Salidroside Anti-inflammatory and antiviral effects
Studies have shown that Salidroside treated PC12 cells in advance significantly reduced MPP+-induced cell apoptosis compared with the control group, and at the same time, the attenuation of mitochondrial membrane potential MMP was also significantly reduced, indicating that salidroside prevented MPP(+) from inducing cell apoptosis in PC12 cells, at least in part through the activation process mediated by the PI3K/Akt pathway.
The above studies show that salidroside also has an important intervention effect in the human body in combating hypoxia and regulating apoptosis pathways. At present, there are relevant important combinations in clinical practice for the treatment of certain hypoxia-related diseases, which deserve further study.
Salidroside also has anti-inflammatory effects. Inflammation is the body's adaptive response to tissue damage and infection caused by the external environment, but excessive inflammatory response can lead to various functional disorders in the human body.
Studies have shown that salidroside inhibits the anti-inflammatory effects of proinflammatory cytokines through NF-κB and MAPK-mediated signaling pathways. Secondly, studies found that the levels of tumor necrosis factor α, interleukin 1β and IL-6 in renal tubular epithelial cells pretreated with salidroside were significantly inhibited.
Similarly, studies have shown that after 2-hour occlusion of the middle cerebral artery and reperfusion, rats were given salidroside for 1 hour. After 24 hours, it was found that salidroside increased the neuronal nuclear protein NeuN and reduced the CD11b markers of microglia and macrophages in the peri-infarct area of the brain, and also reduced the mRNA of IL-6, IL-1β, TNF-α, CD14, CD44, and iNOS.
Other studies have shown that salidroside can reduce the expression of inflammatory cytokines and upregulate the expression of SIRT3, which may be a potential mechanism for preventing endothelial cells from premature aging. Studies have shown that the expression of IL-6 and TNF-α in BV-2 cells pretreated with salidroside was reduced, and salidroside inhibited PC12 cell apoptosis by reducing the release of inflammatory factors in activated microglia and the activation of p38 and JNK.

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