葛根素对激素性股骨头坏死大鼠骨组织及PI3K/Akt信号转导通路的影响

    Effect of puerarin on the bone tissue and PI3K/Akt signal transduction pathway in rats with femoral head osteonecrosis induced by hormone

    • 摘要:
      目的探究葛根素对激素性股骨头坏死大鼠骨组织及PI3K/Akt信号转导通路的影响。
      方法将大鼠分为对照组、模型组和观察组,用臀肌注射甲泼尼龙琥珀酸钠方法复制激素性股骨头坏死大鼠模型。模型复制后观察组大鼠腹腔注射葛根素注射液。比较各组大鼠一般状态、股骨头病理切片和股骨头骨密度、血清血管内皮生长因子(VEGF)和一氧化氮(NO)水平、股骨头中Akt和p-Akt蛋白表达水平。
      结果观察组大鼠给药后活动程度显著提高,毛发有色泽,精神状态良好。模型组大鼠血清中的VEGF和NO水平低于对照组(P < 0.01);观察组大鼠血清中的VEGF和NO水平高于模型组(P < 0.01)。3组大鼠股骨头中Akt蛋白表达水平差异无统计学意义(P>0.05);模型组大鼠股骨头中p-Akt蛋白表达水平显著高于对照组(P < 0.01);观察组大鼠股骨头中p-Akt蛋白表达水平显著高于模型组(P < 0.01)。
      结论葛根素对激素性股骨头坏死模型大鼠有治疗作用,其作用机制可能为升高血清中促进血管新生活性因子水平的升高,进而促进血管新生,重建供血和血液循环,促进坏死部位新骨生成。

       

      Abstract:
      ObjectiveTo explore the effects of puerarin on the bone tissue and PI3K/Akt signal transduction pathway in rats with femoral head osteonecrosis induced by hormone.
      MethodsThe rats were divided into the control group, model group and observation group.The model of femoral head osteonecrosis induced by hormone was established by intramuscular injection of methylprednisolone sodium succinate.The observation group was established by intraperitoneal injection with puerarin in model rat.The general state, pathological change and bone mineral density of femoral head, serum levels of vascular endothelial growth factor(VEGF) and nitric oxide(NO), and levels of Akt and p-Akt protein in femoral head among three groups were compared.
      ResultsThe activity of the rats in observation group increased significantly after administration, and the hair color and spirit were good.The serum levels of VEGF and NO in model group were less than those in control group and observation group(P < 0.01).The differences of the expression levels of Akt protein in femoral head among three groups were not statistically significant(P>0.05), and the expression level of p-Akt protein in model group was significantly higher and lower than that in control group and observation group, respectively(P < 0.01).
      ConclusionsPuerarin plays a therapeutic effect on the femoral head necrosis, and the mechanism of which may be related to increase the level of angiogenic activity factor, form the angiogenesis, reconstruct the blood supply and circulation, and promote the formation of new bone at the necrotic site.

       

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