摘要
目的观察胰岛素联合丹参酮ⅡA抗DPN大鼠周围神经细胞凋亡的作用并初步探讨其机制。方法成年雄性SD大鼠40只,随机分为正常对照组、模型组、胰岛素治疗组和胰岛素+丹参酮ⅡA治疗组,药物干预4周,处死动物后取坐骨神经,检测周围神经细胞凋亡及相关蛋白Bax和Bcl-2、线粒体膜电位、胞浆/线粒体Bax和Cytochrome C表达变化。结果与正常对照组比较,模型组血糖、糖化血红蛋白、细胞凋亡及促凋亡蛋白Bax表达均显著升高,同时线粒体膜电位和抗凋亡蛋白Bcl-2均显著下降;Bax从细胞浆向线粒体转位而Cytochrome C从线粒体向细胞浆转位。胰岛素与丹参酮ⅡA联合比单用胰岛素更能显著改善糖代谢紊乱,抑制周围神经细胞凋亡、升高线粒体膜电位以及抑制Bax和Cytochrome C转位。结论胰岛素联合丹参酮ⅡA能够显著改善DPN大鼠糖代谢紊乱,并能够显著降低周围神经细胞凋亡,其抑制线粒体凋亡途径可能是其抗DPN大鼠周围神经细胞凋亡的主要机制之一。
Objective To investigate the effect of insulin combined with tanshinone ⅡA on peripheral neuropathy in diabetic rats and to elucidate a possible mechanism .Methods Forty male SD rats were randomized equally into control group ,DPN model group , Insulin group and Insulin＋ tanshinoneⅡA group .Four weeks after administration of the corresponding drugs ,cell apoptosis and apoptosis related protein ,such as Bax and Bcl‐2 ,mitochondrial membrane potential and the cytoplasm and mitochondria change of Bax and Cytochrome C amount in sciatic nerve were examined .Results Compared with the control group ,the levels of BG , Hb1Ac ,cell apoptosis and Bax in DPN group significantly increased （P〈0 .01） while mitochondrial membrane potential and Bcl‐2 significantly decreased .In DPN groups ,Bax released from cytoplasm to mitochondrial ,while cytochrome C was opposite with that in the case of Bax .Compared with insulin group ,insulin combined with tanshinoneⅡA group significantly decreased the level of BG and HbA1c ,markedly inhibited the cell apoptosis ,markedly increased the mitochondrial membrane potential and inhibited the translocation of Bax and Cytochrome C .Conclusion Insulin combined with tanshinoneⅡA significantly inhibited the cell apoptosis probably by suppressing the mitochondrial apoptotic pathways .
出处
《西北药学杂志》
CAS
2015年第6期716-720,共5页
Northwest Pharmaceutical Journal
