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Published on: January 7, 2014
Curcumin protects against MPP+-induced neurotoxicity in SH-SY5Y cells by modulating the TRPV4 channel
Ramazan Çınar1, Kenan Yıldızhan2
1Department of Biophysics, Faculty of Medicine, Bilecik Seyh Edebali University, Bilecik, Turkey.
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.
Insights
Curcumin (CUR) protects neuronal cells against Parkinson's disease (PD) by reducing oxidative stress and regulating mitochondrial function. This study shows CUR mitigates MPP+-induced neurotoxicity by modulating TRPV4 channel activity.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Neuroinflammation, mitochondrial dysfunction, and oxidative stress (OS) are implicated in Parkinson's disease (PD) pathogenesis.
- Curcumin (CUR) exhibits neuroprotective effects by scavenging reactive oxygen species (ROS) and suppressing OS.
- This study explores CUR's role in modulating TRPV4 channels in an in vitro PD model.
Purpose of the Study:
- To investigate the therapeutic potential of Curcumin (CUR) in an in vitro Parkinson's disease (PD) model.
- To elucidate the role of the TRPV4 channel in MPP+-induced neurotoxicity and its modulation by CUR.
- To assess the impact of CUR on oxidative stress, mitochondrial dysfunction, and cellular damage in PD models.
Main Methods:
- SH-SY5Y cells were exposed to MPP+ to induce a PD model, divided into control, CUR, MPP+, and MPP++CUR groups.
- TRPV4 channel activity was assessed using agonist GSK1016790A (GSK) and antagonist Ruthenium red (Rr).
- Measurements included ROS production, glutathione (GSH) levels, mitochondrial membrane potential (JC-1), apoptosis, and TRPV4 expression.
Main Results:
- MPP+ exposure elevated ROS and mitochondrial membrane potential while reducing GSH levels.
- CUR treatment and Rr incubation downregulated MPP+-induced neurotoxicity and TRPV4 overstimulation.
- CUR modulated GSH levels, ROS production, apoptosis, and TRPV4 expression, mitigating MPP+-induced cellular damage.
Conclusions:
- Curcumin (CUR) demonstrates neuroprotective effects in an in vitro PD model by alleviating mitochondrial dysfunction and oxidative stress.
- CUR treatment regulates TRPV4 channel activation, reducing neurotoxicity induced by MPP+.
- The antioxidant properties of CUR are key to its protective mechanism against MPP+-induced neurotoxicity.
