Oxidative stress-induced cell damage has long been implicated both in the physiological process of aging and in a variety of neurodegenerative disorders such as Parkinson’s and Alzheimer’s diseases ( [Choi et al., 2006a], [Finkel and Holbrook, 2000] and [Markesbery, 1997]). Oxidative damage, mediated by reactive oxygen species which can be generated following cell lysis, oxidative burst, or the presence of an excess of free transition metals, can attack proteins, deoxynucleic acid, and lipid membranes, thereby disrupting cellular function and integrity ( [Gardner et al., 1997] and [Gorman et al., 1996]). Hydrogen peroxide (H2O2), one of the main reactive oxygen species, is produced during the redox process and is recently considered as a messenger in intracellular signaling cascades

Salidroside which is extracted from Rhodiola rosea L and has long been used as an adaptogen in traditional Tibetan medicine, has been reported to have various pharmacological properties including anti-aging, anticancer, anti-inflammation, hepatoprotective and antioxidative effects and [Kucinskaite et al., 2004]). For example, salidroside has been found to be protective against neuron cell death induced by glutamate and hypoxia/hypoglycemia ( [Cao et al., 2006] and [Zhang et al., 2004]), and against mitochondria dysfunction induced by sodium azide (Cao et al., 2005). Nevertheless, the mechanism underlying its neuroprotective effects remains unclear, especially at cellular level. Clarification of the effects of salidroside on apoptosis in SH-SY5Y cells may provide a new insight into the mechanism of neuroprotection.

the mRNA levels of thioredoxin, heme oxygenase-1 and peroxiredoxin-I were dramatically decreased by H2O2 treatment. However, pretreatment with salidroside notably induced the expressions of these antioxidant enzymes, especially thioredoxin and heme oxygenase-1.

According to the neuroprotective effects of salidroside on hydrogen peroxide (H2O2)-induced apoptosis in SH-SY5Y cells were investigated. Pretreatment with salidroside markedly attenuated H2O2-induced cell viability loss and apoptotic cell death in a dose-dependent manner. The mechanisms by which salidroside protected neuron cells from oxidative stress included the induction of several antioxidant enzymes, thioredoxin, heme oxygenase-1, and peroxiredoxin-I; the downregulation of pro-apoptotic gene Bax and the upregulation of anti-apoptotic genes Bcl-2 and Bcl-XL. Furthermore, salidroside dose-dependently restored H2O2-induced loss of mitochondrial membrane potential as well as the elevation of intracellular calcium level. These results suggest that salidroside has protective effects against oxidative stress-induced cell apoptosis, which might be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress.