Akademik Veri Yönetim Sistemi
Molecular Biology Reports, cilt.52, sa.1, 2025 (SCI-Expanded)
Background: It is well acknowledged that neuroinflammation, mitochondrial dysfunction, and oxidative stress (OS) play a role in the etiology of Parkinson’s disease (PD). Curcumin (CUR) protect neuronal cells by interfering with the production of reactive oxygen species (ROS) in neuronal cells and suppressing OS. In this study, we investigated the role of the TRPV4 channel under CUR stimulation in the PD model induced by MPP+ in SH-SY5Y cells. Methods: The cells were divided into four groups: control, CUR, MPP+ and MPP++CUR. In addition, incubations were performed with TRPV4 channel agonist GSK1016790A (GSK) and its antagonist Ruthenium red (Rr) to follow the Ca2+ current induced through the TRPV4 channel. Results: MPP+ exposure increased mitochondrial and intracellular ROS production and mitochondrial membrane potential in the cell, while decreasing GSH levels. During CUR and Rr incubation, MPP+ exposure and TRPV4 agonist GSK-induced TRPV4 overstimulation were down-regulated. The effects of MPP+ on intracellular damage were changed by CUR treatment, as seen in changes in GSH levels, mROS, iROS, JC/1, apoptosis, and TRPV4 expression value compared to the MPP+ group. Conclusions: The CUR treatment in the in vitro PD model created with MPP+ reduced cellular damage by regulating mitochondrial dysfunction, OS and TRPV4 channel activation in MPP+-induced neurotoxicity with the antioxidant properties of CUR.