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The osteogenesis-promoting effects of alpha-lipoic acid against glucocorticoid-induced osteoporosis through the NOX4, NF-kappaB, JNK and PI3K/AKT pathways
- Source :
- Scientific Reports, Scientific Reports, Vol 7, Iss 1, Pp 1-16 (2017)
- Publication Year :
- 2017
- Publisher :
- Nature Publishing Group UK, 2017.
-
Abstract
- Recently, accumulating evidence has indicated that glucocorticoid-induced osteoporosis (GIOP) is closely related to oxidative stress and apoptosis. Alpha-lipoic acid (LA), a naturally endogenous anti-oxidant, possesses anti-oxidative and anti-apoptosis activities, implicating LA as a therapeutic agent for the treatment of GIOP. In this study, the osteogenesis-promoting effects of LA against GIOP were investigated and the mechanisms were further probed. Here, the results showed that LA inhibited oxidative stress, suppressed apoptosis and improved osteopenia by promoting the expression of osteogenesis markers, including ALP, COL-I, OCN, BMP-2, RUNX2 and OSX. Further study revealed that the osteogenesis-promoting effects of LA likely occur via the regulation of the NOX4, NF-kappaB, JNK and PI3K/AKT pathways. The present study indicated that LA may prevent GIOP and promote osteogenesis and might be a candidate for the treatment of GIOP.
- Subjects :
- 0301 basic medicine
medicine.medical_specialty
MAP Kinase Kinase 4
Alpha-Lipoic Acid
Science
Biology
medicine.disease_cause
Article
Antioxidants
Cell Line
Rats, Sprague-Dawley
03 medical and health sciences
Phosphatidylinositol 3-Kinases
Osteogenesis
Internal medicine
medicine
Animals
Protein kinase B
Glucocorticoids
PI3K/AKT/mTOR pathway
Multidisciplinary
Thioctic Acid
NF-kappa B
NOX4
Rats
RUNX2
030104 developmental biology
Endocrinology
Apoptosis
NADPH Oxidase 4
Cancer research
Medicine
Osteoporosis
Female
Signal transduction
Proto-Oncogene Proteins c-akt
Oxidative stress
Signal Transduction
Subjects
Details
- Language :
- English
- ISSN :
- 20452322
- Volume :
- 7
- Database :
- OpenAIRE
- Journal :
- Scientific Reports
- Accession number :
- edsair.doi.dedup.....23cf38de6c3cb4fdfb6ed967e4c5fccc