Tetrandrine protects mouse retinal ganglion cells from ischemic injury
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Updated: May 1, 2026
Morphometric Analyses of Retinal Sections
Published on: February 19, 2012
Weiyi Li1, Chen Yang2, Jing Lu2
1Department of Ophthalmology, Peking University Third Hospital, Peking University Eye Center, Beijing, People's Republic of China ; Department of Neural and Behavioral Sciences, Penn State University, Hershey, PA, USA.
Abstract:
This study aimed to determine the protective effects of tetrandrine (Tet) on murine ischemia-injured retinal ganglion cells (RGCs). For this, we used serum deprivation cell model, glutamate and hydrogen peroxide (H2O2)-induced RGC-5 cell death models, and staurosporine-differentiated neuron-like RGC-5 in vitro. We also investigated cell survival of purified primary-cultured RGCs treated with Tet. An in vivo retinal ischemia/reperfusion model was used to examine RGC survival after Tet administration 1 day before ischemia. We found that Tet affected RGC-5 survival in a dose- and time-dependent manner. Compared to dimethyl sulfoxide treatment, Tet increased the numbers of RGC-5 cells by 30% at 72 hours. After 48 hours, Tet protected staurosporine-induced RGC-5 cells from serum deprivation-induced cell death and significantly increased the relative number of cells cultured with 1 mM H2O2 (P<0.01). Several concentrations of Tet significantly prevented 25-mM-glutamate-induced cell death in a dose-dependent manner. Tet also increased primary RGC survival after 72 and 96 hours. Tet administration (10 μM, 2 μL) 1 day before retinal ischemia showed RGC layer loss (greater survival), which was less than those in groups with phosphate-buffered saline intravitreal injection plus ischemia in the central (P=0.005, n=6), middle (P=0.018, n=6), and peripheral (P=0.017, n=6) parts of the retina. Thus, Tet conferred protective effects on serum deprivation models of staurosporine-differentiated neuron-like RGC-5 cells and primary cultured murine RGCs. Furthermore, Tet showed greater in vivo protective effects on RGCs 1 day after ischemia. Tet and ciliary neurotrophic factor maintained the mitochondrial transmembrane potential (ΔΨm) of primary cultured RGCs and inhibited the expression of activated caspase-3 and bcl-2 in ischemia/reperfusion-insult retinas.
Insights
Tetrandrine (Tet) protects retinal ganglion cells (RGCs) from injury in vitro and in vivo. This compound demonstrated significant neuroprotective effects against various cell death models and ischemia/reperfusion injury in mice.
Area of Science:
- Neuroscience
- Ophthalmology
- Pharmacology
Background:
- Retinal ganglion cells (RGCs) are crucial for vision and vulnerable to ischemic injury.
- Developing effective neuroprotective strategies for RGCs is essential for treating vision loss.
Purpose of the Study:
- To investigate the protective effects of tetrandrine (Tet) against RGC injury.
- To evaluate Tet's efficacy in both in vitro and in vivo models of RGC damage.
Main Methods:
- Utilized RGC-5 cell death models induced by serum deprivation, glutamate, and hydrogen peroxide (H2O2).
- Assessed Tet's effects on primary cultured murine RGCs and staurosporine-differentiated RGC-5 cells.
- Employed an in vivo retinal ischemia/reperfusion model in mice, administering Tet prior to injury.
Main Results:
- Tetrandrine demonstrated dose- and time-dependent protection of RGC-5 cells.
- Tet significantly increased RGC survival in serum deprivation, H2O2, and glutamate-induced cell death models.
- In vivo, Tet administration before ischemia reduced RGC layer loss, indicating enhanced RGC survival.
Conclusions:
- Tetrandrine confers significant protective effects on RGCs against various injury insults.
- Tetrandrine shows promise as a therapeutic agent for preventing RGC damage in conditions like ischemic retinopathy.
