ABSTRACT
BACKGROUND: It has been found that salidroside can improve diabetic retinopathy. However, it is not clear whether salidroside can protect retinal Müller cells (rMC-1) against damage induced by high glucose. OBJECTIVE: To investigate the effect and mechanism of salidroside on oxidative stress and apoptosis induced by high glucose in rat rMC-1 cells. METHODS: The rMC-1 cells were divided into four groups: normal control group, high glucose group (culture medium with a final glucose concentration of 35.5 mmol/L), salidroside group (treatment with salidroside for 4 hours followed by co-culture with high glucose) and PI3K inhibitor group (treatment with salidroside and PI3K inhibitor for 4 hours followed by co-culture with high glucose). The viability of the rMC-1 cells was measured by cell counting kit-8 assay. Reactive oxygen species production was detected by DCFH-DA. The superoxide dismutase and catalase activities were tested by specific kits. Cell apoptosis was detected by flow cytometry. Western blot was used to detect the expression levels of Cleaved caspase-3, PI3K, AKT and phosphorylated AKT. RESULTS AND CONCLUSION: Compared with the normal control group, the cell viability and the activities of antioxidant enzymes (superoxide dismutase, catalase) in the high glucose group were significantly decreased, the production of reactive oxygen species, apoptotic rate and the level of Cleaved caspase-3 were significantly increased, and the phosphorylated AKT/AKT ratio was down-regulated (P < 0.05). Compared with the high glucose group, salidroside significantly enhanced the cell viability and increased the activities of antioxidant enzymes (superoxide dismutase, catalase), decreased the production of reactive oxygen species, reduced the apoptotic rate of the cells and downregulated the expression level of Cleaved caspase-3 (P < 0.05). Salidroside also activated the phosphorylation of Akt (P < 0.05). Whereas, the addition of LY294002, a pharmacological inhibitor of PI3K, showed similar results in the high glucose group (P < 0.05). To conclude, salidroside can protect rMC-1 cells through inhibiting apoptosis and oxidative stress induced by high glucose. The main mechanism responsible for the inhibition of oxidative stress is the activation of the PI3K/Akt pathway.