大黄酚对青光眼神经退行性病变的保护作用及其信号转导通路
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:


Protective effect of chrysophanol on neural degeneration caused by glaucoma and its mechanism
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的:探讨大黄酚对慢性青光眼大鼠的保护作用及其作用机制。

    方法:采用双极电凝器电凝巩膜表面3组静脉,建立慢性高眼压大鼠模型,分为3组。一组为高眼压模型组,一组为大黄酚低剂量组(25mg/kg),一组为大黄酚高剂量组(50mg/kg),每组各15只,右眼为实验眼,左眼为正常对照眼。连续给药6wk后处死大鼠并摘取眼球,PCR和Western-blot检测PERK和ROCK-1在视网膜中的表达。

    结果:大黄酚高、低剂量组能有效降低大鼠眼内压,与模型眼相比有显著统计学差异(P<0.01)。正常对照视网膜p-PERK蛋白水平表达比较低,青光眼模型组表达显著升高,高、低剂量大黄酚使其表达增高。ROCK-1在视网膜中的表达在青光眼模型组表达最高,各治疗组均可使其表达下降,以高剂量组下降最显著。RT-PCR结果表明,高剂量组大鼠视网膜PERK mRNA水平明显高于模型对照眼; ROCK-1 mRNA水平则显著降低。

    结论:高剂量大黄酚能有效降低青光眼大鼠的眼内压,其作用机制可能是通过激活PERK蛋白磷酸化以调控PERK/ROCK信号转导而发挥其保护作用。

    Abstract:

    AIM:To investigate the effect and mechanism of chrysophanol for rat model with glaucoma.

    METHODS:The glaucoma rat models were made by cauterization of three episcleral veins. Then the glaucoma rats were divided into three groups. Group 1 was the untreated intraocular hypertension group. Group 2 was the low dose of chrysophanol group(25mg/kg). Group 3 was the high dose of chrysophanol group(50mg/kg), 15 rats in each group. The right eyes were the experiment eyes while the left were the control ones. After 6wk treatment, the mRNA and protein of protein kinase-like endoplasmic reticulum kinase(PERK)and Rho kinase 1(ROCK-1)were determined in the retina.

    RESULTS:The chrysophanol reduced intraocular pressure(IOP)of experiment eyes, which was significantly lower than that of control eyes(P<0.01). Compared with the normal group, the p-PERK protein increased significantly in the retina of glaucoma model group and chrysophanol increased the lever of p-PERK protein. The ROCK-1 protein level increased significantly in glaucoma group, it all decreased in these treatment groups, and it decreased significantly in high dose treatment group. Detected by TR-PCR, chrysophanol also could activate the mRNA of PERK and inhibited the mRNA expression of ROCK-1 in a rat model of glaucoma.

    CONCLUSION:These results suggest that chrysophanol can reduce the IOP through the phosphorylation of PERK protein to regulate the PERK/ROCK signaling in glaucoma rat model.

    参考文献
    相似文献
    引证文献
引用本文

胡浩,江灵莉.大黄酚对青光眼神经退行性病变的保护作用及其信号转导通路.国际眼科杂志, 2016,16(1):34-36.

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2015-08-19
  • 最后修改日期:2015-12-14
  • 录用日期:
  • 在线发布日期: 2015-12-28
  • 出版日期: