Abstract: AIM:To explore the protective effects and the underlying mechanism of salidroside (SDS) on lipopolysaccharide (LPS)-induced inflammation in murine macrophage RAW264.7 cells. METHODS: Cells were divided randomly into eight groups: control group (A group), LPS group (B group), SDS 5 group (C group), SDS 5+LPS group (D group), SDS 10 group (E group), SDS 10+LPS group (F group), SDS 20 group (G group) and SDS 20+LPS group (H group). After cells were stimulated with LPS (1 μg/ml) for 6 h in the presence or absence of 0-20 μg/ml SDS for 1 h, activation of nuclear factor kappa B (NF-κB) was detected and analyzed by Western blotting. Supernatant was then used for determination of TNF-α, IL-6, and IL-10 levels by ELISA and lactate dehydrogenase (LDH) activity with corresponding detection kit according to the manufacturer’s instructions. Cells were stimulated with LPS (1 μg/ml) for 24 h in the presence or absence of 0-20 μg/ml SDS for 1 h, and cell viability was measured using the MTT assay. RESULTS: MTT assay showed that 1 μg/ml LPS reduced cell viability, but SDS concentration-dependently reversed LPS-induced reduction of cell viability. Western blotting showed that SDS markedly inhibited the activation of NF-κB in LPS-treated cells. SDS concentration-dependently reduced LPS-induced TNF-α, IL-6, and LDH content and increased IL-10 content. CONCLUSION: Salidroside plays an important role in anti-inflammation of murine macrophage RAW264.7 cells induced by LPS. Protection may be correlated with inhibition of inflammatory factors through NF-κB signal pathway and the balance between pro- and anti-inflammatory systems.