Protective mechanism of salidroside on retinal ganglion cells in diabetic rats

XING Shuang; ZHAO Wei; LIU Li; GUO Ying; GUO Shuo

doi:10.11659/jjssx.07E024138

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Protective mechanism of salidroside on retinal ganglion cells in diabetic rats

Basic Research | 更新时间：2025-07-31

- Protective mechanism of salidroside on retinal ganglion cells in diabetic rats
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 34, Issue 8, Pages: 675-679(2025)
- 作者机构：
  
  秦皇岛市第一医院眼科，河北秦皇岛 066000
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.07E024138
  CLC： R285.5
- Received：25 July 2024，
  
  Published：25 August 2025
- 稿件说明：
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邢爽,赵伟,刘丽等.红景天苷对糖尿病大鼠视网膜神经节细胞的保护机制研究[J].局解手术学杂志,2025,34(08):675-679.

XING Shuang,ZHAO Wei,LIU Li,et al.Protective mechanism of salidroside on retinal ganglion cells in diabetic rats[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(08):675-679.
邢爽,赵伟,刘丽等.红景天苷对糖尿病大鼠视网膜神经节细胞的保护机制研究[J].局解手术学杂志,2025,34(08):675-679. DOI： 10.11659/jjssx.07E024138.

XING Shuang,ZHAO Wei,LIU Li,et al.Protective mechanism of salidroside on retinal ganglion cells in diabetic rats[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(08):675-679. DOI： 10.11659/jjssx.07E024138.

摘要

目的

探讨红景天苷对糖尿病大鼠视网膜神经节细胞（RGC）的保护作用及其可能的分子机制。

方法

选取45只雄性SD大鼠并将其随机分为对照组、模型组和红景天苷组，每组15只。模型组和红景天苷组大鼠均构建糖尿病模型，待建模成功后，红景天苷组大鼠每日给予50 mg/kg红景天苷灌胃，连续12周，模型组大鼠不再做任何处理。对照组大鼠给予等量生理盐水灌胃，连续12周。每隔4周测量大鼠空腹血糖。实验结束后，统计各组大鼠存活率；病理HE染色观察大鼠视网膜组织病理改变，并进行RGC计数；ELISA法检测大鼠视网膜组织中活性氧(ROS)、超氧化物歧化酶（SOD）、丙二醛（MAD）及过氧化氢酶（CAT）含量；Western blot检测Keap1-Nrf2/HO-1通路相关蛋白血红素氧合酶-1（HO-1）、Kelch样ECH关联蛋白1（Keap1）及核因子E2相关因子2（Nrf2）的表达。

结果

3组大鼠存活率比较，差异无统计学意义（

0.05）。对照组大鼠各时间点空腹血糖水平均在正常范围波动；模型组和红景天苷组大鼠空腹血糖水平始终高于对照组（

0.05）；红景天苷组大鼠空腹血糖水平随时间延长逐渐降低（

0.05）。与对照组相比，模型组大鼠的视网膜厚度变薄，细胞排列出现明显紊乱现象，内、外核层中伴随有明显的水肿，有空泡现象出现；红景天苷组大鼠视网膜组织病理改变较模型组改善。与对照组相比，模型组大鼠视网膜组织中ROS、MAD含量及Keap1、Nrf2蛋白表达明显较高（

0.05），CAT、SOD含量及RGC数量、HO-1蛋白表达明显较低/少（

0.05）；给予红景天苷干预后，红景天苷组大鼠各氧化应激因子含量、RGC数量及Keap1、HO-1蛋白表达较模型组均明显逆转（

0.05）。

结论

给予红景天苷干预能够减轻糖尿病大鼠视网膜氧化应激反应，缓解RGC损伤，可能通过调控Keap1-Nrf2/HO-1信号通路发挥作用。

Abstract

Objective

To explore the protective effect of salidroside on retinal ganglion cells （RGC） in diabetic rats and its possible molecular mechanism.

Methods

Forty-five male SD rats were selected and randomly divided into the control group， the model group and the salidroside group， with 15 rats in each group.Diabetes models of rats were established in both the model group and the salidroside group. After successful modeling， rats in the salidroside group were given 50 mg/kg salidroside by gavage daily for 12 consecutive weeks， while rats in the model group received no further treatment. Rats in the control group were given the same amount of normal saline by gavage for 12 consecutive weeks.The fasting blood glucose of rats was detected every 4 weeks.After the experiment， the survival rate of rats in each group was calculated. Pathological HE staining was used to observe the pathological changes of retinal tissue in rats， and RGC counting was performed.The contents of reactive oxygen species （ROS）， superoxide dismutase （SOD）， malondialdehyde （MAD） and catalase （CAT） in the retinal tissue of rats were detected by ELISA.Western blot was used to detect the expressions of heme oxygenase-1 （HO-1）， Kelch-like ECH associated protein 1 （Keap1）， and nuclear factor E2-related factor 2 （Nrf2） in the KEAP1-NrF2 /HO-1 pathway.

Results

There was no statistically significant difference in the survival rate among the three groups of rats （

0.05）.The fasting blood glucose levels of rats in the control group fluctuated within the normal range at each time point. The fasting blood glucose levels of rats in the model group and the salidroside group were consistently higher than those in the control group（

0.05）.The fasting blood glucose level of rats in the salidroside group gradually decreased over time （

0.05）.Compared with the control group， the retinal thickness of rats in the model group became thinner， the cell arrangement showed obvious disordered phenomena， and there was obvious edema in the inner and outer nuclear layers and vacuole phenomena.The pathological changes of retinal tissue of rats in the salidroside group were improved compared with those in the model group.Compared with the control group， the contents of ROS and MAD and the p

rotein expressions of Keap1 and Nrf2 in the retinal tissues of rats in the model group were significantly higher（

0.05），while the contents of CAT and SOD， the number of RGC and the protein expression of HO-1 were significantly lower/less（

0.05）.After intervention with salidroside，the contents of each oxidative stress factor， the number of RGC， and the protein expressions of Keap1 and HO-1 of rats in the salidroside group were significantly reversed compared with the model group（

0.05）.

Conclusion

Intervention with salidroside can alleviate the oxidative stress response in the retina of diabetic rats and relieve RGC injury，which may exert its effect through the Keap1-Nrf2/HO-1 signaling pathway.

关键词

Keywords

references

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