Effect of maca water extract on cobalt chloride-induced hypoxia injury in PC12 cells

  Objective  To explore the effect of maca water extract on cobalt chloride (CoCl₂)-induced hypoxia injury in PC12 cells.

  Methods  PC12 cells were exposed to CoCl₂ at different dose and for different time duration to set up the chemical hypoxia injury model. Cell viability was determined with cell counter kit-8 (CCK-8). The activity of superoxide dismutase (SOD) and nitric oxide synthase (NOS), the quantity of malondialdehyde (MDA), nitric oxide (NO), and lactate dehydrogenase (LDH) in culture medium were measured with kit assay. The intracellular NO was detected using a fluorescent probe (2′,7′-dichlorodihydrofluorescein diacetate, DCFH-DA). The cell apoptotic rate was determined with annexin V-FITC/PI staining.

  Results  Compared with that of the control cells, the viability of PC12 cells exposed to CoCl₂ was inhibited significantly in a dose- and time-dependent manner. Significantly decreased cell viability rate (51.55% ± 2.71%) and increased of SOD and NOS and content of MDA, NO, and LDH in culture medium were observed in PC12 cells exposed to 300 μmol/L CoCl₂ for 24 hours in comparison with those of the control cells. For the PC12 cells treated with maca water extraction of 60 and 120 μg/ml, the viability rate increased obviously (63.99% ± 3.24% and 69.95% ± 2.25%) and the NOS activity and content of MDA, NO, and LDH in culture medium decreased compared to the CoCl₂ exposed PC12 cells. Obviously increased intracellular NO content (61.5% ± 5.7%) and cell apoptotic rate (41.33% ± 3.83%) were observed in the PC12 cells treated with 500 μmol/L CoCl₂ for 24 hours compared to the control cells. Obviously decreased intracellular NO content (36.50% ± 4.70% and 33.40% ± 3.80%) and cell apoptotic rate (34.87 ± 2.50% and 31.33% ± 3.44%) were observed in the PC12 cells treated with maca water extraction of 60 and 120 μg/ml compared to those in the cells exposed to 500 μmol/L CoCl₂.

  Conclusion  Maca water extract has protective effect on cobalt chloride-induced hypoxia injury by inhibiting NO generation, oxidative stress and cell apoptosis in PC12 cells.