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Updated: Jun 6, 2026
A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury
Published on: September 13, 2018
Meloxicam exerts neuroprotection on spinal cord trauma in rats
Tayfun Hakan1, Hale Zerrin Toklu, Necat Biber
1Haydarpasa Numune EAH, Beyin ve Sinir Cerrahisi Klinigi, Tibbiye Caddesi, Istanbul, Turkey. tayfunhakan@yahoo.com
Abstract:
Traumatic injury to the central nervous system results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of the COX2 inhibitor meloxicam in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 2 mg/kg meloxicam or saline 30 min postinjury by intraperitoneal injection. At seven days postinjury, neurological examination was performed and rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and DNA fragmentation. Formation of ROS in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in CL, MDA levels, MPO activity, and DNA damage. On the other hand, meloxicam treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that meloxicam, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion, and DNA fragmentation.
Insights
Meloxicam, a COX2 inhibitor, demonstrated neuroprotective effects in a rat spinal cord injury (SCI) model. It reduced oxidative stress, lipid peroxidation, and DNA fragmentation, improving neurological function after traumatic injury.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Traumatic spinal cord injury (SCI) causes delayed neuronal death and dysfunction.
- Early SCI involves impaired mitochondrial function, reactive oxygen species (ROS) generation, and lipid peroxidation.
- Delayed ROS neutralization contrasts with early oxidative damage.
Purpose of the Study:
- To investigate the neuroprotective potential of meloxicam, a COX2 inhibitor, in a rat model of SCI.
- To assess meloxicam's effects on oxidative stress markers and neurological recovery post-SCI.
Main Methods:
- Induction of moderate SCI at T10 using a weight-drop method in rats.
- Administration of meloxicam (2 mg/kg) or saline 30 minutes post-injury.
- Assessment of neurological function, histopathology, malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity, DNA fragmentation, and ROS via chemiluminescence (CL) at seven days post-injury.
Main Results:
- SCI significantly increased CL, MDA, MPO activity, and DNA fragmentation while decreasing GSH levels.
- Meloxicam treatment reversed these biochemical changes and reduced SCI-induced histopathological alterations.
- Meloxicam administration improved neurological function deficits caused by SCI.
Conclusions:
- Meloxicam effectively reduces oxidative stress following spinal cord injury in rats.
- The drug exerts neuroprotection by inhibiting lipid peroxidation, glutathione depletion, and DNA fragmentation.
- Meloxicam shows promise as a therapeutic agent for managing traumatic SCI.
