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Tibolone Administration Is Associated with Enhanced Motor Recovery and Decreased Cell-Specific NOX2 and NOX4
Tzayaka Castillo-Mendieta1, Stephanie Sánchez-Torres1, Hermelinda Salgado-Ceballos2
1Unidad de Investigación Médica en Farmacología, Hospital de Especialidades Dr. Bernardo Sepúlveda, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Background/Objectives:
This study aimed to investigate the effect of tibolone (TIB) on the expression of the NOX2 and NOX4 isoforms and their co-localization in neurons and astrocytes using an animal model of spinal cord injury (SCI).
Methods:
Male Sprague Dawley rats were subjected to contusive SCI at T9 and treated with TIB (1 or 2.5 mg/kg/day). The expression of NOX2 and NOX4, and their co-localization in neurons and astrocytes, were evaluated at 3, 7, and 15 days post-SCI. Oxidative stress markers and motor recovery were also assessed.
Results:
SCI induced a time-dependent increase in NOX2 protein expression at 15 days compared to 3 days (0.192 ± 0.012 vs. 0.013 ± 0.0007) and in NOX4 protein expression (0.027 ± 0.002 vs. 0.958 ± 0.088), displaying differential cell-specific localization patterns in neurons and astrocytes across time points. TIB treatment significantly attenuated SCI-induced oxidative stress (15,391.8 ± 1047.6 vs. 21,264.4 ± 2669.8) and decreased NOX2 and NOX4 co-localization in both neurons and astrocytes in a dose- and time-dependent manner. Furthermore, TIB-treated animals exhibited a modest but significant restoration of motor function at 15 days post-SCI.
Conclusions:
Our findings indicate that TIB administration reduces oxidative stress, modifies NOX2 and NOX4 immunoreactivity patterns in neurons and astrocytes, and promotes partial functional recovery following SCI.
Insights
Tibolone (TIB) treatment reduced oxidative stress and altered NOX2/NOX4 expression in neurons and astrocytes after spinal cord injury (SCI). This intervention promoted partial motor function recovery in a rat model.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Spinal cord injury (SCI) leads to significant neuronal damage and functional deficits.
- NADPH oxidase (NOX) enzymes, particularly NOX2 and NOX4, are implicated in SCI-induced oxidative stress.
- Tibolone (TIB), a synthetic steroid, has shown neuroprotective potential in other models.
Purpose of the Study:
- To investigate the impact of TIB on NOX2 and NOX4 expression and co-localization in neurons and astrocytes following SCI.
- To assess the effects of TIB on oxidative stress markers and motor function recovery in an animal model of SCI.
Main Methods:
- Male Sprague Dawley rats underwent contusive SCI at T9 and received TIB treatment (1 or 2.5 mg/kg/day).
- NOX2 and NOX4 expression and co-localization in neurons and astrocytes were analyzed at 3, 7, and 15 days post-SCI.
- Oxidative stress markers and motor recovery were quantitatively assessed.
Main Results:
- SCI increased NOX2 and NOX4 protein expression and altered their cellular localization over time.
- TIB treatment dose-dependently attenuated SCI-induced oxidative stress and reduced NOX2/NOX4 co-localization.
- TIB administration resulted in a modest but significant improvement in motor function by 15 days post-SCI.
Conclusions:
- Tibolone administration modulates NOX2 and NOX4 expression and localization in the injured spinal cord.
- TIB effectively reduces oxidative stress and promotes partial functional recovery after SCI.
- These findings suggest TIB as a potential therapeutic agent for managing SCI.
