Effect of valproic acid on astrocyte proliferation around the central canal in rats following spinal cord injury / 中华创伤杂志

ABSTRACT

Objective To investigate the effect and mechanism of valproic acid in preventing astrocyte proliferation around the central canal of rats following spinal cord injury.Methods Forty-five Wister rats were divided into normal control group (n =5),injury group (n =20) and treatment group (n =20) according to random number table.Animal models of acute spinal cord injury were produced at T10 using Allen' s method by dropping a 10 g weight from a 15 mm height.Rats in treatment group received intraperitoneal injection of valproic acid (300 mg · kg-1 · d-1 in two divided doses) at 30 minutes postinjury.Instead,rats in injury group were injected with an equal volume of saline in the same way.Hindlimb function was evaluated using BBB scoring system at 1,3,7,and 14 days postinjury.Astrocytes proliferation around central canal and expression of glial fibrous acid protein (GFAP) were examined.Results In normal control group,few astrocytes around spinal central canal and a low expression of GFAP were detected.In injury group,astrocytes began to increase at 24 hours postinjury; fluorescence intensity for GFAP was 24.6 ± 3.6 at 24 hours,reached a peak of 69.2 ± 6.4 at 3 days,maintained a high level of 56.7 ± 5.6 at 7 days,and reduced to 35.4 ± 4.3 at 14 days,a level that remained higher than that in normal control group (11.2 ± 1.6).Whereas in treatment group at 3 and 7 days,astrocyte proliferation around spinal central canal was lower than that in injury group; GFAP expressions (47.8 ± 5.3 and 42.2 ± 6.7) were lower than those in injury group (F =177.6,P ＜ 0.05).At 3,7,and 14 days,BBB scores in treatment group (7.80 ± 0.83,12.00 ± 1.58,and 16.60 ± 1.12 respectively) were significantly higher than those in injury group (4.60 ± 0.54,6.65 ± 0.67,and 9.40 ± 1.14 respectively) (F =1 113.6,P ＜ 0.05).Conclusion After spinal cord injury,valproic acid reduces astrocyte proliferation around central canal via inhibiting GFAP expression to promote functional recovery.