Curcumin Reduces High-dose Morphine-Induced Apoptosis and Oxidative Neurotoxicity via TRPV4 Cation Channel Suppression

Authors : Hacı Ömer Osmanlıoğlu

Pages : 262-270

Doi:10.26453/otjhs.1702198

View : 51 | Download : 75

Publication Date : 2025-09-15

Article Type : Research Paper

Abstract :Objective: Long-term and high-dose morphine (H-MRP) treatments for neuropathic pain cause the body to become extremely susceptible to morphine tolerance, which increases the amount of toxic reactive oxygen species (ROS), apoptosis, and calcium (Ca2+) entering the neuron. It has been known that curcumin (CRC) decreased these increases in ROS-damaged SH-SY5Y cells by blocking the TRPV4 cation channel. It has not been studied whether CRC can also suppress the high levels of ROS and apoptosis caused by H-MRP in SH-SY5Y cells by affecting TRPV4. So, the study was carried out to investigate whether CRC can suppress the high level of mitochondrial ROS and apoptosis. Materials and Methods: In the SH-SY5Y, four primary groups were induced as control, normal morphine (N-MRP) (50 µM for 24h), H-MRP (500 µM for 24h), H-MRP + CRC (5 µM for 24h). Results: While the incubations of TRPV4 antagonist (ruthenium red) and CRC decreased the H-MRP-induced increases of apoptosis, caspase-3, caspase-8, caspase-9, ROS, mitochondrial dysfunction, debris number, and lipid peroxidation levels, the TRPV4 agonist (GSK1016790A) stimulation further increased these levels. The CRC increased glutathione, glutathione peroxidase, live cell number, and cell viability percentage, all of which were decreased by H-MRP. Conclusions: The levels of H-MRP-induced neuronal death and mitochondrial oxidative stress were reduced by CRC treatment through TRPV4 inhibition. For H-MRP-induced mitochondrial oxidative neuronal injury, CRC is a potential treatment option.
Keywords : Kurkumin, sinir hasarı, mitokondriyal oksidatif stres, morfin, TRPV4 kanalı

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