ArticleDrug design, development and therapy2014
Tetrandrine protects mouse retinal ganglion cells from ischemic injury.
Article in Drug design, development and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Protective effect of Tetrandrine on optic nerve by inhibiting glial activation through NF-κB pathway.Heliyon · 2024Article
- Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Melatonin Alleviates Retinal Ischemia-Reperfusion Injury by Inhibiting p53-Mediated Ferroptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Recent Progress in Chitosan-Based Nanomedicine for Its Ocular Application in Glaucoma.Pharmaceutics · 2023Review
- Chitosan-coated bovine serum albumin nanoparticles for topical tetrandrine delivery in glaucoma:Drug delivery · 2022Article
- Inhibiting multiple forms of cell death optimizes ganglion cells survival after retinal ischemia reperfusion injury.Cell death & disease · 2022Article
- Role of glia in optic nerve.Progress in retinal and eye research · 2021Review
- CRISPR/Cas9‒Mediated Tspo Gene Mutations Lead to Reduced Mitochondrial Membrane Potential and Steroid Formation in MA-10 Mouse Tumor Leydig Cells.Endocrinology · 2018Article
- The role of microglia in the progression of glaucomatous neurodegeneration- a review.International journal of ophthalmology · 2018Review
- Pioglitazone ameliorates retinal ischemia/reperfusion injuryInternational journal of ophthalmology · 2017Article
- Papaverine inhibits lipopolysaccharide-induced microglial activation by suppressing NF-κB signaling pathway.Drug design, development and therapy · 2016Article
- Visual detection of glial cell line-derived neurotrophic factor based on a molecular translator and isothermal strand-displacement polymerization reaction.Drug design, development and therapy · 2015Article
- Neuroprotective therapies for glaucoma.Drug design, development and therapy · 2015Review
- Tetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-κB and ERK signaling pathways in BV2 cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
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.
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