Objective To explore the effect of Nec-1 on cell viability and genes of apoptosis and autophagy of the aluminun-induced nerve cells.
Methods We conducted the study by means of cell culture in vitro, producing aluminum injury model by Al3+(2 mmol/L), then intervented cell death by Necrostatin-1(Nec-1), and investigated the Nec-1's role toward the Alinduced nerve cells using CCK-8 and RT-PCR methods.
Results Cell viability of Nec-1(30 μmol/L)group had statistically difference(P < 0.05), whereas of the Nec-1(60 μmol/L)and Nec-1(90 μmol/L)groups had very significant difference(P < 0.01)as compared with Al3+(2 mmol/L)exposure group(control).The RT-PCR demonstrated that the expression of caspase-3 gene in Al3+(2 mmol/L)group(control)was 0.98& #177;0.120, but that of Nec-1(60 μmol/L)and Nec-1(90 μmol/L)groups were 0.50& #177;0.077 and 0.44& #177;0.050 respectively. Compared with the control group, the expression of caspase-3 gene of the latter two groups decreased with statistical significance(P < 0.01). The expression of LC3-Ⅱ gene of Al3+(2 mmol/L)group(control)was 1.82& #177;0.047, but that of Nec-1(60 μmol/L)and Nec-1(90 μmol/L)groups were 1.00& #177;0.022 and 0.97& #177;0.035 respectively. Compared with the control group, the expression of LC3-Ⅱ gene of the latter two groups also decreased with statistical significance(P < 0.01).
Conclusion In summary, Nec-1 can increase cell viability of Al-induced nerve cells, and decrease the expression of autophagy and apoptosis genes.
DownLoad: