Neuroprotective effects of salidroside against 6-OHDA-induced oxidative stress in PC12 cells

Parkinson's disease (PD) is the second-most common neurodegenerative disease, and the development and progression of PD is characterized by oxidative stress (OS). This study determined the neuroprotective effects of salidroside (Sal). We report that Sal with scavenging ROS capabilities could regulate oxidative stress for the prevention of pathologic α-synuclein (α-syn) transmission in 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells. Sal exhibits effective free radical quenching ability and safe use in biological systems. The protective effects of Sal against 6-OHDA-induced neurotoxicity in PC12 cells were investigated using the DPPH method for free radical scavenging, CCK8 for cell viability, DCFH-DA for ROS levels, immunohistochemical staining for α-syn, and western blot for SOD, CAT, and GPX4 protein detection. The results obtained through our studies showed that 6-OHDA-induced neurotoxicity significantly decreased cell viability, antioxidant enzyme (SOD, CAT, and GPX4) expression, increased ROS levels, and α-syn accumulation, while on Sal (50 mg mL −1 ) pretreatment obviously regulated the cellular redox balance and decreased α-syn accumulation. With further study, these findings may provide new insight into the protective mechanisms against neurodegenerative diseases and synucleinopathies. Neuroprotective effects of salidroside (Sal) in PC12 cells against oxidative stress induced by 6-hydroxydopamine (6-OHDA). Sal scavenges reactive oxygen species (ROS), enhances antioxidant enzyme activity (SOD, CAT, GPX4), and reduces α-synuclein (α-syn) accumulation.