Agmatine protects Müller cells from high-concentration glucose-induced cell damage via N-methyl-D-aspartic acid receptor inhibition

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Abstract

Neural injury is associated with the development of diabetic retinopathy. Muller cells provide structural and metabolic support for retinal neurons. High glucose concentrations are known to induce Muller cell activity. Agmatine is an endogenous polyamine, which is enzymatically formed in the mammalian brain and has exhibited neuroprotective effects in a number of experimental models. The aims of the present study were to investigate whether agmatine protects Muller cells from glucoseinduced damage and to explore the mechanisms underlying this process. Lactate dehydrogenase activity and tumor necrosis factoralpha mRNA expression were significantly reduced in Muller cells exposed to a high glucose concentration, following agmatine treatment, compared with cells not treated with agmatine. In addition, agmatine treatment inhibited glucoseinduced Muller cell apoptosis, which was associated with the regulation of Bax and Bcl2 expression. Agmatine treatment suppressed glucoseinduced phosphorylation of mitogenactivated protein kinase (MAPK) protein in Muller cells. The present study demonstrated that the protective effects of agmatine on Muller cells were inhibited by NmethylDaspartic acid (NMDA). The results of the present study suggested that agmatine treatment protects Muller cells from highconcentration glucoseinduced cell damage. The underlying mechanisms may relate to the antiinflammatory and antiapoptotic effects of agmatine, as well as to the inhibition of the MAPK pathway, via NMDA receptor suppression. Agmatine may be of use in the development of novel therapeutic approaches for patients with diabetic retinopathy.

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Han, N., Yu, L., Song, Z., Luo, L., & Wu, Y. (2015). Agmatine protects Müller cells from high-concentration glucose-induced cell damage via N-methyl-D-aspartic acid receptor inhibition. Molecular Medicine Reports, 12(1), 1098–1106. https://doi.org/10.3892/mmr.2015.3540

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