Repair effect of Wnt3a protein on the contused adult rat spinal cord
Zongsheng Yin, Bo Zu, Jun Chang, Hui Zhang
Abstract
Zongsheng Yin, Bo Zu, Jun Chang, Hui Zhang
Abstract
OBJECTIVE: To explore the repair effect of Wnt3a on injured spinal cord in rats. METHODS: Moderate spinal cord contusion injury was made in 40 adult Sprague-Dawley rats at T10. Fifteen rats served as contusion controls (Group 1). Fifteen rats were treated with Wnt3a 3 days after injury (Group 2). Ten additional rats received only T10 laminectomies to serve as non-injured controls (Group 0). The functional recovery of the rats was observed through Basso-Beattie-Bresnahan (BBB) open field locomotor score. Rats were killed at 14 or 28 days after injury, then spinal cords were removed for histopathologic examinations, and the expression of the bromodeoxyuridine (BrdU) plus neural cell markers was stained with immunohistochemical method. RESULTS: After an initial complete hindlimb paralysis, rats of all groups receiving a contusive injury recovered substantial function within 1 week. By 28 days, the BBB score for rats in Group 2 is better than that for rats in Group 1 by 7 points (Group 2 = 16.94, after 28 days versus Group 1 = 9.89 points; p < 0.05). Light and electron microscopic works showed that the Wnt3a-treated group had moderate repair effect of myelin and axons. Immunohistochemical analysis showed a significant increase in the number of the inducing differentiated neurons in Wnt3a-treated rats compared with control rats 2 weeks after injury. CONCLUSIONS: Exogenous Wnt3a administration can improve axonal conduction and spinal cord function in the injured spinal cord, and the administration of Wnt3a result in the increase in the populations of neurons, suggesting that these cells may be derived from neural precursors and stem cells.
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OBJECTIVE: To explore the repair effect of Wnt3a on injured spinal cord in rats. METHODS: Moderate spinal cord contusion injury was made in 40 adult Sprague-Dawley rats at T10. Fifteen rats served as contusion controls (Group 1). Fifteen rats were treated with Wnt3a 3 days after injury (Group 2). Ten additional rats received only T10 laminectomies to serve as non-injured controls (Group 0). The functional recovery of the rats was observed through Basso-Beattie-Bresnahan (BBB) open field locomotor score. Rats were killed at 14 or 28 days after injury, then spinal cords were removed for histopathologic examinations, and the expression of the bromodeoxyuridine (BrdU) plus neural cell markers was stained with immunohistochemical method. RESULTS: After an initial complete hindlimb paralysis, rats of all groups receiving a contusive injury recovered substantial function within 1 week. By 28 days, the BBB score for rats in Group 2 is better than that for rats in Group 1 by 7 points (Group 2 = 16.94, after 28 days versus Group 1 = 9.89 points; p < 0.05). Light and electron microscopic works showed that the Wnt3a-treated group had moderate repair effect of myelin and axons. Immunohistochemical analysis showed a significant increase in the number of the inducing differentiated neurons in Wnt3a-treated rats compared with control rats 2 weeks after injury. CONCLUSIONS: Exogenous Wnt3a administration can improve axonal conduction and spinal cord function in the injured spinal cord, and the administration of Wnt3a result in the increase in the populations of neurons, suggesting that these cells may be derived from neural precursors and stem cells.
Key concepts: Medicine, Spinal cord, Spinal cord injury, Immunohistochemistry, Hindlimb, WNT3A, Glial scar, Anesthesia