| Neurodegenerative diseases are often associated with spontaneous apoptosis. During hypoxia-ischemic brain injury, intracellular Ca2+ is overloaded, which can cause neuronal apoptosis. Recent findings indicated that Mg2+ could be the protect factor for the injury process by regulating cellular metabolism and function regulation. It also has positive protection effect in neuronal cells. Recent studies demonstrated that the concentration of Mg2+ in serum decreased remarkably after brain injury. Animal experiments, have proved that supplement of Mg2+ could alleviate brain damage, improve neuron function, and reduce neuronal apoptosis.Animal experiments and epidemiology investigations indicated that Mg2+ was deficit in aged animals. Aging also led to the decrease of absorption of Mg2+. In addition, Mg2+ deficiency could influence membranous integrality and its function, enhance susceptibility of oxygenation, thereby induce cardiovascular diseases as well as accelerate process of aging. Further studies are necessary to understand the protective effect of Mg2+ in neuronal apoptosis.1. The effect of Mg2+ on apoptosis in cells cultured in serum free mediumSH-Sy5Y cells were incubated in serum free medium after adding Mg2+ for 2 h. The cells viability was measured by MTT assay. Apoptosis was analyzed with Hochest33342 staining. The expression of NR2B was determined by fluorescence real-time PCR. The results showed that the viability of SH-Sy5Y cells was decreased after cultured in the medium without serum. We have demonstrated that the level of NR2B mRNA was decreased. However, Mg2+ could partial block the apoptosis of the neuronal cells.2. The effect of Mg2+ on apoptosis in aged cellular modelSH-Sy5Y cells were treated with H2O2 after adding Mg2+ for 2 h. The cells viability was measured by MTT assay. Apoptosis was analyzed with Hochest33342 staining. The expression of NR2B was determined by fluorescence real-time PCR. |