毛蕊异黄酮治疗脊髓损伤大鼠的作用机制

Mechanism of Calycosin in the Treatment of Spinal Cord Injury in Rats

目的:探究毛蕊异黄酮治疗脊髓损伤的潜在作用机制。方法:30只大鼠随机分为假手术组、模型组、毛蕊异黄酮组,每组10只。模型组和毛蕊异黄酮组采用改良Allen重物打击法建立大鼠脊髓损伤模型后,毛蕊异黄酮组大鼠给予20 mg/kg毛蕊异黄酮灌胃。造模5周后,测定改良Tarlov评分、皮层体感诱发电位波潜伏期时长和斜板试验,测定SCI大鼠脊髓神经功能。观察HE染色后脊髓损伤的情况;蛋白质印迹法检测脊髓组织中p-Akt、gp130、IL-6蛋白表达。结果:与假手术组比较,模型组中改良Tarlov评分及倾斜平面临界角度显著降低(P<0.05),皮层体感诱发电位波潜伏期时长和p-Akt、gp130、IL-6蛋白表达均显著上调(P<0.05);与模型组比较,毛蕊异黄酮治疗后改良Tarlov评分及斜板试验角度显著上升(P<0.05),皮层体感诱发电位波潜伏期时长和p-Akt、gp130、IL-6蛋白表达均显著下调(P<0.05)。结论:毛蕊异黄酮促进大鼠脊髓损伤后神经功能的恢复,通过抑制gp130、IL-6的蛋白表达和PI3K/Akt信号通路磷酸化起作用。

Objective:To explore the potential mechanism of Calycosin in the treatment of Spinal Cord Injury.Methods:Thirty rats were randomly divided into Sham group,model group and Calycosin group,ten rats in each group.After spinal cord injury model was established by modified Allen heavy hit method in model group and Calycosin group,rats in the Calycosin group were given 20 mg/kg calycosin by gavage.After the 5 weeks,the modified Tarlov score,cortical somatosensory evoked potential latency time and inclined plate test were measured to determine the spinal cord neurological function of SCI rats.The 5 weeks after modeling,the injury of spinal cord tissues were observed by HE staining.The protein expressions of p-Akt,gp130 and IL-6 in spinal cord were detected by Western blotting.Results:Compared with the Sham group,the modified Tarlov score and the critical angle of tilt plane in the model group were significantly decreased(P<0.05),and the latency time of cortical somatosensory evoked potential wave and the expression of p-Akt,gp130 and IL-6 proteins were significantly increased(P<0.05).Compared with the model group,after Calycosin intervention,the modified Tarlov score and the critical angle of inclined plane were significantly increased(P<0.05),and the latency time of cortical somatosensory evoked potential wave and the expression of p-Akt,gp130 and IL-6 proteins were significantly decreased(P<0.05).Conclusion:Calycosin promoted the recovery of neurological function after SCI in rats by inhibiting the protein expression of gp130 and IL-6 and phosphorylation of PI3K/Akt signaling pathway.