Effect and related mechanism of seaweed polysaccharide on apoptosis of fibroblast-like synoviocytes in patients with rheumatoid arthritis.
- Author:
Lie DAI
1
;
Ting LI
;
Lang-jing ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Arthritis, Rheumatoid; pathology; Caspase 3; metabolism; Cells, Cultured; Fibroblasts; cytology; drug effects; Humans; Polysaccharides; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Seaweed; Synovial Membrane; cytology; drug effects; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2011;31(7):961-966
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect and related mechanism of seaweed polysaccharide (SP) on apoptosis of fibroblast-like synoviocytes in patients with rheumatoid arthritis (RA-FLS).
METHODSRA-FLS were in vitro cultured using modified tissue culture method. Effect of SP (0, 15, 20, and 25 mg/mL, respectively) at different time points (0, 3, 4, and 5 days, respectively) on the proliferation and apoptosis of RA-FLS, and protein expressions of Caspase-3, Bax, and Bcl-2 was detected by cell counting kit-8 (CCK-8) assay, Hoechst 33258 staining assay, TUNEL assay, and Western blot, respectively.
RESULTSCompared with 0 mg/mL SP at the same time point, the proliferation of RA-FLS was inhibited, and the apoptosis was promoted 3, 4, and 5 days after intervened by 15, 20, and 25 mg/mL SP, respectively (P<0.01) in time- and dose-dependent manners. RA-FLS Bax protein expression was up-regulated, Bcl-2 protein expression down-regulated, Caspase-3 activated and split by 15, 20, and 25 mg/mL SP, respectively for 4 days (P<0.05, P<0.01). Besides, the changes were in a dose-dependent manner.
CONCLUSIONSSP could inhibit RA-FLS proliferation and induce its apoptosis in dose- and time-dependent manners. Its apoptosis mechanism might be through up-regulating intracellular Bax protein expression and down-regulating Bcl-2 protein expression, thus influencing the mitochondrion signaling pathway, further promoting Caspase-3 activation and split, resulting in the apoptosis of RA-FLS.