05 August 2019 : Laboratory Research
Salidroside Suppresses IL-1β-Induced Apoptosis in Chondrocytes via Phosphatidylinositol 3-Kinases (PI3K)/Akt Signaling Inhibition
Mingzheng Wu1AB, Rui Hu1C, Junwen Wang1AF, Ying An1EF, Lin Lu1EF, Chao Long1DF, Li Yan1ACE*DOI: 10.12659/MSM.917851
Med Sci Monit 2019; 25:5833-5840
Abstract
BACKGROUND: Salidroside, a natural dietary isothiocyanate, has been widely studied for its multiple effects, including promoting proliferation, anti-inflammation, and anti-apoptosis. In the present study, these effects of Salidroside were explored to assess whether it could prevent osteoarthritis (OA) in vitro.
MATERIAL AND METHODS: The cytotoxic and proliferating effects of Salidroside on chondrocytes were detected by use of the Cell Counting Kit 8 assay. The expression levels of proteins were detected by Western blot. The cell apoptosis level was assessed by flow cytometry, and the levels of ROS, NO, caspase 3, and caspase 9 were assessed to evaluate the level of apoptosis. The expression level of pro-inflammatory factors was detected by ELISA.
RESULTS: Our results demonstrated that Salidroside promotes chondrocytes proliferation, inhibits IL-1β-induced apoptosis and inflammation, and scavenges reactive oxygen species (ROS) and NO of chondrocytes. Salidroside upregulates the level of Bcl-2 and downregulates the level of Bax. Salidroside also inhibits the production of caspase 3/9 and suppresses the phosphorylation of PI3K and AKT.
CONCLUSIONS: Our results suggest that Salidroside prevents OA by its powerful pro-proliferating, anti-phlogistic, and anti-apoptotic effects by inhibiting PI3K/AKT.
Keywords: Chondrocytes, Glucosides, Nitric Oxide, Osteoarthritis, Proto-Oncogene Proteins c-bcl-2, bcl-2-Associated X Protein
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