Protective role and related mechanism of Gnaq in neural cells damaged by oxidative stress

<span class="paragraphSection"><div class="boxTitle">Abstract</div>Gnaq is a member of G protein family and is rich in brain tissue. It has attracted the attention of many researchers in melanoma due to its high ratio of mutation. We have previously reported that the expression level of Gnaq in the mouse forebrain cortex was significantly decreased with age. Oxidative stress (OS) is the main cause leading to brain aging and related diseases. The roles and mechanisms of Gnaq in antioxidation in the brain have not been fully explored. In the present study, gene recombinant technique and lentivirus transfection technique were used to generate a Gnaq-overexpression cell model (Gnaq-SY5Y) coupled with H₂O₂ to build an OS model. The viability of cells, concentration of reactive oxygen species (ROS), apoptosis-related proteins (Bcl-2 and Bax), and signal pathways (NF-κB and Erk1/2) were compared between model cells and control cells. Results showed that the antioxidative ability of Gnaq-SY5Y cells was significantly improved. Concomitantly, the ROS level in Gnaq-SY5Y cells was significantly decreased whether the cells were subject to or not to H₂O₂ treatment. Anti-apoptotic protein Bcl-2 was up-regulated and apoptosis-promoting protein Bax was down-regulated in Gnaq-SY5Y cells after treatment with H₂O₂. NF-κB and phosphorylated Erk1/2 (p-Erk1/2) was significantly down-regulated in Gnaq-SY5Y cells. H₂O₂ treatment decreased Gnaq expression but increased NF-κB and p-Erk1/2 expressions in Gnaq-SY5Y cells. It is therefore concluded that Gnaq plays a pivotal role in antioxidation in neural cells. A possible mechanism for this would be that the overexpressed Gnaq inhibits the cellular damaging effect mediated by NF-κB and Erk1/2 signal pathways.</span>

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