Angiotensin signaling may modulate neuronal survival, yet its receptor-specific contribution in dopaminergic injury remains unclear. We tested whether activating AT2 receptors protects human SH-SY5Y cells against 6-hydroxydopamine (6OHDA). Cells were exposed for 72 h to angiotensin II (AngII, 600 nM), the selective AT2 agonist CGP42112A (1 µM), or both, and then challenged for 24 h with the LD50 of 6OHDA. Viability was quantified by trypan blue exclusion and propidium iodide flow cytometry. 6OHDA reduced viable cells versus control (844,167 ± 51,011 vs 1,538,125 ± 73,919; p<0.05). CGP42112A increased viable counts (2,350,000 ± 212,132), and CGP42112A+AngII further increased them (2,750,000 ± 353,553; both p<0.05). Flow cytometry confirmed a 56.92% drop in viability with 6OHDA (p<0.0001), partially rescued by CGP42112A (+9.92%; p=0.0031) and more robustly by CGP42112A+AngII (+20.5%; p<0.0001). The AT2 antagonist PD123319 abolished protection, whereas AT1 blockade with losartan did not blunt it, implicating AT2 signaling. Basal exposure to AngII or CGP42112A alone did not alter viability. All values are means ± SEM of three independent experiments; groups were compared by one-way ANOVA with Tukey’s post hoc test. These preliminary data indicate that AT2 receptor activation confers protection in a 6OHDA model of dopaminergic damage and nominates AT2 as a candidate target to bolster neuronal survival in neurodegenerative settings.