NDLI: Protective effects of paeoniflorin against FasL-induced apoptosis of intervertebral disc annulus fibrosus cells via Fas-FasL signalling pathway

Content Provider	PubMed Central
Author	Chen, Shao-qing Lin, Jian-ping Zheng, Qi-kai Chen, Shui-jin Ming, Li Lin, Xian-zhao Wang, Shi-zhong
Copyright Year	2015
Abstract	In the present study, we demonstrate that the degeneration of intervertebral discs is caused by ageing and apoptosis of matrix cells. Apoptosis is as essential as the function of proteoglycan synthesis in assessing the possible degeneration of intervertebral discs; paeoniflorin (PF) induces cytoprotective effects on various types of cells. In this study, the function of PF in inhibiting Fas ligand (FasL)-induced apoptosis in annulus fibrosus cells was assessed, and the correlation between apoptosis and the Fas-FasL pathway was determined. Annulus fibrosus cells were derived from the intervertebral discs of 1-month-old Sprague Dawley rats; the cells were characterised by toluidine blue staining and subjected to apoptosis with FasL. PF was diluted to various concentrations and added to annulus fibrosus cells at various times. The impact of PF and FasL on cell apoptosis of annulus fibrosus cells was determined by flow cytometry. Western blot analysis was performed to determine the protein expression levels of Fas and caspase-3. The percentages of apoptotic annulus fibrosus cells as well as the expression levels of caspase-3 and Fas were significantly reduced following treatment with 208, 20.8 or 2.08 µM PF. PF inhibits the activation of the Fas-FasL signal pathway and decreases FasL-induced apoptosis of annulus fibrosus cells.
Related Links	http://dx.doi.org/10.3892/etm.2015.2776
Ending Page	2355
Page Count	5
Starting Page	2351
File Format	PDF
ISSN	17921015
e-ISSN	17921015
Journal	Experimental and Therapeutic Medicine
Issue Number	6
Volume Number	10
Language	English
Publisher	D.A. Spandidos
Publisher Date	2015-12-01
Access Restriction	Open
Rights Holder	D.A. Spandidos
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research 2400/2401

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