Neuroprotective effect of omega‐3 fatty acids on spinal cord injury induced rats

Introduction In this study, the effects of omega‐3 fatty acids were examined in a rat model of spinal cord injury. Methods The rats were classified into sham, control, spinal cord injury plus 50 mg/kg Omega‐3 fatty acids and spinal cord injury plus 100 mg/kg Omega‐3 fatty acids. The levels of oxidat...

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Veröffentlicht in:Brain and behavior 2019-08, Vol.9 (8), p.e01339-n/a
Hauptverfasser: Bi, Jiaqi, Chen, Chong, Sun, Peiyu, Tan, Haining, Feng, Fan, Shen, Jianxiong
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Sprache:eng
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Zusammenfassung:Introduction In this study, the effects of omega‐3 fatty acids were examined in a rat model of spinal cord injury. Methods The rats were classified into sham, control, spinal cord injury plus 50 mg/kg Omega‐3 fatty acids and spinal cord injury plus 100 mg/kg Omega‐3 fatty acids. The levels of oxidative, apoptotic, and inflammatory markers were examined in each of these groups. Results Altered lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (Gpx), and catalase were normalized. Omega‐3 fatty acid supplementation decreased tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6) levels by >50%. TNF‐α and IL‐6 mRNA expression were reduced. Caspase‐3, p53, bax, and pro‐NGF mRNA expression levels were increased by 1.3‐, 1.4‐, 1.2‐, and 0.9‐fold, respectively, whereas bcl‐2 mRNA expression was decreased by 0.77‐fold in control rats. Omega‐3 fatty acid supplementation decreased p53, caspase‐3, bax, and pro‐NGF mRNA expression by >40%, while the level of bcl‐2 mRNA expression was increased by 286.9%. Omega‐3 fatty acid supplementation decreased caspase‐3 and p53 protein expression by >30%. Conclusion Taken together, our results suggested that omega‐3 fatty acid supplementation reduced oxidative stress, apoptosis, and the levels of inflammatory markers in ischemia‐reperfusion‐induced rats. Omega‐3 fatty acid supplementation reduced oxidative stress, apoptosis, and the levels of inflammatory markers in ischemia‐reperfusion‐induced rats.
ISSN:2162-3279
2162-3279
DOI:10.1002/brb3.1339