Salidroside Suppresses IL-1β-Induced Apoptosis in Chondrocytes via Phosphatidylinositol 3-Kinases (PI3K)/Akt Signaling Inhibition
Mingzheng Wu, Rui Hu, Junwen Wang, Ying An, Lin Lu, Chao Long, Li Yan
Department of Orthopedics, Pu’ai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China (mainland)
Med Sci Monit 2019; 25:5833-5840
DOI: 10.12659/MSM.917851
Available online: 2019-08-05
Published: 2019-08-05

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-1ß-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, Phosphatidylinositol 3-Kinases