BACKGROUND: Neurite outgrowth inhibitor-A (Nogo-A), myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein are three myelin-associated proteins that act as inhibitors to central nervous system regeneration. Neurite outgrowth inhibitor-A imposes the strongest effect on inhibiting axonal regeneration after traumatic brain injury. Alpha-tocopherol, a member of the vitamin E family, is recognized as an active antioxidative substance. Its use has not been well studied in brain injury research, especially in axonal regeneration research. METHODS: We obtained 99 intact adult male Sprague-Dawley rats (200-250 g) from the Experimental Animal Center of Central South University. We used the modified method of Freeney to generate moderate brain injury in the rats. We injected 600 mg/kg α-tocopherol intraperitoneally daily as traumatic brain injury (TBI) treatment. Then, we performed behavioral tests in the corresponding time point, examined brain tissues after hematoxylin-eosin staining to identify changes in cell morphology, and performed immunohistochemical staining and quantitative real-time polymerase chain reaction to detect the expression of NoGo and Nogo receptor (NgR) in brain tissue. RESULTS: For the Neurological Severity Scores of rats, there were obvious differences among the three groups at the corresponding time points. Standard hematoxylin-eosin staining showed that the brain structure of a sham-operated group of rats was clear, uniform, and compact. A TBI group exhibited hemorrhage, edema, inflammatory cell infiltration, condensed nuclei, and necrosis. We also saw glial cells and fibrous tissue proliferation. The α-tocopherol-treated TBI group had similar but less severe changes than the TBI group. Expression of Nogo-A and NgR increased after TBI compared with the sham-operated group. However, Nogo-A and NgR expression was significantly lower in the α-tocopherol-treated TBI group compared with the TBI group. Similarly, results showed that functional neurological deficits among rats in the α-tocopherol-treated TBI group were less pronounced than in the TBI group (model group). CONCLUSIONS: Our data demonstrate that α-tocopherol-treated rats had reduced microscopic evidence of brain damage. Alpha-tocopherol reduced Nogo-A and NgR expression in brain tissue after traumatic brain injury and promoted nerve regeneration. Alpha-tocopherol treatment of TBI rats had a neuroprotective role in their recovery.
BACKGROUND:Neurite outgrowth inhibitor-A (Nogo-A), myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein are three myelin-associated proteins that act as inhibitors to central nervous system regeneration. Neurite outgrowth inhibitor-A imposes the strongest effect on inhibiting axonal regeneration after traumatic brain injury. Alpha-tocopherol, a member of the vitamin E family, is recognized as an active antioxidative substance. Its use has not been well studied in brain injury research, especially in axonal regeneration research. METHODS: We obtained 99 intact adult male Sprague-Dawley rats (200-250 g) from the Experimental Animal Center of Central South University. We used the modified method of Freeney to generate moderate brain injury in the rats. We injected 600 mg/kg α-tocopherol intraperitoneally daily as traumatic brain injury (TBI) treatment. Then, we performed behavioral tests in the corresponding time point, examined brain tissues after hematoxylin-eosin staining to identify changes in cell morphology, and performed immunohistochemical staining and quantitative real-time polymerase chain reaction to detect the expression of NoGo and Nogo receptor (NgR) in brain tissue. RESULTS: For the Neurological Severity Scores of rats, there were obvious differences among the three groups at the corresponding time points. Standard hematoxylin-eosin staining showed that the brain structure of a sham-operated group of rats was clear, uniform, and compact. A TBI group exhibited hemorrhage, edema, inflammatory cell infiltration, condensed nuclei, and necrosis. We also saw glial cells and fibrous tissue proliferation. The α-tocopherol-treated TBI group had similar but less severe changes than the TBI group. Expression of Nogo-A and NgR increased after TBI compared with the sham-operated group. However, Nogo-A and NgR expression was significantly lower in the α-tocopherol-treated TBI group compared with the TBI group. Similarly, results showed that functional neurological deficits among rats in the α-tocopherol-treated TBI group were less pronounced than in the TBI group (model group). CONCLUSIONS: Our data demonstrate that α-tocopherol-treated rats had reduced microscopic evidence of brain damage. Alpha-tocopherol reduced Nogo-A and NgR expression in brain tissue after traumatic brain injury and promoted nerve regeneration. Alpha-tocopherol treatment of TBI rats had a neuroprotective role in their recovery.
Authors: Alice Jacquens; Edward J Needham; Elisa R Zanier; Vincent Degos; Pierre Gressens; David Menon Journal: Int J Mol Sci Date: 2022-09-23 Impact factor: 6.208
Authors: Valentina Di Pietro; Kamal M Yakoub; Giuseppe Caruso; Giacomo Lazzarino; Stefano Signoretti; Aron K Barbey; Barbara Tavazzi; Giuseppe Lazzarino; Antonio Belli; Angela Maria Amorini Journal: Antioxidants (Basel) Date: 2020-03-22