title: Porcine placenta hydrolysates enhance osteoblast differentiation through their antioxidant activity and effects on ER stress.
abstract: 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.
authors.affiliation: Department of Pharmacology and Institute of Drug Development, Chonbuk National University, Jeonju, 560-182, Republic of Korea.
authors.forename: Hwa-Young
authors.initials: HY
authors.lastname: Lee
authors.affiliation: Department of Pharmacology and Institute of Drug Development, Chonbuk National University, Jeonju, 560-182, Republic of Korea.
authors.forename: Han-Jung
authors.initials: HJ
authors.lastname: Chae
authors.affiliation: CODEBIO CO., LTD, Busong 1gil 62, Jiksan-eup, Seobuk-gu, Cheonan, Chungnam, 331-815, Republic of Korea.
authors.forename: Sun-Young
authors.initials: SY
authors.lastname: Park
authors.affiliation: Department of Obstetrics and Gynecology, Institute for Medical Sciences, Chonbuk National University Medical School, Jeonju, 560-182, Republic of Korea. obgyn2001@naver.com.
authors.forename: Jong-Hyun
authors.initials: JH
authors.lastname: Kim
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001688:Biological Products / Q000737:chemistry / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D005260:Female; D006861:Hydrogen Peroxide; D051379:Mice; D010006:Osteoblasts / Q000187:drug effects*; D010920:Placenta / Q000737:chemistry*; D011247:Pregnancy; D013552:Swine
chemical_list: D000975:Antioxidants; D001688:Biological Products; D006861:Hydrogen Peroxide
keywords: Alkaline phosphatase; Apoptosis; Osteoporosis; Oxidative damage; ROS