, alkaline phosphatase, alternative medicine, antioxidant activity, apoptosis, bone density, bone metabolism, bone strength, caspases, cell viability, enzyme activity, hydrogen peroxide, hydrolysates, immunoblotting, osteoblasts, osteocalcin, osteoporosis, placenta, reverse transcriptase polymerase chain reaction, superoxide dismutase, swine
BACKGROUND: Osteoporosis is a disease characterized by decreased bone strength, decreased bone mass, and bone deterioration. Oxidative damage is an important contributor to functional changes in the development of osteoporosis. Here we found that porcine placenta hydrolysates (PPHs) protect MC3T3-E1 osteoblastic cells against hydrogen peroxide (H₂O₂)-induced oxidative damage. METHODS: In vitro cell viability was determined using trypan blue dye exclusion. ER stress and apoptosis were evaluated using immunoblotting and a commercially available caspase kit. ALP, osteocalcin, Runx2, and osterix expression levels were evaluated by RT-PCR using isolated RNA. ROS, NADPH oxidase, and SOD activity levels were also measured. RESULTS: We investigated the mechanisms underlying PPH-mediated inhibition of H₂O₂-induced ER stress and ROS production. PPHs also regulated osteoblast differentiation via the upregulation of alkaline phosphatase (ALP) expression in MC3T3-E1 osteoblastic cells. Also, treatment with PPHs enhanced the transcription of osteocalcin, Runx2, and osterix. These effects were all associated with the antioxidant actions of PPHs. Moreover, PPHs reversed the decrease in SOD activity, decreased ROS release, and inhibited NADPH oxidase activity in H₂O₂-treated MC3T3-E1 osteoblastic cells. CONCLUSIONS: PPHs protect cells against H₂O₂-induced cell damage when ER stress is involved. In addition, PPHs enhance osteoblast differentiation. This enhancement likely explains the regulatory effect of PPHs on bone metabolism disturbances, i.e. PPHs control ER stress and the related ROS production in osteoblasts.