In Vitro Ameliorative Effects of Sinapic Acid on Parkinson Related Neurotoxicity in SHSY5Y Cell Lines

The neuroprotective effects of polyphenols have been reported in the prevention of the early onset or delay of the progression of various neurodegenerative diseases, including Parkinson disease (PD). Neuroinflammation, oxidative stress, and mitochondrial dysfunction play significant roles in the pathophysiology of PD. Sinapic acid (SNP) is a naturally occurring polyphenol belonging to a group of hydroxycinnamic acids, which has gained importance owing to its beneficial effects, including antioxidant and anti-inflammatory properties. The present study aimed to develop an insight into the effects of sinapic acid on mitigating the inflammatory markers, oxidative stress, and deranged mitochondrial dynamics in human neuroblastoma cells (SHSY5Y) intoxicated with MPP+. The modulating variations of SNP on apoptosis, mitochondrial membrane potential (MMP), intracellular reactive oxygen species (ROS), and expression of proteins like PARKIN, PINK1, DJ-1, Bax, and BCl2 were analyzed in MPP+ induced PD-like toxic conditions. Pre-treatment with SNP decreased the levels of ROS and improved MMP. Also, SNP down-regulated the expression of PARKIN1, caspase-3, and DJ-1, along with a reduction in the expression of inflammatory markers such as IL-1β and TNF-α. Further, SNP was observed to increase the levels of BCl2, an anti-apoptotic protein, and the activity of superoxide dismutase (SOD), an enzymatic antioxidant. Based on the above results, the authors concluded that SNP exhibited neurotherapeutic potential in PD-like neurotoxic conditions. The present study reported the preclinical and mechanistic approach to identify the exact mechanism of action of SNP in PD.