Porcine placenta hydrolysates regulate calcium disturbance in MC3T3-E1 osteoblastic cells.
BMC Complement Altern Med
; 16: 237, 2016 Jul 25.
Article
em En
| MEDLINE
| ID: mdl-27457075
ABSTRACT
BACKGROUND:
In bone metabolism, Ca(2+) disturbance and oxidative damage are the main biochemical factors related to pathology. Osteoblasts are bone-forming cells that also control bone endocrinology. Endocrine hormones and proteins are matured, folded, and secreted in the endoplasmic reticulum (ER). ER stress has emerged as a new pathological mechanism to explain bone disturbance. Here we studied the role of porcine placenta hydrolysates (PPHs) in the regulation of ER stress.METHODS:
Cell viability was determined in vitro using trypan blue dye exclusion. ER stress and apoptosis were evaluated using immunoblotting and a caspase kit. The fluorescent Ca(2+)-binding dye Fura-2/AM was used to measure changes in intracellular Ca(2+) ([Ca(2+)]i). ROS levels, NADPH oxidase activity, and superoxide dismutase (SOD) activity were also measured.RESULTS:
PPHs protected MC3T3-E1 osteoblastic cells against thapsigargin (Tg)-induced ER stress. Moreover, PPHs regulated caspase-12 and -3 activities, thereby protecting against cell death, and also regulated Tg-induced Ca(2+) release. The Ca(2+) chelator BAPT/AM also regulated caspase-12 and -3 activities and prevented Ca(2) stress-induced cell death. In the presence of PPHs or BAPTA/AM, Ca(2+)-related ROS were also regulated, as demonstrated by alterations in NADPH oxidase and SOD activity.CONCLUSIONS:
PPHs appear to regulate bone metabolism disturbance by controlling Ca(2+) concentrations, and thus ER stress and ROS, in osteoblasts cultured in vitro.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Osteoblastos
/
Placenta
/
Produtos Biológicos
/
Estresse Oxidativo
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Sinalização do Cálcio
Limite:
Animals
/
Pregnancy
Idioma:
En
Revista:
BMC Complement Altern Med
Assunto da revista:
TERAPIAS COMPLEMENTARES
Ano de publicação:
2016
Tipo de documento:
Article