芪麝颈康丸对颈椎间盘细胞凋亡的影响

目的探讨芪麝颈康丸抑制颈椎间盘退变的细胞分子机制.方法将48只大鼠分成四组,切除其中36只(A、B、C三组)颈后部浅、中层肌,造成颈椎间盘退变模型,D组为正常假手术组.分别给予芪麝颈康丸(A)、颈复康(B)等药物治疗,C、D组不给药.4月后将动物处死,采用原位末端脱氧核苷酸转移酶标记法观察大鼠颈椎间盘退变模型椎间盘组织中细胞凋亡的情况及芪麝颈康丸等对细胞凋亡的影响.同时观察各组椎间盘退变程度的变化.结果模型空白组(C)椎间盘退变明显,与A、D组比较,差异有显著意义(P＜0.05,P＜0.01).正常组D组椎间盘细胞凋亡指数低于其余各组,分别与A、B、C组比较差异有显著意义(P＜0.05);空白对照组C组细胞凋亡指数偏高,A组、B组细胞凋亡指数低于C组,但差异没有显著意义(P＜0.05).结论动物颈椎间盘退变与椎间盘细胞凋亡有关.A组细胞凋亡指数明显低于C组,差异虽无显著意义,却预示芪麝颈康丸有抑制椎间盘细胞凋亡的可能性.

Effect of QiSheJingKang Pill on the Apoptosis of the Cells in Cervical Intervertebral Disc

Objective:To elucidate the molecular mechanism of QiSheJingKang Pill to inhibit the degeneration of intervertebral disc.Methods:48 aged,14 months old,female SD rats were randomly separated into four groups.A,B and C group were experimental model of cervical intervertebral disc degeneration which was established by resection of the posterior paravertebral muscles from cervical vertebrae,D group was the normal control group (sham-surgery).The rats of A and B group were treated with QiSeJing Kang Pill and JingFuKang respectively.Using HE staining and terminal deoxynucleotidy1 transferase-mediated dUTP nick end labeling (TUNEL) technique,we assessed the morphologic state of the discs,and observed the density of apoptosis cells of the intervertebral disc in every group,then compared with each other separately.Results:The degree of intervertebral disc degeneration was significant higher in the discs of C group compared with that in A and D group respectively (P<0.05).The apoptosis index of the discs was significant lower in D group compared with A group,B group and C group separately (P<0.05),and the index was higher in C group than that in A or B group,but there were not significant difference (P<0.05).Conclusion:Apoptosis of the cells in intervertebral discs played a important role during intervertebral disc degeneration.The apoptosis index in A group was lower than that in C group,this predicts it is possible that QiShenJingKang Pill can inhibit the apoptosis of the cells in the intervertebral discs.