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 RESEARCH ARTICLE
Year : 2013  |  Volume : 45  |  Issue : 2  |  Page : 149-154

Nimodipine inhibits N-methyl-N-nitrosourea-induced retinalphotoreceptor apoptosis in vivo


1 Department of Histology and Embryology, College of Basic Medical Science, China Medical University, Shenyang- 110 001; Department of Pharmacology, HE's University, Liaoning Shenyang-110163, People's Republic of China
2 Department of Pharmacology, HE's University, Liaoning Shenyang-110163, People's Republic of China
3 Experimental Teaching Center of Pharmacology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, Liaoning Shenyang-110 016, People's Republic of China
4 Echo Lab, The First Affiliated Hospital of China Medical University, Liaoning Shenyang-110 016, People's Republic of China
5 Department of Histology and Embryology, College of Basic Medical Science, China Medical University, Shenyang- 110 001, People's Republic of China

Correspondence Address:
Gui Yuan Sun
Department of Histology and Embryology, College of Basic Medical Science, China Medical University, Shenyang- 110 001
People's Republic of China
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Source of Support: This work was supported by China Medical University, Conflict of Interest: None


DOI: 10.4103/0253-7613.108297

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Purpose: The purpose of the present study was to investigate the effect of nimodipine (NMD), a calcium channel blocker, on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration. Materials and Methods: 60 mg/kg MNU was given intraperitoneally to 6-week-old female Sprague-Dawley rats, and NMD was injected intraperitoneally for up to 5 days after MNU. The effect of NMD was evaluated by electron microscopy and electroretinography (ERG). Proteins of Bax, Bcl-2, Caspase-3, and mitochondrial membrane potential (MMP) were analyzed with flow cytometry. The expressions of phosphodiesterase (PDE) and Caspase-3 were detected by reverse transcriptase polymerase chain reaction (RT-PCR). Results: The apparent preservation of NMD to the photoreceptor cell was demonstrated by electron microscopy. After NMD treatment, both a- and b-waves of ERG were significantly higher compared with the control group, and had a protective effect on MNU-damaged retinal ERG. Flow cytometric assays showed that NMD decreased the level of Bax and Caspase-3 and increased the activity of Bcl-2 in retina. NMD significantly restored the mitochondrial membrane potential (MMP). RT-PCR analysis demonstrated that NMD treatment significantly decreased mRNA level of Caspase-3, and mRNA level of PDE was clearly upregulated. Conclusions: These data suggest that NMD may regulate the expressions of Bax, Bcl-2, Caspases-3, and PDE, and protection on the functions of retinal cell mitochondria inhibit MNU-induced photoreceptor cell apoptosis and protect retinal function in rats.






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