丙泊酚干预对大鼠视神经损伤的影响及机制研究
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NeuroProtective mechanisms of ProPofol to retinal ganglion cells in a Partial oPtic nerve crush rat model
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    目的 探讨大鼠视神经损伤后丙泊酚干预对损伤视神经及视网膜神经节的影响及机制。方法 SD大鼠67只,随机取20只为正常组,不予任何处理。余行视神经钳夹法造模,造模成功42只纳入实验。随机分为:模型对照组和丙泊酚组,各21只/组。造模后4 d,以TUNEL法检测大鼠视网膜和视神经细胞凋亡,造模后7 d,RT-PCR、Western-blot检测视网膜和视神经节细胞组织Caspase-3、BCL-2基因和蛋白表达。造模后14 d,行闪光视觉诱发电位检测,处死大鼠取眼球,观察各组大鼠视网膜和视神经的病理形态,行视网膜神经节细胞计数。结果 造模后4 d,丙泊酚组视网膜神经节细胞凋亡数量明显低于模型对照组(P<0.05),造模后7 d与模型对照组相比,丙泊酚组Caspase-3的表达显著降低(P<0.05);BCL-2的表达显著升高(P<0.05)。造模后14 d,荧光金阳性RGC数:模型对照组最少,丙泊酚组较多,正常组最多,且各组之间差异有统计学意义(P<0.05)。丙泊酚组大鼠闪光视觉诱发电位伏期较模型对照组大鼠短(P<0.05)、波幅明显高于模型对照组(P<0.05)。结论 丙泊酚干预通过减少大鼠视神经钳夹后RGCs的凋亡,降低视网膜Caspase-3的表达,升高BCL-2的表达,对视神经损伤起到保护作用。

    Abstract:

    Objective To investigate the Protective effect of propofol on the retinal ganglion cells of the rat optic nerve crush model. Methods 67 SD rats. Randomly selected 20 rats, don't do any processing for the normal group. With more than 47 rats optic clamps for optic nerve contusion model, legal system building 5 failure, success of 42 rats were randomly divided into the optic nerve damage and propofol group, 21/group. Will not be any treatment after optic nerve injury group building, 4 hours after propofol group for propofol therapy. After 4 days of successful modeling, the apoptosis of retinal ganglion cells were detected by TUNEL staining. After 7 days of successful modeling, the expression of Caspase-3, BCL-2 in retina and optic nerve cells of rats were detected by RT-PCR and Western-blot.After 14 days of successful modeling, The amplitude and latent period of P1 wave of flash visual evoked potential were detected.The animals were sacrificed and the optic nerve was taken to observe the pathological morphology of retina and optic nerve in rats, and the retinal ganglion cells (RGC) were counted. Results After 4 days of successful modeling,the apoptosis of the propofol group was significantly lower than that of the optic nerve injury group (P<0.05).After 7 days of successful modeling,the expression of Caspase-3 in the propofol group was significantly lower than that in the propofol group (P<0.05), the expression of BCL-2 in the propofol group was significantly higher than that in the propofol group (P<0.05).After 14 days of successful modeling, FG Positive RGC numbers:normal group>propofol group> optic nerve injury group and between groups difference was statistically significant (P<0.05). The flash visual evoked potential of the rats in propofol group was significantly shorter than that in the optic nerve injury group (P<0.05) and the amplitude of the visual evoked Potential was significantly higher than that of the optic nerve injury group (P<0.05).Conclusions Propofol treatment can through an early reduction in rats after optic nerve crush RGCs apoptosis, decreased Caspase-3 expression, increased BCL-2 expression and improve number of optic nerve crush of RGCs survival.

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李学东,陈家康,覃军,麦用军,肖振勇.丙泊酚干预对大鼠视神经损伤的影响及机制研究[J].中国比较医学杂志,2016,26(7):42~47.

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  • 最后修改日期:2015-09-01
  • 在线发布日期: 2016-07-28
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