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Abstract: (3 Views)
Background: Depression is a common and disabling complication of spinal cord injury (SCI), yet effective treatments that simultaneously improve neurological and neuropsychiatric outcomes remain limited. Astaxanthin possesses potent neuroprotective properties, but its effects on post-SCI depression have not been reported.
Methods: Adult male Wistar rats were subjected to compressive SCI and randomly assigned to Sham, SCI, Vehicle, oral astaxanthin (100 mg/kg), or fluoxetine (10 mg/kg) groups. Treatments were administered once daily for 7 days beginning 2 h after injury. Locomotor recovery was assessed using the Basso–Beattie–Bresnahan (BBB) scale, whereas depressive-like behavior was evaluated using the sucrose preference and tail suspension tests on days 7, 14, 21, and 28 after SCI. Hippocampal brain-derived neurotrophic factor (BDNF) protein expression was determined by Western blot analysis on day 28.
Results: Oral astaxanthin significantly improved locomotor recovery from day 7 onward and produced greater functional improvement than fluoxetine. SCI induced persistent depressive-like behavior. Astaxanthin significantly attenuated these behavioral deficits from day 21 onward, with antidepressant-like efficacy comparable to fluoxetine. In parallel, astaxanthin restored hippocampal BDNF protein expression reduced after SCI.
Conclusions: Oral astaxanthin improves both neurological and neuropsychiatric outcomes following compressive SCI. Its antidepressant-like effects are associated by restoration of hippocampal BDNF expression, while its superior locomotor benefits compared with fluoxetine further support its multimodal neuroprotective profile. These findings identify oral astaxanthin as a promising therapeutic candidate for mitigating both motor dysfunction and depression after SCI.
Methods: Adult male Wistar rats were subjected to compressive SCI and randomly assigned to Sham, SCI, Vehicle, oral astaxanthin (100 mg/kg), or fluoxetine (10 mg/kg) groups. Treatments were administered once daily for 7 days beginning 2 h after injury. Locomotor recovery was assessed using the Basso–Beattie–Bresnahan (BBB) scale, whereas depressive-like behavior was evaluated using the sucrose preference and tail suspension tests on days 7, 14, 21, and 28 after SCI. Hippocampal brain-derived neurotrophic factor (BDNF) protein expression was determined by Western blot analysis on day 28.
Results: Oral astaxanthin significantly improved locomotor recovery from day 7 onward and produced greater functional improvement than fluoxetine. SCI induced persistent depressive-like behavior. Astaxanthin significantly attenuated these behavioral deficits from day 21 onward, with antidepressant-like efficacy comparable to fluoxetine. In parallel, astaxanthin restored hippocampal BDNF protein expression reduced after SCI.
Conclusions: Oral astaxanthin improves both neurological and neuropsychiatric outcomes following compressive SCI. Its antidepressant-like effects are associated by restoration of hippocampal BDNF expression, while its superior locomotor benefits compared with fluoxetine further support its multimodal neuroprotective profile. These findings identify oral astaxanthin as a promising therapeutic candidate for mitigating both motor dysfunction and depression after SCI.
Keywords: Astaxanthin, Spinal cord injury, Depression, Brain-derived neurotrophic factor (BDNF), Fluoxetine
Type of Manuscript: Experimental research article |
Subject:
Neurophysiology/Pharmacology
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