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Updated: May 1, 2026
Morphometric Analyses of Retinal Sections
Published on: February 19, 2012
Tetrandrine protects mouse retinal ganglion cells from ischemic injury
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.
