Salvianolic acid B protects against MPP+-induced neuronal injury via repressing oxidative stress and restoring mitochondrial function.

Maintaining normal conditions in the mitochondria and repressing oxidative stress has emerged as a crucial therapeutic strategy to ameliorate neuron damage in Parkinson's disease. Salvianolic acid B (SalB) is a polyphenolic compound isolated from Salvia miltiorrhiza, which has been prescribed for various biological properties, including antioxidative stress, anti-inflammation and neuroprotection in pathological conditions. Previously, SalB was reported to be of benefit in slowing Parkinson's disease pathology, but whether the neuroprotective role of SalB is associated with a mitochondrial protective action is still elusive. Here we aimed to explore the effects of SalB on mitochondrial function in Parkinson's disease to uncover the underlying cellular mechanisms. The results showed that SalB significantly alleviated 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial disruption in line with ameliorated oxidative injury, which is evidenced by inhibited mitochondrial membrane potential collapse, reduced reactive oxygen species (ROS) generation, increased expression of NAD(P)H: quinone oxidoreductase, and enhanced mitochondrial biosynthesis - the upregulation of nuclear respiratory factor 1 and mitochondrial transcription factor A expressions. Mechanistically, SalB not only increased AMP-activated protein kinase (AMPK) activation and sirtuin3 mRNA and protein levels, but also attenuated ROS-triggered neuroinflammation by downregulating the expressions of NOD-like receptor family pyrin domain containing 3, caspase-1 and Interleukin-1β (IL-1β). In conclusion, these in-vitro findings, for the first time, demonstrate that SalB offers protection against MPP+-induced neuronal injury via upregulating sirtuin3 expression and activating the AMPK signaling to restore mitochondrial function.