Ginsenoside Rg1 Prevents H₂O₂-induced Lens Opacity

ABSTRACT

Purpose: To investigate the potential function of Ginsenoside Rg1 (Rg1) against lens opacification.

Methods: Eyeballs from adult Sprague-Dawley rats were enucleated and lenses were dissected for ex vivo culture under H₂O₂ treatment. Water soluble protein (WSP) content, the level of superoxide dismutase (SOD), total glutathione (GSH), and reduced GSH were detected by indicated assays. Cell viability was performed by Cell Counting Kit-8 experiment.

Results

Exposure of 0.2 mM H₂O₂ in lenses resulted in obvious cloudiness and typical pathological changes of cataract such as rupture of the lens capsule, degenerative lens epithelial cells (LECs), etc. Rg1 effectively prevented lens opacity caused by H₂O₂. After Rg1 treatment, lens WSP content, the level of SOD, total GSH, and reduced GSH were increased, while the level of MDA and oxidized GSH were decreased. In addition, MDA concentration of lens by Rg1 treatment only was found to be lower than the controls. Rg1 attenuated H₂O₂-induced cell injury at the concentration of 0.4 mM that it elevated cell activity, and peaked at 0.6 mM.

Conclusions

This study demonstrated that Rg1 might have the capability to protect lens against oxidative stress-induced cataract, at least by local administration.

Abbreviations: LECs: lens epithelial cells; Rg1: Ginsenoside Rg1; SD: Sprague-Dawley; ROS: reactive oxygen species; SOD: Superoxide Dismutase; GSH: glutathione; MDA: Malonediadehyde; H₂O_2: Hydrogen peroxide

KEYWORDS:

• Cataract
• lens opacity
• antioxidant
• ginsenoside Rg1
• hydrogen peroxide

Author contributions

G.Z., M.Z., F.Y.: substantial contributions to the conception or design of the work; or the acquisition, analysis, or interpretation of data for the work. L.K.: drafting the article. H.G.: final approval of the version to be published. G.Z., M.Z., F.Y., L.K., and H.G.: agreement to be accountable for all aspects of the work including questions related to the accuracy.

Disclosure statement

We declare that we have no conflict of interest.

Statement of ethics

The study protocol was approved by Committee on Animal Research of Nantong University (No. S20200313-006).

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

This work was supported by the National Science Foundation of China (81974129 and 81500706), the Postdoctoral Science Foundation of China (2020M671562), the Postdoctoral Science Foundation of Jiangsu Province (2020Z318), the Science and Technology Project of Nantong Municipality (JCZ19088, MS22019012 and MS12019030, Nantong, Jiangsu, China), and the Project of Nantong Municipal Health Commission (QA2019061, Nantong, Jiangsu, China).