Salidroside, a primary active component of Rhodiola rosea, has attracted scientific interest for its potential neuroprotective properties. Several preclinical studies have explored its effects in models of nerve damage, including oxidative stress-induced neuronal injury, peripheral nerve injury, and neurodegenerative diseases. Laboratory research, primarily in cell cultures and animal models, suggests that salidroside may reduce neuronal apoptosis, mitigate oxidative stress, and promote nerve regeneration by modulating signaling pathways such as PI3K/Akt and Nrf2/ARE. For example, studies published in journals like Brain Research and Neuroscience Letters have reported that salidroside administration can reduce cell death and promote functional recovery after nerve injury in rodents.

However, despite promising preclinical data, there is currently a lack of robust human clinical trials directly evaluating salidroside’s efficacy in treating or supporting nerve damage or neuropathies. Most available evidence is limited to animal or in vitro models, and optimal dosing, safety, and long-term effects in humans have not been established. Therefore, while the scientific rationale exists and preliminary findings are encouraging, the overall evidence remains preliminary and insufficient for strong clinical recommendations at this time.